International Journal of Pediatric Otorhinolaryngology 78 (2014) 882–884
Contents lists available at ScienceDirect
International Journal of Pediatric Otorhinolaryngology journal homepage: www.elsevier.com/locate/ijporl
Case Report
The nasogastric tube syndrome in infants§ Jeffrey Harmon a, Karthik Balakrishnan b,*, Alessandro de Alarcon b,c, Catherine K. Hart b,c a
University of Cincinnati College of Medicine, Office of Student Affairs, Medical Sciences Building E-251, PO Box 670552, Cincinnati, OH 45267, United States Division of Pediatric Otolaryngology – Head & Neck Surgery, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Avenue, MLC-2018, Cincinnati, OH 45229, United States c Department of Otolaryngology – Head & Neck Surgery, University of Cincinnati College of Medicine, 231 Albert Sabin Way ML 0528, Cincinnati, OH 45267, United States b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 16 January 2014 Received in revised form 7 February 2014 Accepted 8 February 2014 Available online 20 February 2014
This series of three patients is the first description of the presentation, clinical course, and endoscopic findings of nasogastric tube-related airway distress, or nasogastric tube syndrome, in infants. We identify key differences in disease features from those described in adults, based on our literature review. Specifically, infant nasogastric tube syndrome presented as significant respiratory distress and postcricoid inflammation without vocal fold immobility. Symptoms resolved more quickly (mean SD, 2 1 days) than reported in adults. We suggest that nasogastric tube syndrome should be considered in infants with otherwise unexplained respiratory distress, even in the absence of impaired vocal fold mobility. ß 2014 Elsevier Ireland Ltd. All rights reserved.
Keywords: Infant Stridor Respiratory distress Nasogastric tube
1. Introduction Iglauer and Molt [1] first described damage to the larynx due to an indwelling enteric tube in a case series in 1939, with the majority of their reported cases showed laryngeal chondritis, edema, and vocal fold immobility. Nasogastric tube syndrome was later formally defined by Sofferman et al. [2] in 1990 as an uncommon phenomenon involving throat pain, vocal fold dysfunction, and respiratory distress in adult patients as a result of post-cricoid mucosal damage due to the presence of a nasogastric (NG) tube. Suggested mechanisms by which this syndrome might occur include friction from the motion of the larynx sliding up and down against the nasogastric tube, cricopharyngeus muscle contraction forcing the tube against the mucosa overlying the posterior cricoid cartilage, and pinching of the tube between the cricoid cartilage and anterior cervical spine while the patient is in a supine position [2]. Mechanical irritation and compression-related ischemia are thought to result in inflammation, ulceration, and possible infection of the interarytenoid and post-cricoid mucosa, cricoarytenoid muscle (vocal fold abductor), and cricoid cartilage. Subsequent bilateral vocal fold dysfunction may occur, leading to respiratory
distress [3,4]. A study on dogs by Friedman et al. [5] suggested midline nasogastric tube placement predisposes patients to development of nasogastric tube syndrome. Management, though not defined specifically in the literature, includes removal of the NG tube and medical treatment with steroids, antibiotics, and antireflux therapy. Many reported cases have also required tracheostomy [1,4]. To our knowledge, 37 cases of nasogastric tube syndrome have been reported as of 2013 [1–11]. Of these cases, only 2 were children, aged 4 and 5 years, respectively. Both were reported by Iglauer and Molt long before the development of flexible nasopharyngoscopy [1,3]. Both patients required tracheotomy, with subsequent direct laryngoscopy showing laryngeal inflammation, arytenoid edema, and significantly reduced vocal fold mobility. Despite the frequent use of nasogastric and orogastric tubes in infants and young children, associated laryngeal injury has not been described in this younger age group. We present three cases encountered in the otolaryngology division of a tertiary children’s hospital specializing in aerodigestive disorders. This study was approved by the Institutional Review Board at Cincinnati Children’s Hospital Medical Center. 1.1. Case 1
§
Presented at the American Society of Pediatric Otolaryngology 2013 Annual Meeting, Washington, DC. * Corresponding author at: 3333 Burnet Avenue, MLC 2018, Cincinnati, OH 45227, United States. Tel.: +1 513 636 4355; fax: +1 513 636 8133. E-mail address: [email protected] (K. Balakrishnan). http://dx.doi.org/10.1016/j.ijporl.2014.02.013 0165-5876/ß 2014 Elsevier Ireland Ltd. All rights reserved.
