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Bilateral Vocal Cord Paralysis After Disc Battery Ingestion...cause transient vocal cord paralysis...

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Poster Design & Printing by Genigraphics ® - 800.790.4001 CASE 1 DISCUSSION CASE 2 Figure 2. Patient 1 underwent direct laryngoscopy, which revealed immobile vocal folds in a paramedian position. Figure 4. Patient 2 underwent balloon dilatation to treat her glottic stenosis. Unfortunately, the results were temporary. ABSTRACT CONTACT DISCUSSION Figure 1. PA and lateral x-rays reveal a metallic, round foreign body in the upper esophagus. Note the peripheral halo of reduced density on the PA image and the step-off on the lateral view, which raise the suspicion of a disc battery. A 15-month-old girl with no significant medical history was brought to her pediatrician’s office after her grandmother saw her playing with a disc battery and suspected ingestion. PA and lateral chest x-rays were obtained and showed a battery at the level of the upper esophagus. She was immediately sent to the emergency room of a tertiary care hospital. Upon arrival, the otolaryngology service was consulted and arranged for emergency direct laryngoscopy and esophagoscopy. A disc battery was encountered at the level of the cricopharyngeus and was removed about four hours after ingestion. The esophageal mucosa was severely discolored and showed circumferential damage consistent with a burn injury. The patient was extubated in the operating room and was started on intravenous antibiotics. She did well in the immediate postoperative period. After tolerating nasogastric tube feeds, a barium esophagram showed the development of a stricture. She was discharged from the hospital and followed by a pediatric surgeon for esophageal dilatation. Ten weeks after the initial esophagoscopy, the pediatric surgeon noted the patient to have inspiratory stridor. She was referred to a pediatric otolaryngologist, who discovered bilateral true vocal fold paralysis on fiberoptic laryngoscopy. She was subsequently admitted to the hospital for direct laryngoscopy, bronchoscopy, and tracheostomy. The patient was followed as an outpatient and did not regain vocal fold mobility. Eleven months after ingestion, she underwent an endoscopic posterior cricoid split with rib graft interposition but failed to be decannulated. She subsequently had six separate procedures to alleviate her stenosis, including balloon dilatation and carbon dioxide laser ablation, but she still required tracheostomy. She then underwent a second laryngotracheal reconstruction with anterior and posterior rib grafts and, nearly five years after the initial insult, was decannulated. ingestion. Tissue damage due to alkali exposure persists until the solution is neutralized and may continue for days to weeks [3]. This may explain the delayed nature of the paralysis. Presumably, the vocal fold paralysis in these cases is due to extension of the burn injury to involve the recurrent laryngeal nerves. Another plausible explanation is that the inflammatory reaction and fibrosis extended to include either the recurrent laryngeal nerves or the cricoarytenoid joints. The number of major or fatal outcomes from battery ingestion has increased 6.7 fold over the past 25 years, paralleling the increased use of large diameter (20 mm) lithium cells. Large diameter batteries are more likely to lodge in the esophagus. Furthermore, 20 mm lithium batteries generate greater current more rapidly due to increased voltage (3V) and capacitance compared to other disc batteries. As a result, they pose a greater risk to children, and 12.6% of children younger than six who ingest a battery at least 20 mm in diameter will suffer a serious complication or death [3]. These two cases offer several important lessons. First, given the rapidity and severity of tissue damage, efforts must focus on primary prevention. A large study of battery ingestions showed that children younger than six removed the battery directly from a product in 61.8% of cases and from battery packaging in 8.2% [4]. Manufacturers should produce more secure battery compartments, and parents must keep batteries away from children [4]. Second, parents and medical professionals must be educated about the potential disasters of battery ingestion in order to avoid delays in treatment. If there is any suspicion of battery ingestion, the child should be brought immediately to a tertiary care center with the ability to provide appropriate and timely treatment. Finally, the length of time of impaction, location in the esophagus relative to surrounding structures, type of battery, and orientation of the battery may help predict a delayed complication and should help guide the length of hospitalization. Close follow up with a pediatrician and otolaryngologist is necessary in all cases. A 