AM ER IC AN JOURNAL OF OT OLARYNGOLOGY – H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 3 03– 3 0 5
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Acute vocal fold dystonic reaction to propofol: a case report☆,☆☆ Rachel C. Steckelberg, MD, MPH a,⁎, David Tsiang, MD a , Kelly Pettijohn, MD b , Abie Mendelsohn, MD b , Nir Hoftman, MD a a b
Department of Anesthesiology and Perioperative Care, UCLA Ronald Reagan Medical Center, 757 Westwood Plaza, Los Angeles, California Department of Head and Neck Surgery, UCLA Ronald Reagan Medical Center, 757 Westwood Plaza, Los Angeles, California
ARTI CLE I NFO
A BS TRACT
Article history:
A 67-year old male underwent uneventful robotic-assisted thoracoscopic resection of a
Received 4 November 2014
solitary pulmonary fibrous tumor. Immediately following extubation at the completion of the surgical procedure, the patient developed respiratory distress that did not resolve with treatment. Benadryl provided only temporary relief. Midazolam and hydromorphone were given for anxiolysis and analgesia respectively, which provided transient relief of symptoms. Propofol was given to decrease upper airway reflexes. Adequate reversal from nondepolarizing neuromuscular blockade was confirmed with nerve stimulator. A flexible laryngoscope was introduced nasally to visualize the vocal cords, which revealed intermittent tremulousness of the vocal cords, adduction of bilateral vocal cords to the midline, and minimal to absent opening with inspiration, without any apparent injury or blood, saliva, or vomit noted in or around the glottic opening. The patient was then given diazepam and reintubated. Given the patient's history of difficulty breathing after previous surgery and the lack of vocal cord movement, dystonic reaction to propofol was suspected. The patient remained intubated for two hours in the post-anesthesia care unit before being extubated uneventfully. © 2015 Elsevier Inc. All rights reserved.
1.
Introduction
Propofol is the most commonly used anesthetic induction agent. At present, there have been a limited number of described cases of propofol-related seizure-like and/or dystonic reactions [1,2]. Dystonic reactions have most frequently been reported as jerky movements of the extremities or opisthotonos [2]. Despite
☆
numerous case reports, no clear consensus regarding the neurogenic origin and therapeutic strategy for these adverse reactions has been reached. This report describes a case of vocal fold dystonia, observed as postoperative stridor. Given the widespread use of propofol, this treatable and potentially lifethreatening medication reaction should be considered when assessing any patient with postoperative stridor and abnormal
Disclosures: The authors have no financial or other competing interests to disclose. Author contributions: All authors had full access to all of the data in the study and take full responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: All authors. Acquisition of data: RS, DT, KP. Analysis and interpretation of data: All authors. Drafting of the manuscript: RS, DT, KP. Critical revision of the manuscript for important intellectual content: All authors. Study supervision: NH, AM. ⁎ Corresponding author at: Ronald Reagan Medical Center, 757 Westwood Plaza, Suite 3304, Los Angeles, California 90025, USA. Tel.: +1 310 267 8655; fax: +1 310 825 6301. E-mail address: [email protected] (R.C. Steckelberg).
☆☆
http://dx.doi.org/10.1016/j.amjoto.2014.11.006 0196-0709/© 2015 Elsevier Inc. All rights reserved.
304
AM ER IC AN JOURNAL OF OT OLA RYNGOLOGY– H E A D A N D NE CK M E D ICI N E AN D S U RGE RY 3 6 (2 0 1 5) 3 03 – 3 0 5
vocal fold motion in a patient who has been given propofol. It is important to review cases such as this to determine an appropriate therapeutic treatment plan, as well as to identify potential strategies to prevent further adverse outcomes.
2.
Materials and methods
2.1.