The first patient is a 2-month old male with coarctation of the aorta status post repair. An NG tube was placed six weeks later due to feeding difficulties. Two days after placement of the NG tube, the
[(Fig._1)TD$IG]
[(Fig._2)TD$IG]
J. Harmon et al. / International Journal of Pediatric Otorhinolaryngology 78 (2014) 882–884
883
Fig. 1. Patient 1, endoscopic view prior to NG tube removal. Note the significant postcricoid edema and granulation.
Fig. 2. Patient 2, endoscopic view prior to NG tube removal. Note the significant postcricoid edema and granulation.
patient developed acute inspiratory stridor, retractions, and desaturations worsening over the next 5 days. These symptoms were unresponsive to systemic steroids, inhaled racemic epinephrine, gastric acid suppression with ranitidine and proton pump inhibitors, and change in body position. Fiberoptic laryngoscopy showed normal bilateral vocal fold motion. Microlaryngoscopy and bronchoscopy performed 5 days after the onset of respiratory symptoms showed interarytenoid edema, erythema, and postcricoid granulation tissue around the NG tube. The nasogastric tube was removed immediately and replaced with total parenteral nutrition followed by gastrostomy tube placement. His stridor improved within one day of NG tube removal; the stridor and retractions resolved completely within five days. Follow up fiberoptic laryngoscopy showed improving post-cricoid granulation (Fig. 1).
increased work of breathing had completely resolved. Fiberoptic examination one week after the disappearance of airway symptoms showed resolution of post-cricoid edema.
1.2. Case 2 The second patient is a 3-month old female status-post slide tracheoplasty with cardiopulmonary bypass for complete tracheal rings. After an NG tube had been in place for approximately 11 days, she developed increased work of breathing. Serial microlaryngoscopy and bronchoscopies showed persistent severe postcricoid edema. Flexible laryngoscopy showed normal bilateral true vocal fold motion. The increased work of breathing and inspiratory stridor persisted over seven weeks despite twice daily proton pump inhibitor therapy, after which the NG tube was replaced with a gastrostomy tube. The stridor resolved two days later. Repeat microlaryngoscopy and bronchoscopy one month later showed improved post-cricoid edema (Fig. 2). 1.3. Case 3 Patient 3 is a 3-month old male, born at 30 weeks, intubated for bradycardia after emergent cesarean section due to preterm premature rupture of membranes. An orogastric tube was placed four days after intubation, and the patient was extubated nearly two months later. The orogastric tube remained in place. The patient remained on twice daily ranitidine therapy for gastric acid suppression. One month after removal of the endotracheal tube, the patient was noted to have intermittent biphasic stridor. Fiberoptic laryngoscopy showed normal bilateral vocal fold motion and no obvious lesions. Microlaryngoscopy and bronchoscopy showed post-cricoid edema. The orogastric tube was removed and a gastrostomy tube was placed. Three days later, the stridor and
2. Discussion NG tube syndrome is a rare but serious condition reported primarily in adult patients, comprising bilateral vocal fold dysfunction with associated respiratory compromise [2,4]. The only two cases described in children were reported more than 70 years ago. In both cases, vocal fold dysfunction was again described [1]. This case series is the first description of the presentation and outcomes of NG tube syndrome in infants. As in previously reported adult cases, the three infants at our institution developed significant respiratory distress that was temporally