The Journal of Craniofacial Surgery • Volume 25, Number 4, July 2014
correlation between any platelet indices including platelet count, MPV, platelet mass, platelet distribution width, as well as plateletcrit and platelet aggregation responses induced with adenosine diphosphate, collagen, and epinephrine. Recently, De Luca et al4 reported a study that investigated whether MPV was associated with platelet reactivity and the extent of coronary artery disease among patients with diabetes. They performed a cohort study including 1016 consecutive patients with diabetes undergoing coronary angiography. They found that MPV was not related to platelet reactivity and concluded that MPV may not be considered a risk factor for coronary artery disease among patients with diabetes. Therefore, it does not seem possible to use MPV as a marker of platelet function. On the other hand, the reliable detection of MPV is dependent on a number of variables, including time of analysis, method of analysis, anticoagulant used, and specimen storage temperature.5 The MPV is reported routinely in complete blood count, but it is not suitable because ethylenediaminetetraacetic acid (EDTA) induced changes over time.5 Platelet size changes induced by EDTA cause a progressive increase in MPV with impedance technology. When measured by optical methods, the MPV decreases nearly 10% because of a fall in the refractile index of the platelets because of dilution of cytoplasmic contents. Jackson and Carter6 showed that the MPV increases up to 30% within 5 minutes of exposure and increases further by 10% to 15% over the next 2 hours when using the impedance method. Lancé et al7 suggested that timing was important when measuring MPV and that optimal measuring time with EDTA should be 120 minutes after venipuncture. Also, the reference range of MPV is specific to the individual technologies. Different technologies for measuring the MPV give different results. Studies comparing results from these instruments have shown MPV differences of up to 40%.8 Because the measurement times of samples, method of analysis, and used technologies were unknown in this study, the validity and reliability of data were questionable. In conclusion, MPV may not be beneficial for the management of patients with adenoid hypertrophy. Cengiz Beyan, MD Department of Hematology Gulhane Military Medical Academy Ankara, Turkey [email protected]; [email protected] Esin Beyan, MD Department of Internal Medicine Kecioren Training and Research Hospital Ankara, Turkey
REFERENCES 1. Kucur C, Kulekci S, Zorlu A, et al. Mean platelet volume levels in children with adenoid hypertrophy. J Craniofac Surg 2014;25:e29–e31 2. Harrison P. Platelet function testing [UpToDate web site]. Available at: http://www.uptodate.com/contents/platelet-function-testing. Accessed January 17, 2014 3. Beyan C, Kaptan K, Ifran A. Platelet count, mean platelet volume, platelet distribution width, and plateletcrit do not correlate with optical platelet aggregation responses in healthy volunteers. J Thromb Thrombolysis 2006;22:161–164 4. De Luca G, Verdoia M, Cassetti E, et al. Mean platelet volume is not associated with platelet reactivity and the extent of coronary artery disease in diabetic patients. Blood Coagul Fibrinolysis 2013;24:619–624 5. Lancé MD, Sloep M, Henskens YM, et al. Mean platelet volume as a diagnostic marker for cardiovascular disease: drawbacks of preanalytical conditions and measuring techniques. Clin Appl Thromb Hemost 2012;18:561–568
Correspondence
6. Jackson SR, Carter JM. Platelet volume: laboratory measurement and clinical application. Blood Rev 1993;7:104–113 7. Lancé MD, van Oerle R, Henskens YM, et al. Do we need time adjusted mean platelet volume measurements? Lab Hematol 2010;16:28–31 8. George TI. Automated hematology instrumentation [UpToDate web site]. Available at: http://www.uptodate.com/contents/automated-hematologyinstrumentation. Accessed January 17, 2014
Hypoglossal Paralysis After Intubation for Nasal Surgery To the Editor: Hypoglossal nerve palsy is a multietiologic condition and a rare complication of general anesthesia because XII nerve palsies have more frequently been reported in association with tumors, head trauma, stroke, multiple sclerosis, carotid endarterectomy, Guillain-Barré syndrome, and infection.1–6 The hypoglossal nerve innervates the muscles of the tongue and controls swallowing and speech.4 Hypoglossal nerve palsies usually present unilaterally with signs of dysarthria and dysphagia, and they are frequently associated with involvement of other cranial nerves and neurologic structures.3 The knowledge of the pathway of the hypoglossal nerve is fundamental to hypothesize the mechanism that may be responsible for hypoglossal nerve injury. The XII