13-month-old girl with a history of congenital hearing loss and bilateral hearing aid use presented to an outside emergency room after the acute onset of drooling and several episodes of vomiting that began while she was playing. A PA and lateral chest x-ray revealed the presence of a metallic, round foreign body in the upper esophagus, which was believed to be a coin. Transfer was arranged to a tertiary care institution having pediatric otolaryngology staff. Upon arrival, repeat imaging confirmed the location of the foreign object. In addition, a halo seen on the PA image and a step-off seen on the lateral image raised the concern for disc battery ingestion. The patient was immediately brought to the operating room for direct laryngoscopy and esophagoscopy. A lithium disc battery was removed from just below the cricopharyngeus muscle. Though removed six hours after ingestion, examination of the local esophageal mucosa showed circumferential black discoloration and tissue damage. The patient was extubated and transferred to the pediatric intensive care unit. Intravenous ampicillin/sulbactam and dexamethasone were initiated. On the second postoperative day, steroids were discontinued and oral feeds were initiated. She was discharged home on postoperative day three. Two days after discharge, the patient was brought to the emergency room with worsening inspiratory stridor and subcostal retractions. Fiberoptic laryngoscopy revealed bilateral true vocal fold immobility with paramedian vocal fold positions. The patient was readmitted to the PICU and restarted on systemic steroids. Direct laryngoscopy and bronchoscopy with spontaneous ventilation were performed and showed bilateral vocal cord immobility and mild subglottic erythema but an otherwise unremarkable larynx and trachea. Her respiratory status improved such that she had mild inspiratory stridor upon exertion. Tracheostomy was not needed, and she was discharged home on a steroid taper after four days. On outpatient follow-up, she was noted to have limited return of function of her left true vocal cord three months after the incident. The most recent fiberoptic examination at six- month follow-up was unchanged. She continues to have intermittent inspiratory stridor and tolerates regular diet. More than 3700 cases of disc battery ingestion were reported in the U.S. in 2008 [1]. Batteries that pass into the stomach generally follow a benign course through the GI tract and can be treated conservatively [2]. Conversely, those that lodge in the esophagus must be treated as true emergencies, even in the absence of symptoms, because tissue damage can be rapid and severe injury may occur after just two hours [3,4]. Reported complications of esophageal disc batteries may be catastrophic and include esophageal stricture, tracheoesophageal fistula [5,6], aorto-esophageal fistula [7,8], fistulization into other vessels [5], and esophageal perforation [9,10]. Many of these complications develop days to weeks after removal [3,5-10]. The initial challenge facing physicians is to distinguish an ingested battery from a coin, which is the most common foreign body ingested by children in the U.S. and Europe [11]. Occasionally, a strong history or witnessed event will help. More often, symptomatic patients will have a neck or chest x-ray that reveals a round, metallic esophageal foreign body. PA x- rays of a disc battery often reveal a peripheral halo of reduced density, and lateral views show a step-off or greater depth than a coin [12]. Physicians should specifically look for these features in all cases because the consequences of misdiagnosis and delay of treatment can be devastating. Three mechanisms of battery-induced local tissue damage have been proposed: leakage of alkaline electrolyte, pressure necrosis, and generation of an external current through physiologic electrolyte solutions [3,4]. Animal models suggest that external current generation is the major mechanism [13]. The battery’s negative pole generates sodium hydroxide and an alkaline tissue pH, while the positive end creates hydrochloric acid and an acidic pH. Tissue damage at the alkaline terminal – manifested by liquefactive necrosis, fat saponification, and inflammatory cell invasion – is much more severe and infiltrative. This creates a polarity of induced tissue damage suggesting that complications may be more likely when an impacted battery’s negative pole faces anteriorly, allowing damage to reach the trachea, larynx, recurrent laryngeal nerves, and aorta or other vessels. Though esophageal foreign bodies have been noted to cause transient vocal cord paralysis [14], only two previous reports of bilateral vocal cord paralysis specifically due to esophageal disc batteries have been reported [8,12]. Both reports suggest the paralysis was immediate, and one patient had some return of vocal cord mobility at six-month follow-up. The two cases reported here describe infants who had esophageal disc batteries removed several hours after Objectives: 1. Reinforce the need to educate medical professionals and parents about the importance of the prevention and urgent workup and treatment of battery ingestion. 