related to NG tube placement. In contrast to previously reported cases in adults and older children, these infants developed post-cricoid edema, inflammation, and mucosal damage without developing impaired vocal fold mobility. Sofferman et al. [2] noted that NG tubes are typically present for days to weeks before the manifestation of symptoms. A metaanalysis by Brousseau et al. [4] estimated a range of NG tube syndrome onset from 12 h after intubation to 2 weeks after extubation. Apostolakis et al. [3] found their patients experienced symptoms within 48 hours of NG intubation. While the time to onset has varied between studies, time to recovery from respiratory symptoms and vocal fold dysfunction in adults has generally been estimated at 1–2 weeks [4,10]. In our case series, the stridor, respiratory distress, and post-cricoid inflammation in these children resolved much more quickly (mean SD, 2 1 days). The role of gastroesophageal reflux in the pathophysiology of infant nasogastric tube syndrome is unclear. Reflux is known to cause airway distress in infants, with a variety of common manifestations [12]. NG tubes have been shown to increase reflux in both preterm infants [13] and adults [14]. Furthermore, changing from NG tube feeding to gastrostomy tube feeding may reduce reflux, at least in adults [15,16]. All three patients in our series were on acid suppressive therapy with one or more medications at the time of onset of their airway symptoms, and continued therapy with these agents did appear to alter their symptoms. Non-acidic reflux may also be an agent of laryngeal injury. For example, pepsin has been shown to cause intracellular damage to hypopharyngeal epithelial cells at pH 7 [17]. Accordingly, leaving the NG tube in place and simply continuing acid suppressive therapy may not be sufficient to prevent NG tube syndrome.
884
J. Harmon et al. / International Journal of Pediatric Otorhinolaryngology 78 (2014) 882–884
3. Conclusion NG tube syndrome should be considered in infants with otherwise unexplained respiratory distress in the presence of NG or orogastric tubes. Normal vocal fold motion does not rule out this syndrome in infants. Removal of the offending tube may lead to quick resolution of respiratory distress, while acid suppression alone may not be adequate to prevent this syndrome. Future investigation is necessary to clarify the pathophysiologic mechanisms for the different presentations in adults or older children and infants. Authors’ contributions Harmon contributed to manuscript preparation, editing, and final approval. Balakrishnan contributed to conception, design, data collection, manuscript preparation, editing, and final approval. De Alarcon and Hart contributed to conception, design, data collection, editing, and final approval. Conflict of interest None declared. References [1] S. Iglauer, W.F. Molt, Severe injury to the larynx resulting from the indwelling duodenal tube, Ann. Otol. Rhinol. Laryngol. 48 (1939) 886–904. [2] R.A. Sofferman, C.E. Haisch, J.A. Kirchner, N.J. Hardin, The nasogastric tube syndrome, Laryngoscope 100 (1990) 962–968.
[3] L.W. Apostolakis, G.F. Funk, L.F. Urdaneta, T.M. McCulloch, M.M. Jeyapalan, The nasogastric tube syndrome: two case reports and a review of the literature, Head Neck 23 (2001) 59–63. [4] V.J. Brousseau, K.M. Kost, A rare but serious entity: nasogastric tube syndrome, Otolaryngol. Head Neck Surg. 135 (2006) 677–679. [5] M. Friedman, H. Baim, V. Shelton, M. Stobnicki, T. Chilis, T. Ferrara, et al., Laryngeal injuries secondary to nasogastric tubes, Am. Otol. Rhinol. Laryngol. 90 (1981) 469–474. [6] V.J. Brousseau, K.M. Kost, Nasogastric tube syndrome, J. Otolaryngol. 