Initial case presentation
A 67-year old 85-kilogram man underwent an uneventful thoracoscopic robotic assisted left upper lobe wedge resection of a solitary fibrous tumor under general anesthesia. The patient's medical history included well-controlled hypertension, coronary artery disease (status post drug-eluting stent placement), chronic atrial fibrillation, and a chronic left basal ganglia lacunar infarct. The patient denied drug allergies, although he did describe an episode of “difficulty breathing” after a previous inguinal hernia surgery under sedation using propofol that resolved with an unknown “reversal agent”. During this thoracic procedure the patient was intubated atraumatically with a 39Fr double lumen endotracheal tube for the duration of the five-hour operation. On indirect video laryngoscopy, the pharmacologically paralyzed vocal cords appeared without any visible pathology. Immediately after extubation, the patient developed respiratory distress and stridor that did not resolve with jaw thrust and continuous positive airway pressure, the standard treatments for suspected laryngospasm. Midazolam 3 mg and hydromorphone 0.4 mg were given for anxiolysis and analgesia respectively, which provided transient relief of symptoms. Propofol 20 mg was given to decrease upper airway reflexes. Adequate reversal from nondepolarizing neuromuscular blockade was confirmed with nerve stimulator. The patient's preoperative calcium level was within normal limits. The patient's oropharynx had been thoroughly suctioned prior to extubation and he was alert, oriented, and following commands as we attempted our various interventions. A flexible laryngoscope was introduced nasally to visualize the vocal cords, which revealed intermittent tremulousness of the vocal cords, adduction of bilateral vocal cords to the midline, and minimal to absent opening with inspiration, without any apparent injury or blood, saliva, or vomit noted in or around the glottic opening.
3.
Results
A dystonic reaction to propofol was suspected after ruling out other causes of stridor and considering both the pattern of vocal cord movement and the patient's previous history of respiratory distress following surgery under propofol sedation. Diphenhydramine 50 mg was administered for its anticholinergic properties since the first agent of choice (benztropine) was not available in our hospital in intravenous formulation. Given that this treatment proved temporary as the previous ones had, the decision was made to re-intubate the patient and wake him slowly in the post-anesthesia care unit (PACU), to provide time for the effects of the propofol to resolve spontaneously. The patient was thus given diazepam 10 mg (for both sedation/anxiolysis and for treatment of the dystonic reaction), ketamine 50 mg (for a non-propofol
induction), succinylcholine 100 mg (for paralysis), and then reintubated. The patient was transported to the PACU, where he remained sedated for 2 hours before being awakened and extubated uneventfully, without any return of the dystonia. The patient was monitored overnight for precaution and discharged home the next day.
4.
Discussion
Stridor is a relatively common postoperative finding that warrants prompt evaluation. When consulted regarding a patient with such symptoms, diagnoses such as laryngeal edema, laryngospasm, and vocal cord immobility are typically considered. In the case of abnormal bilateral vocal fold mobility on fiberoptic laryngoscopy, the following etiologies are considered: surgical trauma related to local procedures such as thyroidectomy/parathyroidectomy etc. (an estimated 44% of observed cases), malignancy (17%), endotracheal intubation (15%), neurologic disease (12%), and idiopathic causes (12%) [1]. In the immediate postoperative patient, the expected causes of stridor include laryngeal edema, laryngospasm, cord paralysis related to recurrent laryngeal nerve (RLN) damage from local surgery, or intubation-related causes. Intubation-related causes include arytenoid dislocation, RLN damage from anterior displacement of the cricoid cartilage relative to the thyroid cartilage, extreme hyperextension of the neck resulting in vagus nerve stretch injury, or excessive endotracheal tube cuff pressure that compresses the RLN as it enters the larynx. Short-term intubation most frequently results in a unilateral vocal cord palsy, with an estimated incidence of 1 per 1000 procedures [3]. Laryngospasm is caused by excessive stimulation of the laryngeal adductor reflex mediated by the superior laryngeal nerve. It is a common etiology of perioperative stridor characterized by upper airway obstruction, usually lasting less than 1–2 minutes, and is responsive to medications that would decrease stimulation of the reflex (such as lidocaine or paralytic agents). In the case of our patient, standard