2. Suggest the need for close and prolonged follow-up of patients sustaining mucosal injury due to battery ingestion. Methods: Two cases of bilateral vocal cord paralysis as a delayed complication after the ingestion of a disc battery are reported. The anatomical basis for this sequela and the literature regarding this topic are reviewed. Results: A 13-month-old and a 15-month- old were referred to two different tertiary care centers after x-rays taken at outside institutions confirmed the presence of round foreign bodies in the upper esophagus. Direct laryngoscopy, rigid esophagoscopy, and foreign body removal were completed within six and four hours, respectively. Circumferential corrosive injuries of the esophageal mucosa were noted in both. The first patient was discharged home on postoperative day three but returned two days later with stridor. Laryngoscopy was significant for bilateral vocal cord immobility and paramedian vocal cord position. She was followed closely and has regained partial mobility of her left vocal cord at three months follow up. The second patient was noted to be stridorous ten weeks after ingestion. Laryngoscopy also revealed bilateral vocal cord paralysis, and tracheostomy was required. Nearly five years later, after numerous airway procedures, she was decannulated. Conclusion: Bilateral vocal cord paralysis is an uncommon yet potentially catastrophic complication of disc battery ingestion, and active follow-up with an otolaryngologist is necessary for timely identification and management. David H. Burstein, MD SUNY Downstate Medical Center Department of Otolaryngology [email protected] 718-270-1638 REFERENCES 1. Bronstein AC, Spyker DA, Cantilena LR, Green JL, Rumack BH, Giffin SL. 2008 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 26 th Annual Report. Clinical Toxicology 2009; 47: 911-1084. 2. Litovitz T, Schmitz BF. Ingestion of Cylindrical and Button Batteries: An Analysis of 2382 Cases. Pediatrics 1992; 89: 747-757. 3. Litovitz T, Whitaker N, Clark L, White NC, Marsolek M. Emerging Battery-Ingestion Hazard: Clinical Implications. Pediatrics 2010; 125: 1168-1177. 4. Litovitz T, Whitaker N, Clark L. Preventing Battery Ingestions: An Analysis of 8648 Cases. Pediatrics 2010; 125: 1178-1183. 5. Blatnik DS, Toohill RJ, Lehman RH. Fatal complicaion from an alkaline battery foreign body in the esophagus. Annals of Otology, Rhinology, and Laryngology 1977; 86: 611-615. 6. Sigalet D, Lees G. Tracheoesophageal injury secondary to disc battery ingestion. Journal of Pediatric Surgery 1988; 23: 996-998. 7. Shabino CL, Feinberg AN. Esophageal perforation secondary to alkaline battery ingestion. Journal of the American College of Emergency Physicians 1979; 8(9): 360-362. 8. Hamilton JM, Schraff SA, Notrica DM. Severe injuries from coin cell battery ingestions: 2 case reports. Journal of Pediatric Surgery 2009; 44: 644-647. 9. Samad L, Ali M, Ramzi H. Button battery ingestion: hazards of esophageal impaction. Journal of Pediatric Surgery 1999; 34: 1527-1531. 10. Gordon AC, Gough MH. Oesophageal perforation after button battery ingestion. Annals of the Royal College of Surgeons of England 1993; 75: 362-364. 11. Kay M, Wyllie R. Pediatric Foreign Bodies and Their Management. Current Gastroenterology Reports 2005; 7: 212-218. 12. Bernstein JM, Burrows SA, Saunders MW. Lodged oesophageal button battery masquerading as a coin: an unusual cause of bilateral vocal cord paralysis. Emergency Medicine Journal 2007; 24: e15 13. Yoshikawa T, Asai S, Takekawa Y, Kida A, Ishikawa K. Experimental investigation of battery- induced esophageal burn injury in rabbits. Critical Care Medicine 1997; 25: 2039-2044. 14. Virgilis D, Weinberger JM, Fisher D, Goldberg S, Picard E, Kerem E. Vocal Cord Paralysis Secondary to Impacted Esophageal Foreign Bodies in Young Children. Pediatrics 2001; 107(6): e101.6 David H. Burstein, MD 1 ; Mark J. Burstein, MD 2 ; Jason Mouzakes, MD 2 ; Perminder S. Parmar, MD 1 ; and Sydney C. Butts, MD 1 1 SUNY Downstate Medical Center, Brooklyn, NY; 2 Albany Medical Center, Albany, NY Bilateral Vocal Cord Paralysis After Disc Battery Ingestion Bilateral Vocal Cord Paralysis After Disc Battery Ingestion Figure 5. Attempts to ablate posterior glottic scar tissue using a CO 2 laser in Patient 2 also failed. Figure 3. At 6-month follow up, Patient 1 had regained limited function of her left vocal fold, as seen on fiberoptic laryngoscopy.
Transcript
Page 1: Bilateral Vocal Cord Paralysis After Disc Battery Ingestion...cause transient vocal cord paralysis [14], only two previous reports of bilateral vocal cord paralysis specifically due