36 (2007) E96–E97. [7] B.V. del Campo, D.M. Perez, D.S. Garrido, Nasogastric tube syndrome: a case report, Acta Otorrinolaringol. Esp. 61 (2010) 85–86. [8] E. Isozaki, S. Tobisawa, R. Naito, T. Mizutani, H. Hayashi, E.L. Marcus, et al., A variant form of nasogastric tube syndrome, Intern. Med. 44 (2005) 1286–1290. [9] E.L. Marcus, Y. Caine, K. Hamdan, M. Gross, Nasogastric tube syndrome: a lifethreatening laryngeal obstruction in a 72-year-old patient, Age Ageing 35 (2006) 538–539. [10] V.I.N. Nehru, H.J. Al Shammari, A.M. Jaffer, Nasogastric tube syndrome: the unilateral variant, Med. Princ. Pract. 12 (2003) 44–46. [11] M. Ohshima, E. Hori, A. Suzuki, H. Katoh, T. Itagaki, Y. Adachi, et al., Nasogastric tube syndrome suspected at the end of anesthesia, Masui 59 (2010) 495–497 (abstract). [12] S.R. Orenstein, An overview of reflux-associated disorders in infants: apnea, laryngospasm, and aspiration, Am. J. Med. 111 (2001) 60S–63S. [13] C.S. Peter, C. Wiechers, B. Bohnhorst, J. Silnry, C.F. Poets, Influence of nasogastric tubes on gastroesophageal reflux in preterm infants: a multiple intraluminal impedance study, J. Pediatr. 141 (2002) 277–279. [14] B.J. Manning, D.C. Winter, G. McGreal, W.O. Kirwan, H.P. Redmond, Nasogastric intubation causes gastroesophageal reflux in patients undergoing elective laparotomy, Surgery 130 (2001) 788–791. [15] S.H. Jung, S.H. Dong, J.Y. Lee, N.H. Kim, J.Y. Jang, H.J. Kim, et al., Percutaneous endosopic gastrostomy prevents gastroesophageal reflux in patients with nasogastric tube feeding: a prospective study with 24-hour pH monitoring, Gut Liver 5 (2011) 288–292. [16] T.H. Lee, Y.C. Shiun, Changes in gastroesophageal reflux in patients with nasogastric tube followed by percutaneous endoscopic gastrostomy, J. Formos. Med. Assoc. 110 (2011) 115–119. [17] N. Johnson, C.W. Wells, T.L. Samuels, J.H. Blumin, Rationale for targeting pepsin in the treatment of reflux disease, Ann. Otol. Rhinol. Laryngol. 119 (2010) 547–558.
Contents lists available at ScienceDirect
International Journal of Pediatric Otorhinolaryngology journal homepage: www.elsevier.com/locate/ijporl
Case Report
The nasogastric tube syndrome in infants§ Jeffrey Harmon a, Karthik Balakrishnan b,*, Alessandro de Alarcon b,c, Catherine K. Hart b,c a
University of Cincinnati College of Medicine, Office of Student Affairs, Medical Sciences Building E-251, PO Box 670552, Cincinnati, OH 45267, United States Division of Pediatric Otolaryngology – Head & Neck Surgery, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Avenue, MLC-2018, Cincinnati, OH 45229, United States c Department of Otolaryngology – Head & Neck Surgery, University of Cincinnati College of Medicine, 231 Albert Sabin Way ML 0528, Cincinnati, OH 45267, United States b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 16 January 2014 Received in revised form 7 February 2014 Accepted 8 February 2014 Available online 20 February 2014
This series of three patients is the first description of the presentation, clinical course, and endoscopic findings of nasogastric tube-related airway distress, or nasogastric tube syndrome, in infants. We identify key differences in disease features from those described in adults, based on our literature review. Specifically, infant nasogastric tube syndrome presented as significant respiratory distress and postcricoid inflammation without vocal fold immobility. Symptoms resolved more quickly (mean SD, 2 1 days) than reported in adults. We suggest that nasogastric tube syndrome should be considered in infants with otherwise unexplained respiratory distress, even in the absence of impaired vocal fold mobility. ß 2014 Elsevier Ireland Ltd. All rights reserved.