nerve originates from the hypoglossal nerve nucleus in the medulla oblongata between the olive and pyramid, leaves the cranium through the hypoglossal canal in the occipital bone, and descends between the internal jugular vein and the internal carotid artery until it reaches the lower border of the posterior belly of the digastric muscle, where it turns forward and medially. The nerve then continues anterior and superior to the greater cornu of the hyoid bone and enters the floor of the mouth deep to the posterior margin of the mylohyoid muscle, supplying motor innervation to both intrinsic and extrinsic lingual muscles.1–6 We present a case of isolated unilateral hypoglossal nerve paralysis after an uneventful tracheal intubation for nasal surgery. A 34-year-old man was scheduled for a rhinoseptoplasty with turbinoplasty under general anesthesia because of nasal respiratory insufficiency associated with nasal septal deviation and turbinate hypertrophy. His medical history included arterial hypertension in treatment with β-blockers. He was otherwise well and did not take any regular medication. General anesthesia was induced through intravenous administration of fentanyl 2 mcg/kg and propofol 2 mg/kg, and vecuronium 0.1 mg/kg was used for muscle paralysis and for the prevention of laryngospasm during insertion of the endotracheal tube. Then, a size-4 Macintosh blade was used and an orotracheal intubation was obtained with an 8-mm tube. No problems were encountered during the intubation. The endotracheal tube cuff was inflated, and the cuff air pressure was checked so that it did not exceed 20 cm H2O. Then, proper placement of the endotracheal tube was confirmed by bilateral breath sounds. During surgery, general anesthesia was maintained by sevoflurane in oxygen/air supplemented with remifentanil. The surgery was completed uneventfully within 60 minutes. No significant changes in cardiovascular or respiratory parameters occurred during the operation. The patient’s spontaneous ventilation was satisfactory. Finally, the endotracheal tube was carefully removed and the patient was transferred to the recovery unit. After 2 hours, the patient
© 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
1581
Correspondence
The Journal of Craniofacial Surgery • Volume 25, Number 4, July 2014
complained of dysarthria and dysphagia without any pain. The patient had his natural sensation of the tongue and taste unaltered. On clinical examination, his tongue deviated to the right on protrusion and there was no visible fasciculation, whereas there were no further detectable cranial nerve abnormalities. Magnetic resonance imaging of his brain did not demonstrate any evidence of an ischemic event or focal abnormality. A neurologist confirmed the diagnosis of an isolated paralysis of the right hypoglossal nerve because of an apparent peripheral lesion. Conservative management was undertaken, and corticosteroid therapy and vitamin B complex were administered for 3 weeks. During hospital stay, no significant improvement was appreciated. On the third postoperative day, the patient was discharged. During the follow-up, progressive improvements of dysphagia and dysarthria were noticed. Four months after the surgery, a complete resolution of symptoms was observed and tongue mobility was normal. Most cases of hypoglossal nerve palsy are caused by tumors or other conditions such as trauma, stroke, multiple sclerosis, surgery, Guillain-Barre neuropathy, or infection. Of course, an oropharyngeal surgical procedure may determine hypoglossal nerve injury too.1 Instead, when surgery is not performed in proximity to the affected nerve, other causes such as endotracheal intubation have to be considered.4 After general anesthesia procedures, both isolated and associated hypoglossal nerve palsies have been observed. In particular, a combination of a lesion affecting the XIIth and Xth cranial nerves has been described and called Tapia syndrome.3 The peripheral Tapia syndrome is determined by an extracranial lesion of the hypoglossal nerve and recurrent laryngeal branch of the vagal nerve, thus causing an ipsilateral palsy of the vocal fold and the muscles of the tongue.2 Possible mechanisms of injury of hypoglossal nerve during general anesthesia include indirect trauma or direct trauma.6 As for indirect trauma, the peculiar positioning or stretching of the neck may be a possible cause of such injury, whereas direct trauma may be determined through laryngoscopy, bronchoscopy, or from continuous pressure of laryngeal mask airways or endotracheal tube.3 In particular, as for direct trauma, several hypotheses have been postulated, although no complete explanation has been reported yet and the exact mechanism is still unknown. The cuff pressure