Poster Design & Printing by Genigraphics® - 800.790.4001

CASE 1 DISCUSSION

CASE 2

Figure 2. Patient 1 underwent direct laryngoscopy, which

revealed immobile vocal folds in a paramedian position.

Figure 4. Patient 2 underwent balloon dilatation to treat her glottic stenosis. Unfortunately, the results were temporary.

ABSTRACT

CONTACT

DISCUSSION

Figure 1. PA and lateral x-rays reveal a metallic, round foreign body in the upper esophagus. Note the peripheral halo of reduced density on

the PA image and the step-off on the lateral view, which raise the suspicion of a disc battery.

A 15-month-old girl with no significant medical history was brought to her pediatrician’s office after her grandmother saw her playing with a disc battery and suspected ingestion. PAand lateral chest x-rays were obtained and showed a battery at the level of the upper esophagus. She was immediately sent to the emergency room of a tertiary care hospital.

Upon arrival, the otolaryngology service was consulted and arranged for emergency direct laryngoscopy and esophagoscopy. A disc battery was encountered at the level of the cricopharyngeus and was removed about four hours after ingestion. The esophageal mucosa was severely discolored and showed circumferential damage consistent with a burn injury. The patient was extubated in the operating room and was started on intravenous antibiotics. She did well in the immediate postoperative period. After tolerating nasogastric tube feeds, a barium esophagram showed the development of a stricture. She was discharged from the hospital and followed bya pediatric surgeon for esophageal dilatation.

Ten weeks after the initial esophagoscopy, the pediatric surgeon noted the patient to have inspiratory stridor. She was referred to a pediatric otolaryngologist, who discovered bilateral true vocal fold paralysis on fiberoptic laryngoscopy. She was subsequently admitted to the hospital for direct laryngoscopy, bronchoscopy, and tracheostomy.

The patient was followed as an outpatient and did not regain vocal fold mobility. Eleven months after ingestion, she underwent an endoscopic posterior cricoid split with rib graft interposition but failed to be decannulated. She subsequently had six separate procedures to alleviate her stenosis, includingballoon dilatation and carbon dioxide laser ablation, but she still required tracheostomy. She then underwent a second laryngotracheal reconstruction with anterior and posterior rib grafts and, nearly five years after the initial insult, was decannulated.

ingestion. Tissue damage due to alkali exposure persists until the solution is neutralized and may continue for days to weeks [3]. This may explain the delayed nature of the paralysis. Presumably, the vocal fold paralysis in these cases is due to extension of the burn injury to involve the recurrent laryngeal nerves. Another plausible explanation is that the inflammatoryreaction and fibrosis extended to include either the recurrent laryngeal nerves or the cricoarytenoid joints.