Keywords: Infant Stridor Respiratory distress Nasogastric tube
1. Introduction Iglauer and Molt [1] first described damage to the larynx due to an indwelling enteric tube in a case series in 1939, with the majority of their reported cases showed laryngeal chondritis, edema, and vocal fold immobility. Nasogastric tube syndrome was later formally defined by Sofferman et al. [2] in 1990 as an uncommon phenomenon involving throat pain, vocal fold dysfunction, and respiratory distress in adult patients as a result of post-cricoid mucosal damage due to the presence of a nasogastric (NG) tube. Suggested mechanisms by which this syndrome might occur include friction from the motion of the larynx sliding up and down against the nasogastric tube, cricopharyngeus muscle contraction forcing the tube against the mucosa overlying the posterior cricoid cartilage, and pinching of the tube between the cricoid cartilage and anterior cervical spine while the patient is in a supine position [2]. Mechanical irritation and compression-related ischemia are thought to result in inflammation, ulceration, and possible infection of the interarytenoid and post-cricoid mucosa, cricoarytenoid muscle (vocal fold abductor), and cricoid cartilage. Subsequent bilateral vocal fold dysfunction may occur, leading to respiratory
distress [3,4]. A study on dogs by Friedman et al. [5] suggested midline nasogastric tube placement predisposes patients to development of nasogastric tube syndrome. Management, though not defined specifically in the literature, includes removal of the NG tube and medical treatment with steroids, antibiotics, and antireflux therapy. Many reported cases have also required tracheostomy [1,4]. To our knowledge, 37 cases of nasogastric tube syndrome have been reported as of 2013 [1–11]. Of these cases, only 2 were children, aged 4 and 5 years, respectively. Both were reported by Iglauer and Molt long before the development of flexible nasopharyngoscopy [1,3]. Both patients required tracheotomy, with subsequent direct laryngoscopy showing laryngeal inflammation, arytenoid edema, and significantly reduced vocal fold mobility. Despite the frequent use of nasogastric and orogastric tubes in infants and young children, associated laryngeal injury has not been described in this younger age group. We present three cases encountered in the otolaryngology division of a tertiary children’s hospital specializing in aerodigestive disorders. This study was approved by the Institutional Review Board at Cincinnati Children’s Hospital Medical Center. 1.1. Case 1
§
Presented at the American Society of Pediatric Otolaryngology 2013 Annual Meeting, Washington, DC. * Corresponding author at: 3333 Burnet Avenue, MLC 2018, Cincinnati, OH 45227, United States. Tel.: +1 513 636 4355; fax: +1 513 636 8133. E-mail address: [email protected] (K. Balakrishnan). http://dx.doi.org/10.1016/j.ijporl.2014.02.013 0165-5876/ß 2014 Elsevier Ireland Ltd. All rights reserved.
The first patient is a 2-month old male with coarctation of the aorta status post repair. An NG tube was placed six weeks later due to feeding difficulties. Two days after placement of the NG tube, the
[(Fig._1)TD$IG]
[(Fig._2)TD$IG]
J. Harmon et al. / International Journal of Pediatric Otorhinolaryngology 78 (2014) 882–884
883
Fig. 1. Patient 1, endoscopic view prior to NG tube removal. Note the significant postcricoid edema and granulation.
Fig. 2. Patient 2, endoscopic view prior to NG tube removal. Note the significant postcricoid edema and granulation.
patient developed acute inspiratory stridor, retractions, and desaturations worsening over the next 5 days. These symptoms were unresponsive to systemic steroids, inhaled racemic epinephrine, gastric acid suppression with ranitidine and proton pump inhibitors, and change in body position. Fiberoptic laryngoscopy showed normal bilateral vocal fold motion. Microlaryngoscopy and bronchoscopy performed 5 days after the onset of respiratory symptoms showed interarytenoid edema, erythema, and postcricoid granulation tissue around the NG tube. The nasogastric tube was removed immediately and replaced with total parenteral nutrition followed by gastrostomy tube placement. His stridor improved within one day of NG tube removal; the stridor and retractions resolved completely within five days. Follow up fiberoptic laryngoscopy showed improving post-cricoid granulation (Fig. 1).
increased work of breathing had completely resolved. Fiberoptic examination one week after the disappearance of airway symptoms showed resolution of post-cricoid edema.