might be too high (although in almost all reported case, the cuff pressure was checked).2 The use of nitrous oxide has been considered responsible for some cases of hypoglossal nerve palsy after general anesthesia.4 Then, the tracheal tube may press on a localized area just at the crossing of the vagal and hypoglossal nerves. In fact, when cricoid pressure is applied or laryngeal displacement is used to facilitate the visualization of the larynx, the hyoid bone is immobilized, whereas the tongue is displaced anteriorly; the lingual and hypoglossal nerves may be stretched as they cross the hyoglossus muscle. In our patient, no problems were encountered during the intubation. The endotracheal tube cuff was inflated, and the cuff air pressure was checked so that it did not exceed 20 cm H2O. Then, proper placement of the endotracheal tube was confirmed by bilateral breath sounds. Furthermore, 2 anatomic conditions have been recognized as risk factors: a calcification of the ligamentum stylohyoideum and the malformation of the skull base such as Arnold Chiari type I.5 Other lesions that can cause peripheral hypoglossal nerve palsy must be ruled out. In fact, the hypoglossal nerve may also be injured by compression by a kinked vertebral artery (hypoglossal-vertebral entrapment syndrome) and occipital condylar fracture, isolation in the neck or in its more distal course near the tongue from carotid aneurysms, aneurysms of a persistent hypoglossal artery, vascular entrapment, spontaneous dissection of the extracranial internal carotid
1582
artery, local infections, surgical or accidental trauma, neck radiation, and tumors of the retroparotid or retropharyngeal spaces, neck, salivary glands, and base of the tongue.1–6 First of all, a differential diagnosis to distinguish the hypoglossal nerve, lingual nerve, and recurrent laryngeal nerve deficits is necessary and it depends on clinical signs and symptoms. In fact, hypoglossal nerve injury causes dysarthria and dysphagia, with patients showing accumulation of saliva, forcing the patient to swallow frequently, dysphagia due to inability to propel food to the pharynx, and respiratory embarrassment due to prolapse of the tongue into the pharynx (mainly in the supine position). Lingual nerve injury usually presents as loss of taste and sensation of the anterior tongue. Recurrent laryngeal nerve injury manifests as dysarthria, stridor, or postoperative aspiration.1–6 Hypoglossal nerve imaging such as magnetic resonance imaging could be useful to provide information for exclusion of a cerebrovascular accident or a mass lesion.1–6 Finally, the treatment of hypoglossal nerve palsy is mostly supportive with courses of systemic steroids, vitamins, and speech therapy,4 although there are no convincing data regarding the efficacy of such management strategy in nerve injuries.4,5 Nevertheless, almost all patients show a progressive but total recovery of the function, thus suggesting a neuropraxic type of nerve damage, as previously mentioned.3,4 In conclusion, although hypoglossal nerve palsy after general anesthesia seems to be extremely rare, anesthesiologists and surgeons should be aware of this possible complication. Despite the still unknown exact causative mechanism, it could be useful to remember that a difficult airway and anatomic anomalies might be involved in neurologic damage. Andrea Carboni, MD Division of Anesthesiology Aosta Hospital, Aosta, Italy Stefano Righi, MD Paolo Boffano, MD Paolo Rossi, MD Laura Malvè, MD Dimitrios Pateras, MD Pierluigi De Matteis, MD Maurizio Boson, MD Division of Otolaryngology Maxillofacial Surgery and Dentistry Aosta Hospital, Aosta, Italy
REFERENCES 1. Rubio-Nazábal E, Marey-Lopez J, Lopez-Facal S, et al. Isolated bilateral paralysis of the hypoglossal nerve after transoral intubation for general anesthesia. Anesthesiology 2002;96:245–247 2. Cinar SO, Seven H, Cinar U, et al. Isolated bilateral paralysis of the hypoglossal and recurrent laryngeal nerves (Bilateral Tapia’s syndrome) after transoral intubation for general anesthesia. Acta Anaesthesiol Scand 2005;49:98–99 3. Hong SJ, Lee JY. Isolated unilateral paralysis of the hypoglossal nerve after transoral intubation for general anesthesia. Dysphagia 2009;24:354–356 4. Hung NK, Lee CH, Chan SM, et al. Transient unilateral hypoglossal nerve palsy after orotracheal intubation for general anesthesia. Acta Anaesthesiol Taiwan 2009;47:48–50 5. Lopes G, Denoel C, Desuter G, et al. Two cases of isolated unilateral paralysis of hypoglossal nerve after uncomplicated orotracheal intubation. Acta Anaesthesiol Belg 2009;60:191–193 6. Al-Benna S. Right hypoglossal nerve paralysis after tracheal intubation for aesthetic breast surgery. Saudi J Anaesth 2013;7:341–343