methods of management of laryngospasm were ineffective, leading to consideration of alternative etiologies [3]. Numerous cases of generalized dystonia related to propofol, the most common induction agent presently used, have been documented in the literature, and summarized in a case report by Schramm and Orser [1]. In their report, cases demonstrating both seizure-like reaction to propofol and dystonic reaction were described. Interestingly, 17 of the total 21 dystonic-type cases reported were in females, predominantly under the age of 30. The most common movements described were jerky limb/trunk movements and opisthotonos [3]. Previous reports have documented cases of laryngeal dystonia in reaction to antipsychotics, but no previous case of vocal cord dystonia related to propofol has been described [2]. Propofol exerts its hypnotic effects through modulation of GABAA receptors, which are ligand-gated ion channels coupled to a central chloride channel that produce an inhibitory effect when they bind the neurotransmitter GABA, which acts primarily in the cerebral cortex. Simultaneously, neuroexcitation, in the form of myoclonus, tremor, dystonic
AM ER IC AN JOURNAL OF OT OLARYNGOLOGY – H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 3 03– 3 0 5
posturing, etc. may be secondary to the depression of subcortical areas of the brain [2]. Specifically, an in vivo study in mice suggested that propofol might increase the motor manifestations, e.g. opisthotonos and athetoid movements, of agonists acting at glycine receptors. Glycine is a central nervous system amino acid that acts as an inhibitory neurotransmitter primarily in subcortical areas of the brain [4], which would include the basal ganglia. An imbalance in the dopaminergic and cholinergic pathways that integrate areas of the cerebral cortex with the basal ganglia may explain the hyper- and hypo-kinetic symptoms of movement disorders such as Parkinson's disease and dystonia. Normally, activation of D2 dopamine receptors in the striatum, which contains projection neurons to the basal ganglia, decreases interneuron excitation and reduces their release of acetylcholine. Furthermore, muscarinic autoreceptors expressed on these interneurons provide feedback control of acetylcholine release. Some forms of primary dystonia (i.e. sporadic or genetic) have been found to be the result of aberrant mutations in enzymes involved in dopamine biosynthesis, e.g. tyrosine hydroxylase and GTP cyclohydrolase. In other forms of dystonia, an alteration in D2 receptor coupling resulted in an increase in interneuron spiking and hence acetylcholine release. In both cases, the underlying theme seems to be an excess of acetylcholine release, which might explain the efficacy of anticholinergic medications in the treatment of dystonia [1,5]. A review of the literature shows dystonic reactions to propofol have been successfully treated with a number of medications. In particular, Schramm and Orser found benztropine 2 mg IV to be successful in treating a dystonic reaction to propofol, since it had a shorter recovery time with fewer side effects when compared to diphenhydramine, which itself has been known to cause acute dystonia [1]. Other investigators have found increasing levels of sedation (with a secure airway in place) and/or anesthesia with medications other than propofol to be effective [6–9]. Benzodiazepines have also been found to be successful in treating propofol dystonia. Zabani and Vaghadia initially used diazepam 5 mg to treat dystonic movements in a patient suspected of having a dystonic reaction to propofol. In the same case, they later used a 100 mg thiopentone bolus and subsequent thiopentone 1% infusion (titrated to effect) when dystonic reactions returned. Other medications used to treat dystonic reactions to propofol include lidocaine, phenytoin, midazolam, lorazepam, muscle relaxants, and procyclidine [1]. For those reactions that are characterized as more “seizure-like” (versus dystonic), the recommended treatment plan is the same as for any general “tonic-clonic type” seizure, and would include treatment with benzodiazepines and/or other anticonvulsant medications [10].
305
In addition to the direct effect from propofol, it is possible that the left basal ganglia lacunar infarct seen on the patient's brain MRI may have made him more susceptible to developing a dystonic reaction, though the lesion was unilateral and the vocal fold dystonia was observed bilaterally. Nevertheless, the vocal fold dystonia responded to medications similar to classically described extremity dystonia, improving with administration of midazolam, hydromorphone, diphenhydramine, and diazepam. Unfortunately, benztropine was not available at our institution, as it may have served to expedite resolution of symptoms and prevent reintubation.