1.2. Case 2 The second patient is a 3-month old female status-post slide tracheoplasty with cardiopulmonary bypass for complete tracheal rings. After an NG tube had been in place for approximately 11 days, she developed increased work of breathing. Serial microlaryngoscopy and bronchoscopies showed persistent severe postcricoid edema. Flexible laryngoscopy showed normal bilateral true vocal fold motion. The increased work of breathing and inspiratory stridor persisted over seven weeks despite twice daily proton pump inhibitor therapy, after which the NG tube was replaced with a gastrostomy tube. The stridor resolved two days later. Repeat microlaryngoscopy and bronchoscopy one month later showed improved post-cricoid edema (Fig. 2). 1.3. Case 3 Patient 3 is a 3-month old male, born at 30 weeks, intubated for bradycardia after emergent cesarean section due to preterm premature rupture of membranes. An orogastric tube was placed four days after intubation, and the patient was extubated nearly two months later. The orogastric tube remained in place. The patient remained on twice daily ranitidine therapy for gastric acid suppression. One month after removal of the endotracheal tube, the patient was noted to have intermittent biphasic stridor. Fiberoptic laryngoscopy showed normal bilateral vocal fold motion and no obvious lesions. Microlaryngoscopy and bronchoscopy showed post-cricoid edema. The orogastric tube was removed and a gastrostomy tube was placed. Three days later, the stridor and
2. Discussion NG tube syndrome is a rare but serious condition reported primarily in adult patients, comprising bilateral vocal fold dysfunction with associated respiratory compromise [2,4]. The only two cases described in children were reported more than 70 years ago. In both cases, vocal fold dysfunction was again described [1]. This case series is the first description of the presentation and outcomes of NG tube syndrome in infants. As in previously reported adult cases, the three infants at our institution developed significant respiratory distress that was temporally related to NG tube placement. In contrast to previously reported cases in adults and older children, these infants developed post-cricoid edema, inflammation, and mucosal damage without developing impaired vocal fold mobility. Sofferman et al. [2] noted that NG tubes are typically present for days to weeks before the manifestation of symptoms. A metaanalysis by Brousseau et al. [4] estimated a range of NG tube syndrome onset from 12 h after intubation to 2 weeks after extubation. Apostolakis et al. [3] found their patients experienced symptoms within 48 hours of NG intubation. While the time to onset has varied between studies, time to recovery from respiratory symptoms and vocal fold dysfunction in adults has generally been estimated at 1–2 weeks [4,10]. In our case series, the stridor, respiratory distress, and post-cricoid inflammation in these children resolved much more quickly (mean SD, 2 1 days). The role of gastroesophageal reflux in the pathophysiology of infant nasogastric tube syndrome is unclear. Reflux is known to cause airway distress in infants, with a variety of common manifestations [12]. NG tubes have been shown to increase reflux in both preterm infants [13] and adults [14]. Furthermore, changing from NG tube feeding to gastrostomy tube feeding may reduce reflux, at least in adults [15,16]. All three patients in our series were on acid suppressive therapy with one or more medications at the time of onset of their airway symptoms, and continued therapy with these agents did appear to alter their symptoms. Non-acidic reflux may also be an agent of laryngeal injury. For example, pepsin has been shown to cause intracellular damage to hypopharyngeal epithelial cells at pH 7 [17]. Accordingly, leaving the NG tube in place and simply continuing acid suppressive therapy may not be sufficient to prevent NG tube syndrome.
884
J. Harmon et al. / International Journal of Pediatric Otorhinolaryngology 78 (2014) 882–884
3. Conclusion NG tube syndrome should be considered in infants with otherwise unexplained respiratory distress in the presence of NG or orogastric tubes. Normal vocal fold motion does not rule out this syndrome in infants. Removal of the offending tube may lead to quick resolution of respiratory distress, while acid suppression alone may not be adequate to prevent this syndrome. Future investigation is necessary to clarify the pathophysiologic mechanisms for the different presentations in adults or older children and infants. Authors’ contributions Harmon contributed to manuscript preparation, editing, and final approval. Balakrishnan contributed to conception, design, data collection, manuscript preparation, editing, and final approval. De Alarcon and Hart contributed to conception, design, data collection, editing, and final approval. Conflict of interest None declared. References [1] S. Iglauer, W.F. Molt, Severe injury to the larynx resulting from the indwelling duodenal tube, Ann. Otol. Rhinol. Laryngol. 48 (1939) 886–904. [2] R.A. Sofferman, C.E. Haisch, J.A. Kirchner, N.J. Hardin, The nasogastric tube syndrome, Laryngoscope 100 (1990) 962–968.