© 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
correlation between any platelet indices including platelet count, MPV, platelet mass, platelet distribution width, as well as plateletcrit and platelet aggregation responses induced with adenosine diphosphate, collagen, and epinephrine. Recently, De Luca et al4 reported a study that investigated whether MPV was associated with platelet reactivity and the extent of coronary artery disease among patients with diabetes. They performed a cohort study including 1016 consecutive patients with diabetes undergoing coronary angiography. They found that MPV was not related to platelet reactivity and concluded that MPV may not be considered a risk factor for coronary artery disease among patients with diabetes. Therefore, it does not seem possible to use MPV as a marker of platelet function. On the other hand, the reliable detection of MPV is dependent on a number of variables, including time of analysis, method of analysis, anticoagulant used, and specimen storage temperature.5 The MPV is reported routinely in complete blood count, but it is not suitable because ethylenediaminetetraacetic acid (EDTA) induced changes over time.5 Platelet size changes induced by EDTA cause a progressive increase in MPV with impedance technology. When measured by optical methods, the MPV decreases nearly 10% because of a fall in the refractile index of the platelets because of dilution of cytoplasmic contents. Jackson and Carter6 showed that the MPV increases up to 30% within 5 minutes of exposure and increases further by 10% to 15% over the next 2 hours when using the impedance method. Lancé et al7 suggested that timing was important when measuring MPV and that optimal measuring time with EDTA should be 120 minutes after venipuncture. Also, the reference range of MPV is specific to the individual technologies. Different technologies for measuring the MPV give different results. Studies comparing results from these instruments have shown MPV differences of up to 40%.8 Because the measurement times of samples, method of analysis, and used technologies were unknown in this study, the validity and reliability of data were questionable. In conclusion, MPV may not be beneficial for the management of patients with adenoid hypertrophy. Cengiz Beyan, MD Department of Hematology Gulhane Military Medical Academy Ankara, Turkey [email protected]; [email protected] Esin Beyan, MD Department of Internal Medicine Kecioren Training and Research Hospital Ankara, Turkey
REFERENCES 1. Kucur C, Kulekci S, Zorlu A, et al. Mean platelet volume levels in children with adenoid hypertrophy. J Craniofac Surg 2014;25:e29–e31 2. Harrison P. Platelet function testing [UpToDate web site]. Available at: http://www.uptodate.com/contents/platelet-function-testing. Accessed January 17, 2014 3. Beyan C, Kaptan K, Ifran A. Platelet count, mean platelet volume, platelet distribution width, and plateletcrit do not correlate with optical platelet aggregation responses in healthy volunteers. J Thromb Thrombolysis 2006;22:161–164 4. De Luca G, Verdoia M, Cassetti E, et al. Mean platelet volume is not associated with platelet reactivity and the extent of coronary artery disease in diabetic patients. Blood Coagul Fibrinolysis 2013;24:619–624 5. Lancé MD, Sloep M, Henskens YM, et al. Mean platelet volume as a diagnostic marker for cardiovascular disease: drawbacks of preanalytical conditions and measuring techniques. Clin Appl Thromb Hemost 2012;18:561–568
Correspondence
6. Jackson SR, Carter JM. Platelet volume: laboratory measurement and clinical application. Blood Rev 1993;7:104–113 7. Lancé MD, van Oerle R, Henskens YM, et al. Do we need time adjusted mean platelet volume measurements? Lab Hematol 2010;16:28–31 8. George TI. Automated hematology instrumentation [UpToDate web site]. Available at: http://www.uptodate.com/contents/automated-hematologyinstrumentation. Accessed January 17, 2014
Hypoglossal Paralysis After Intubation for Nasal Surgery To the Editor: Hypoglossal nerve palsy is a multietiologic condition and a rare complication of general anesthesia because XII nerve palsies have more frequently been reported in association with tumors, head trauma, stroke, multiple sclerosis, carotid endarterectomy, Guillain-Barré syndrome, and infection.1–6 The hypoglossal nerve innervates the muscles of the tongue and controls swallowing and speech.4 Hypoglossal nerve palsies usually present unilaterally with signs of dysarthria and dysphagia, and they are frequently associated with involvement of other cranial nerves and neurologic structures.3 The knowledge of the pathway of the hypoglossal nerve is fundamental to hypothesize the mechanism that may be responsible for hypoglossal nerve injury. The XII nerve originates from the hypoglossal