5.
Conclusions
In conclusion, prompt recognition of propofol-induced vocal fold dystonia and treatment with anticholinergic agents (preferably Benztropine) may firstly aid in the diagnosis, and secondly, if therapeutic, could obviate the need for reintubation. However, should these treatment options fail, sedation with benzodiazepines and reintubation for a “cooling off period” are recommended; once the dystonia resolves spontaneously the patient can be safely extubated and monitored for any recurrent symptoms.
REFERENCES
[1] Schramm BM, Orser BA. Dystonic reaction to propofol attenuated by benztropine (Cogentin). Anesth Analg 2002;94: 1237–40. [2] Vanlersberghe C, Camu F. Propofol. Handb Exp Pharmacol 2008;182:227–52. [3] Feldman MA, Patel A. Anesthesia for eye, ear, nose, and throat surgery. In: Miller RD, editor. Miller's Anesthesia. Philadelphia: Churchill Livingstone; 2009. p. 2357–88. [4] Bansinath M, Shukla VK, Turndorf H. Propofol modulates the effects of chemoconvulsants acting at GABAergic, glycinergic, and glutamate receptor subtypes. Anesthesiology 1995;83:809–15. [5] Pisani A, Bernardi G, Ding J, et al. Re-emergence of striatal cholinergic interneurons in movement disorders. Trends Neurosci 2007;30:545–53. [6] Ananthanarayan C. Dystonic reaction after anesthesia. Can J Anaesth 2001;48:101–3. [7] Strachan A, Raithatha H. Propofol myoclonus. Can J Anaesth 1996;43:536–7. [8] Dingwall A. Oculogyric crisis after daycase anaesthesia. Anaesthesia 1987:542–65. [9] McHugh P. Acute choreoathetoid reaction to propofol. Anaesthesia 1991;46:425. [10] Bevan JC. Propofol-related convulsions (Editorial). Can J Anaesth 1993;40:805–9.
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Acute vocal fold dystonic reaction to propofol: a case report☆,☆☆ Rachel C. Steckelberg, MD, MPH a,⁎, David Tsiang, MD a , Kelly Pettijohn, MD b , Abie Mendelsohn, MD b , Nir Hoftman, MD a a b
Department of Anesthesiology and Perioperative Care, UCLA Ronald Reagan Medical Center, 757 Westwood Plaza, Los Angeles, California Department of Head and Neck Surgery, UCLA Ronald Reagan Medical Center, 757 Westwood Plaza, Los Angeles, California
ARTI CLE I NFO
A BS TRACT
Article history:
A 67-year old male underwent uneventful robotic-assisted thoracoscopic resection of a
Received 4 November 2014
solitary pulmonary fibrous tumor. Immediately following extubation at the completion of the surgical procedure, the patient developed respiratory distress that did not resolve with treatment. Benadryl provided only temporary relief. Midazolam and hydromorphone were given for anxiolysis and analgesia respectively, which provided transient relief of symptoms. Propofol was given to decrease upper airway reflexes. Adequate reversal from nondepolarizing neuromuscular blockade was confirmed with nerve stimulator. A flexible laryngoscope was introduced nasally to visualize the vocal cords, which revealed intermittent tremulousness of the vocal cords, adduction of bilateral vocal cords to the midline, and minimal to absent opening with inspiration, without any apparent injury or blood, saliva, or vomit noted in or around the glottic opening. The patient was then given diazepam and reintubated. Given the patient's history of difficulty breathing after previous surgery and the lack of vocal cord movement, dystonic reaction to propofol was suspected. The patient remained intubated for two hours in the post-anesthesia care unit before being extubated uneventfully. © 2015 Elsevier Inc. All rights reserved.
1.