[3] L.W. Apostolakis, G.F. Funk, L.F. Urdaneta, T.M. McCulloch, M.M. Jeyapalan, The nasogastric tube syndrome: two case reports and a review of the literature, Head Neck 23 (2001) 59–63. [4] V.J. Brousseau, K.M. Kost, A rare but serious entity: nasogastric tube syndrome, Otolaryngol. Head Neck Surg. 135 (2006) 677–679. [5] M. Friedman, H. Baim, V. Shelton, M. Stobnicki, T. Chilis, T. Ferrara, et al., Laryngeal injuries secondary to nasogastric tubes, Am. Otol. Rhinol. Laryngol. 90 (1981) 469–474. [6] V.J. Brousseau, K.M. Kost, Nasogastric tube syndrome, J. Otolaryngol. 36 (2007) E96–E97. [7] B.V. del Campo, D.M. Perez, D.S. Garrido, Nasogastric tube syndrome: a case report, Acta Otorrinolaringol. Esp. 61 (2010) 85–86. [8] E. Isozaki, S. Tobisawa, R. Naito, T. Mizutani, H. Hayashi, E.L. Marcus, et al., A variant form of nasogastric tube syndrome, Intern. Med. 44 (2005) 1286–1290. [9] E.L. Marcus, Y. Caine, K. Hamdan, M. Gross, Nasogastric tube syndrome: a lifethreatening laryngeal obstruction in a 72-year-old patient, Age Ageing 35 (2006) 538–539. [10] V.I.N. Nehru, H.J. Al Shammari, A.M. Jaffer, Nasogastric tube syndrome: the unilateral variant, Med. Princ. Pract. 12 (2003) 44–46. [11] M. Ohshima, E. Hori, A. Suzuki, H. Katoh, T. Itagaki, Y. Adachi, et al., Nasogastric tube syndrome suspected at the end of anesthesia, Masui 59 (2010) 495–497 (abstract). [12] S.R. Orenstein, An overview of reflux-associated disorders in infants: apnea, laryngospasm, and aspiration, Am. J. Med. 111 (2001) 60S–63S. [13] C.S. Peter, C. Wiechers, B. Bohnhorst, J. Silnry, C.F. Poets, Influence of nasogastric tubes on gastroesophageal reflux in preterm infants: a multiple intraluminal impedance study, J. Pediatr. 141 (2002) 277–279. [14] B.J. Manning, D.C. Winter, G. McGreal, W.O. Kirwan, H.P. Redmond, Nasogastric intubation causes gastroesophageal reflux in patients undergoing elective laparotomy, Surgery 130 (2001) 788–791. [15] S.H. Jung, S.H. Dong, J.Y. Lee, N.H. Kim, J.Y. Jang, H.J. Kim, et al., Percutaneous endosopic gastrostomy prevents gastroesophageal reflux in patients with nasogastric tube feeding: a prospective study with 24-hour pH monitoring, Gut Liver 5 (2011) 288–292. [16] T.H. Lee, Y.C. Shiun, Changes in gastroesophageal reflux in patients with nasogastric tube followed by percutaneous endoscopic gastrostomy, J. Formos. Med. Assoc. 110 (2011) 115–119. [17] N. Johnson, C.W. Wells, T.L. Samuels, J.H. Blumin, Rationale for targeting pepsin in the treatment of reflux disease, Ann. Otol. Rhinol. Laryngol. 119 (2010) 547–558.