The number of major or fatal outcomes from battery ingestion has increased 6.7 fold over the past 25 years, paralleling the increased use of large diameter (20 mm) lithium cells. Large diameter batteries are more likely to lodge in theesophagus. Furthermore, 20 mm lithium batteries generate greater current more rapidly due to increased voltage (3V) and capacitance compared to other disc batteries. As a result, theypose a greater risk to children, and 12.6% of children younger than six who ingest a battery at least 20 mm in diameter will suffer a serious complication or death [3].

These two cases offer several important lessons. First, given the rapidity and severity of tissue damage, efforts must focus on primary prevention. A large study of battery ingestions showed that children younger than six removed the battery directly from a product in 61.8% of cases and from battery packaging in 8.2% [4]. Manufacturers should produce more secure battery compartments, and parents must keep batteries away from children [4]. Second, parents and medical professionals must be educated about the potential disasters of battery ingestion in order to avoid delays in treatment. If there is any suspicion of battery ingestion, the child should be brought immediately to a tertiary care center with the ability to provide appropriate and timely treatment. Finally, the length of time of impaction, location in the esophagus relative to surrounding structures, type of battery, and orientation of the battery may help predict a delayed complication and should help guide the length of hospitalization. Close follow up with a pediatrician and otolaryngologist is necessary in all cases.

A 13-month-old girl with a history of congenital hearing loss and bilateral hearing aid use presented to an outside emergency room after the acute onset of drooling and several episodes of vomiting that began while she was playing. A PA and lateral chest x-ray revealed the presence of a metallic, round foreign body in the upper esophagus, which was believed to be a coin. Transfer was arranged to a tertiary care institution having pediatric otolaryngology staff. Upon arrival, repeat imaging confirmed the location of the foreign object. In addition, a halo seen on the PA image and a step-off seen on the lateral image raised the concern for disc battery ingestion.

The patient was immediately brought to the operating room for direct laryngoscopy and esophagoscopy. A lithium disc battery was removed from just below the cricopharyngeusmuscle. Though removed six hours after ingestion, examination of the local esophageal mucosa showed circumferential black discoloration and tissue damage. The patient was extubatedand transferred to the pediatric intensive care unit. Intravenous ampicillin/sulbactam and dexamethasone were initiated. On the second postoperative day, steroids were discontinued and oral feeds were initiated. She was discharged home on postoperative day three.

Two days after discharge, the patient was brought to the emergency room with worsening inspiratory stridor and subcostal retractions. Fiberoptic laryngoscopy revealed bilateral true vocal fold immobility with paramedian vocal fold positions. The patient was readmitted to the PICU and restarted on systemic steroids. Direct laryngoscopy and bronchoscopy with spontaneous ventilation were performed and showed bilateral vocal cord immobility and mild subglottic erythema but an otherwise unremarkable larynx and trachea. Her respiratory status improved such that she had mild inspiratory stridor upon exertion. Tracheostomy was not needed, and she was discharged home on a steroid taper after four days.

On outpatient follow-up, she was noted to have limited return of function of her left true vocal cord three months after the incident. The most recent fiberoptic examination at six-month follow-up was unchanged. She continues to have intermittent inspiratory stridor and tolerates regular diet.

More than 3700 cases of disc battery ingestion were reported in the U.S. in 2008 [1]. Batteries that pass into the stomach generally follow a benign course through the GI tract and can be treated conservatively [2]. Conversely, those that lodge in the esophagus must be treated as true emergencies, even in the absence of symptoms, because tissue damage can be rapid and severe injury may occur after just two hours [3,4].Reported complications of esophageal disc batteries may be catastrophic and include esophageal stricture, tracheoesophageal fistula [5,6], aorto-esophageal fistula [7,8], fistulization into other vessels [5], and esophageal perforation[9,10]. Many of these complications develop days to weeks after removal [3,5-10].