Introduction
Propofol is the most commonly used anesthetic induction agent. At present, there have been a limited number of described cases of propofol-related seizure-like and/or dystonic reactions [1,2]. Dystonic reactions have most frequently been reported as jerky movements of the extremities or opisthotonos [2]. Despite
☆
numerous case reports, no clear consensus regarding the neurogenic origin and therapeutic strategy for these adverse reactions has been reached. This report describes a case of vocal fold dystonia, observed as postoperative stridor. Given the widespread use of propofol, this treatable and potentially lifethreatening medication reaction should be considered when assessing any patient with postoperative stridor and abnormal
Disclosures: The authors have no financial or other competing interests to disclose. Author contributions: All authors had full access to all of the data in the study and take full responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: All authors. Acquisition of data: RS, DT, KP. Analysis and interpretation of data: All authors. Drafting of the manuscript: RS, DT, KP. Critical revision of the manuscript for important intellectual content: All authors. Study supervision: NH, AM. ⁎ Corresponding author at: Ronald Reagan Medical Center, 757 Westwood Plaza, Suite 3304, Los Angeles, California 90025, USA. Tel.: +1 310 267 8655; fax: +1 310 825 6301. E-mail address: [email protected] (R.C. Steckelberg).
☆☆
http://dx.doi.org/10.1016/j.amjoto.2014.11.006 0196-0709/© 2015 Elsevier Inc. All rights reserved.
304
AM ER IC AN JOURNAL OF OT OLA RYNGOLOGY– H E A D A N D NE CK M E D ICI N E AN D S U RGE RY 3 6 (2 0 1 5) 3 03 – 3 0 5
vocal fold motion in a patient who has been given propofol. It is important to review cases such as this to determine an appropriate therapeutic treatment plan, as well as to identify potential strategies to prevent further adverse outcomes.
2.
Materials and methods
2.1.
Initial case presentation
A 67-year old 85-kilogram man underwent an uneventful thoracoscopic robotic assisted left upper lobe wedge resection of a solitary fibrous tumor under general anesthesia. The patient's medical history included well-controlled hypertension, coronary artery disease (status post drug-eluting stent placement), chronic atrial fibrillation, and a chronic left basal ganglia lacunar infarct. The patient denied drug allergies, although he did describe an episode of “difficulty breathing” after a previous inguinal hernia surgery under sedation using propofol that resolved with an unknown “reversal agent”. During this thoracic procedure the patient was intubated atraumatically with a 39Fr double lumen endotracheal tube for the duration of the five-hour operation. On indirect video laryngoscopy, the pharmacologically paralyzed vocal cords appeared without any visible pathology. Immediately after extubation, the patient developed respiratory distress and stridor that did not resolve with jaw thrust and continuous positive airway pressure, the standard treatments for suspected laryngospasm. Midazolam 3 mg and hydromorphone 0.4 mg were given for anxiolysis and analgesia respectively, which provided transient relief of symptoms. Propofol 20 mg was given to decrease upper airway reflexes. Adequate reversal from nondepolarizing neuromuscular blockade was confirmed with nerve stimulator. The patient's preoperative calcium level was within normal limits. The patient's oropharynx had been thoroughly suctioned prior to extubation and he was alert, oriented, and following commands as we attempted our various interventions. A flexible laryngoscope was introduced nasally to visualize the vocal cords, which revealed intermittent tremulousness of the vocal cords, adduction of bilateral vocal cords to the midline, and minimal to absent opening with inspiration, without any apparent injury or blood, saliva, or vomit noted in or around the glottic opening.
3.
Results
A dystonic reaction to propofol was suspected after ruling out other causes of stridor and considering both the pattern of vocal cord movement and the patient's previous history of respiratory distress following surgery under propofol sedation. Diphenhydramine 50 mg was administered for its anticholinergic properties since the first agent of choice (benztropine) was not available in our hospital in intravenous formulation. Given that this treatment proved temporary as the previous ones had, the decision was made to re-intubate the patient and wake him slowly in the post-anesthesia care unit (PACU), to provide time for the effects of the propofol to resolve spontaneously. The patient was thus given diazepam 10 mg (for both sedation/anxiolysis and for treatment of the dystonic reaction), ketamine 50 mg (for a non-propofol
induction), succinylcholine 100 mg (for paralysis), and then reintubated. The patient was transported to the PACU, where he remained sedated for 2 hours before being awakened and extubated uneventfully, without any return of the dystonia. The patient was monitored overnight for precaution and discharged home the next day.