nerve nucleus in the medulla oblongata between the olive and pyramid, leaves the cranium through the hypoglossal canal in the occipital bone, and descends between the internal jugular vein and the internal carotid artery until it reaches the lower border of the posterior belly of the digastric muscle, where it turns forward and medially. The nerve then continues anterior and superior to the greater cornu of the hyoid bone and enters the floor of the mouth deep to the posterior margin of the mylohyoid muscle, supplying motor innervation to both intrinsic and extrinsic lingual muscles.1–6 We present a case of isolated unilateral hypoglossal nerve paralysis after an uneventful tracheal intubation for nasal surgery. A 34-year-old man was scheduled for a rhinoseptoplasty with turbinoplasty under general anesthesia because of nasal respiratory insufficiency associated with nasal septal deviation and turbinate hypertrophy. His medical history included arterial hypertension in treatment with β-blockers. He was otherwise well and did not take any regular medication. General anesthesia was induced through intravenous administration of fentanyl 2 mcg/kg and propofol 2 mg/kg, and vecuronium 0.1 mg/kg was used for muscle paralysis and for the prevention of laryngospasm during insertion of the endotracheal tube. Then, a size-4 Macintosh blade was used and an orotracheal intubation was obtained with an 8-mm tube. No problems were encountered during the intubation. The endotracheal tube cuff was inflated, and the cuff air pressure was checked so that it did not exceed 20 cm H2O. Then, proper placement of the endotracheal tube was confirmed by bilateral breath sounds. During surgery, general anesthesia was maintained by sevoflurane in oxygen/air supplemented with remifentanil. The surgery was completed uneventfully within 60 minutes. No significant changes in cardiovascular or respiratory parameters occurred during the operation. The patient’s spontaneous ventilation was satisfactory. Finally, the endotracheal tube was carefully removed and the patient was transferred to the recovery unit. After 2 hours, the patient
© 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
1581
Correspondence
The Journal of Craniofacial Surgery • Volume 25, Number 4, July 2014
complained of dysarthria and dysphagia without any pain. The patient had his natural sensation of the tongue and taste unaltered. On clinical examination, his tongue deviated to the right on protrusion and there was no visible fasciculation, whereas there were no further detectable cranial nerve abnormalities. Magnetic resonance imaging of his brain did not demonstrate any evidence of an ischemic event or focal abnormality. A neurologist confirmed the diagnosis of an isolated paralysis of the right hypoglossal nerve because of an apparent peripheral lesion. Conservative management was undertaken, and corticosteroid therapy and vitamin B complex were administered for 3 weeks. During hospital stay, no significant improvement was appreciated. On the third postoperative day, the patient was discharged. During the follow-up, progressive improvements of dysphagia and dysarthria were noticed. Four months after the surgery, a complete resolution of symptoms was observed and tongue mobility was normal. Most cases of hypoglossal nerve palsy are caused by tumors or other conditions such as trauma, stroke, multiple sclerosis, surgery, Guillain-Barre neuropathy, or infection. Of course, an oropharyngeal surgical procedure may determine hypoglossal nerve injury too.1 Instead, when surgery is not performed in proximity to the affected nerve, other causes such as endotracheal intubation have to be considered.4 After general anesthesia procedures, both isolated and associated hypoglossal nerve palsies have been observed. In particular, a combination of a lesion affecting the XIIth and Xth cranial nerves has been described and called Tapia syndrome.3 The peripheral Tapia syndrome is determined by an extracranial lesion of the hypoglossal nerve and recurrent laryngeal branch of the vagal nerve, thus causing an ipsilateral palsy of the vocal fold and the muscles of the tongue.2 Possible mechanisms of injury of hypoglossal nerve during general anesthesia include indirect trauma or direct trauma.6 As for indirect trauma, the peculiar positioning or stretching of the neck may be a possible cause of such injury, whereas direct trauma may be determined through laryngoscopy, bronchoscopy, or from continuous pressure of laryngeal mask airways or endotracheal tube.3 In particular, as for direct trauma, several hypotheses have been postulated, although no complete explanation has been reported yet and the exact mechanism is still unknown. The cuff pressure might be too high (although in