4.
Discussion
Stridor is a relatively common postoperative finding that warrants prompt evaluation. When consulted regarding a patient with such symptoms, diagnoses such as laryngeal edema, laryngospasm, and vocal cord immobility are typically considered. In the case of abnormal bilateral vocal fold mobility on fiberoptic laryngoscopy, the following etiologies are considered: surgical trauma related to local procedures such as thyroidectomy/parathyroidectomy etc. (an estimated 44% of observed cases), malignancy (17%), endotracheal intubation (15%), neurologic disease (12%), and idiopathic causes (12%) [1]. In the immediate postoperative patient, the expected causes of stridor include laryngeal edema, laryngospasm, cord paralysis related to recurrent laryngeal nerve (RLN) damage from local surgery, or intubation-related causes. Intubation-related causes include arytenoid dislocation, RLN damage from anterior displacement of the cricoid cartilage relative to the thyroid cartilage, extreme hyperextension of the neck resulting in vagus nerve stretch injury, or excessive endotracheal tube cuff pressure that compresses the RLN as it enters the larynx. Short-term intubation most frequently results in a unilateral vocal cord palsy, with an estimated incidence of 1 per 1000 procedures [3]. Laryngospasm is caused by excessive stimulation of the laryngeal adductor reflex mediated by the superior laryngeal nerve. It is a common etiology of perioperative stridor characterized by upper airway obstruction, usually lasting less than 1–2 minutes, and is responsive to medications that would decrease stimulation of the reflex (such as lidocaine or paralytic agents). In the case of our patient, standard methods of management of laryngospasm were ineffective, leading to consideration of alternative etiologies [3]. Numerous cases of generalized dystonia related to propofol, the most common induction agent presently used, have been documented in the literature, and summarized in a case report by Schramm and Orser [1]. In their report, cases demonstrating both seizure-like reaction to propofol and dystonic reaction were described. Interestingly, 17 of the total 21 dystonic-type cases reported were in females, predominantly under the age of 30. The most common movements described were jerky limb/trunk movements and opisthotonos [3]. Previous reports have documented cases of laryngeal dystonia in reaction to antipsychotics, but no previous case of vocal cord dystonia related to propofol has been described [2]. Propofol exerts its hypnotic effects through modulation of GABAA receptors, which are ligand-gated ion channels coupled to a central chloride channel that produce an inhibitory effect when they bind the neurotransmitter GABA, which acts primarily in the cerebral cortex. Simultaneously, neuroexcitation, in the form of myoclonus, tremor, dystonic
AM ER IC AN JOURNAL OF OT OLARYNGOLOGY – H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 3 03– 3 0 5
posturing, etc. may be secondary to the depression of subcortical areas of the brain [2]. Specifically, an in vivo study in mice suggested that propofol might increase the motor manifestations, e.g. opisthotonos and athetoid movements, of agonists acting at glycine receptors. Glycine is a central nervous system amino acid that acts as an inhibitory neurotransmitter primarily in subcortical areas of the brain [4], which would include the basal ganglia. An imbalance in the dopaminergic and cholinergic pathways that integrate areas of the cerebral cortex with the basal ganglia may explain the hyper- and hypo-kinetic symptoms of movement disorders such as Parkinson's disease and dystonia. Normally, activation of D2 dopamine receptors in the striatum, which contains projection neurons to the basal ganglia, decreases interneuron excitation and reduces their release of acetylcholine. Furthermore, muscarinic autoreceptors expressed on these interneurons provide feedback control of acetylcholine release. Some forms of primary dystonia (i.e. sporadic or genetic) have been found to be the result of aberrant mutations in enzymes involved in dopamine biosynthesis, e.g. tyrosine hydroxylase and GTP cyclohydrolase. In other forms of dystonia, an alteration in D2 receptor coupling resulted in an increase in interneuron spiking and hence acetylcholine release. In both cases, the underlying theme seems to be an excess of acetylcholine release, which might explain the efficacy of anticholinergic medications in the treatment of dystonia [1,5]. A review of the literature shows dystonic reactions to propofol have been successfully treated with a number of medications. In particular, Schramm and Orser found benztropine 2 mg IV to be successful in treating a dystonic reaction to propofol, since it had a shorter recovery time with fewer side effects when compared to diphenhydramine, which itself has been known to cause acute dystonia [1]. Other investigators have found increasing levels of sedation (with a secure airway in place) and/or anesthesia with medications other than propofol to be effective [6–9]. Benzodiazepines have also been found to be successful in treating propofol dystonia. Zabani and Vaghadia initially used diazepam 5 mg to treat dystonic movements in a patient suspected of having a dystonic reaction to propofol. In the same case, they later used a 100 mg thiopentone bolus and subsequent thiopentone 1% infusion (titrated to effect) when dystonic reactions returned. Other medications used to treat dystonic reactions to propofol include lidocaine, phenytoin, midazolam, lorazepam, muscle relaxants, and procyclidine [1]. For those reactions that are characterized as more “seizure-like” (versus dystonic), the recommended treatment plan is the same as for any general “tonic-clonic type” seizure, and would include treatment with benzodiazepines and/or other anticonvulsant medications [10].
305
In addition to the direct effect from propofol, it is possible that the left basal ganglia lacunar infarct seen on the patient's brain MRI may have made him more susceptible to developing a dystonic reaction, though the lesion was unilateral and the vocal fold dystonia was observed bilaterally. Nevertheless, the vocal fold dystonia responded to medications similar to classically described extremity dystonia, improving with administration of midazolam, hydromorphone, diphenhydramine, and diazepam. Unfortunately, benztropine was not available at our institution, as it may have served to expedite resolution of symptoms and prevent reintubation.
5.
Conclusions
In conclusion, prompt recognition of propofol-induced vocal fold dystonia and treatment with anticholinergic agents (preferably Benztropine) may firstly aid in the diagnosis, and secondly, if therapeutic, could obviate the need for reintubation. However, should these treatment options fail, sedation with benzodiazepines and reintubation for a “cooling off period” are recommended; once the dystonia resolves spontaneously the patient can be safely extubated and monitored for any recurrent symptoms.
REFERENCES
[1] Schramm BM, Orser BA. Dystonic reaction to propofol attenuated by benztropine (Cogentin). Anesth Analg 2002;94: 1237–40. [2] Vanlersberghe C, Camu F. Propofol. Handb Exp Pharmacol 2008;182:227–52. [3] Feldman MA, Patel A. Anesthesia for eye, ear, nose, and throat surgery. In: Miller RD, editor. Miller's Anesthesia. Philadelphia: Churchill Livingstone; 2009. p. 2357–88. [4] Bansinath M, Shukla VK, Turndorf H. Propofol modulates the effects of chemoconvulsants acting at GABAergic, glycinergic, and glutamate receptor subtypes. Anesthesiology 1995;83:809–15. [5] Pisani A, Bernardi G, Ding J, et al. Re-emergence of striatal cholinergic interneurons in movement disorders. Trends Neurosci 2007;30:545–53. [6] Ananthanarayan C. Dystonic reaction after anesthesia. Can J Anaesth 2001;48:101–3. [7] Strachan A, Raithatha H. Propofol myoclonus. Can J Anaesth 1996;43:536–7. [8] Dingwall A. Oculogyric crisis after daycase anaesthesia. Anaesthesia 1987:542–65. [9] McHugh P. Acute choreoathetoid reaction to propofol. Anaesthesia 1991;46:425. [10] Bevan JC. Propofol-related convulsions (Editorial). Can J Anaesth 1993;40:805–9.