almost all reported case, the cuff pressure was checked).2 The use of nitrous oxide has been considered responsible for some cases of hypoglossal nerve palsy after general anesthesia.4 Then, the tracheal tube may press on a localized area just at the crossing of the vagal and hypoglossal nerves. In fact, when cricoid pressure is applied or laryngeal displacement is used to facilitate the visualization of the larynx, the hyoid bone is immobilized, whereas the tongue is displaced anteriorly; the lingual and hypoglossal nerves may be stretched as they cross the hyoglossus muscle. In our patient, no problems were encountered during the intubation. The endotracheal tube cuff was inflated, and the cuff air pressure was checked so that it did not exceed 20 cm H2O. Then, proper placement of the endotracheal tube was confirmed by bilateral breath sounds. Furthermore, 2 anatomic conditions have been recognized as risk factors: a calcification of the ligamentum stylohyoideum and the malformation of the skull base such as Arnold Chiari type I.5 Other lesions that can cause peripheral hypoglossal nerve palsy must be ruled out. In fact, the hypoglossal nerve may also be injured by compression by a kinked vertebral artery (hypoglossal-vertebral entrapment syndrome) and occipital condylar fracture, isolation in the neck or in its more distal course near the tongue from carotid aneurysms, aneurysms of a persistent hypoglossal artery, vascular entrapment, spontaneous dissection of the extracranial internal carotid
1582
artery, local infections, surgical or accidental trauma, neck radiation, and tumors of the retroparotid or retropharyngeal spaces, neck, salivary glands, and base of the tongue.1–6 First of all, a differential diagnosis to distinguish the hypoglossal nerve, lingual nerve, and recurrent laryngeal nerve deficits is necessary and it depends on clinical signs and symptoms. In fact, hypoglossal nerve injury causes dysarthria and dysphagia, with patients showing accumulation of saliva, forcing the patient to swallow frequently, dysphagia due to inability to propel food to the pharynx, and respiratory embarrassment due to prolapse of the tongue into the pharynx (mainly in the supine position). Lingual nerve injury usually presents as loss of taste and sensation of the anterior tongue. Recurrent laryngeal nerve injury manifests as dysarthria, stridor, or postoperative aspiration.1–6 Hypoglossal nerve imaging such as magnetic resonance imaging could be useful to provide information for exclusion of a cerebrovascular accident or a mass lesion.1–6 Finally, the treatment of hypoglossal nerve palsy is mostly supportive with courses of systemic steroids, vitamins, and speech therapy,4 although there are no convincing data regarding the efficacy of such management strategy in nerve injuries.4,5 Nevertheless, almost all patients show a progressive but total recovery of the function, thus suggesting a neuropraxic type of nerve damage, as previously mentioned.3,4 In conclusion, although hypoglossal nerve palsy after general anesthesia seems to be extremely rare, anesthesiologists and surgeons should be aware of this possible complication. Despite the still unknown exact causative mechanism, it could be useful to remember that a difficult airway and anatomic anomalies might be involved in neurologic damage. Andrea Carboni, MD Division of Anesthesiology Aosta Hospital, Aosta, Italy Stefano Righi, MD Paolo Boffano, MD Paolo Rossi, MD Laura Malvè, MD Dimitrios Pateras, MD Pierluigi De Matteis, MD Maurizio Boson, MD Division of Otolaryngology Maxillofacial Surgery and Dentistry Aosta Hospital, Aosta, Italy
REFERENCES 1. Rubio-Nazábal E, Marey-Lopez J, Lopez-Facal S, et al. Isolated bilateral paralysis of the hypoglossal nerve after transoral intubation for general anesthesia. Anesthesiology 2002;96:245–247 2. Cinar SO, Seven H, Cinar U, et al. Isolated bilateral paralysis of the hypoglossal and recurrent laryngeal nerves (Bilateral Tapia’s syndrome) after transoral intubation for general anesthesia. Acta Anaesthesiol Scand 2005;49:98–99 3. Hong SJ, Lee JY. Isolated unilateral paralysis of the hypoglossal nerve after transoral intubation for general anesthesia. Dysphagia 2009;24:354–356 4. Hung NK, Lee CH, Chan SM, et al. Transient unilateral hypoglossal nerve palsy after orotracheal intubation for general anesthesia. Acta Anaesthesiol Taiwan 2009;47:48–50 5. Lopes G, Denoel C, Desuter G, et al. Two cases of isolated unilateral paralysis of hypoglossal nerve after uncomplicated orotracheal intubation. Acta Anaesthesiol Belg 2009;60:191–193 6. Al-Benna S. Right hypoglossal nerve paralysis after tracheal intubation for aesthetic breast surgery. Saudi J Anaesth 2013;7:341–343
© 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