The initial challenge facing physicians is to distinguish an ingested battery from a coin, which is the most common foreign body ingested by children in the U.S. and Europe [11]. Occasionally, a strong history or witnessed event will help. More often, symptomatic patients will have a neck or chest x-ray that reveals a round, metallic esophageal foreign body. PA x-rays of a disc battery often reveal a peripheral halo of reduceddensity, and lateral views show a step-off or greater depth than a coin [12]. Physicians should specifically look for these features in all cases because the consequences of misdiagnosis and delay of treatment can be devastating.

Three mechanisms of battery-induced local tissue damage have been proposed: leakage of alkaline electrolyte, pressure necrosis, and generation of an external current through physiologic electrolyte solutions [3,4]. Animal models suggest that external current generation is the major mechanism [13]. The battery’s negative pole generates sodium hydroxide and an alkaline tissue pH, while the positive end creates hydrochloric acid and an acidic pH. Tissue damage at the alkaline terminal – manifested by liquefactive necrosis, fat saponification, and inflammatory cell invasion – is much more severe and infiltrative. This creates a polarity of induced tissue damage suggesting that complications may be more likely when an impacted battery’s negative pole faces anteriorly, allowing damage to reach the trachea, larynx, recurrent laryngeal nerves,and aorta or other vessels.

Though esophageal foreign bodies have been noted to cause transient vocal cord paralysis [14], only two previous reports of bilateral vocal cord paralysis specifically due to esophageal disc batteries have been reported [8,12]. Both reports suggest the paralysis was immediate, and one patient had some return of vocal cord mobility at six-month follow-up.

The two cases reported here describe infants who hadesophageal disc batteries removed several hours after

Objectives: 1. Reinforce the need to educate medical professionals and parents about the importance of the prevention and urgent workup and treatment of battery ingestion. 2. Suggest the need for close and prolonged follow-up of patients sustaining mucosal injury due to battery ingestion.

Methods: Two cases of bilateral vocal cord paralysis as a delayed complication after the ingestion of a disc battery are reported. The anatomical basis for this sequela and the literature regarding this topic are reviewed.

Results: A 13-month-old and a 15-month-old were referred to two different tertiary care centers after x-rays taken at outside institutions confirmed the presence of round foreign bodies in the upper esophagus. Direct laryngoscopy, rigid esophagoscopy, and foreign body removal were completed within six and four hours, respectively. Circumferential corrosive injuries of the esophageal mucosa were noted in both. The first patient was discharged home on postoperative daythree but returned two days later with stridor. Laryngoscopy was significant for bilateral vocal cord immobility and paramedian vocal cord position. She was followed closely and has regained partial mobility of her left vocal cord at three months follow up. The second patient was noted to be stridorous ten weeks after ingestion. Laryngoscopy also revealed bilateral vocal cord paralysis, and tracheostomy was required. Nearly five years later, after numerous airway procedures, she was decannulated.

Conclusion: Bilateral vocal cord paralysis is an uncommon yet potentially catastrophic complication of disc battery ingestion, and active follow-up with an otolaryngologist is necessary for timely identification and management.

David H. Burstein, MDSUNY Downstate Medical Center

Department of [email protected]

718-270-1638

REFERENCES1. Bronstein AC, Spyker DA, Cantilena LR, Green JL, Rumack BH, Giffin SL. 2008 Annual Report of

the American Association of Poison Control Centers’ National Poison Data System (NPDS): 26th

Annual Report. Clinical Toxicology 2009; 47: 911-1084.2. Litovitz T, Schmitz BF. Ingestion of Cylindrical and Button Batteries: An Analysis of 2382 Cases.

Pediatrics 1992; 89: 747-757.3. Litovitz T, Whitaker N, Clark L, White NC, Marsolek M. Emerging Battery-Ingestion Hazard:

Clinical Implications. Pediatrics 2010; 125: 1168-1177.4. Litovitz T, Whitaker N, Clark L. Preventing Battery Ingestions: An Analysis of 8648 Cases.

Pediatrics 2010; 125: 1178-1183.5. Blatnik DS, Toohill RJ, Lehman RH. Fatal complicaion from an alkaline battery foreign body in the

esophagus. Annals of Otology, Rhinology, and Laryngology 1977; 86: 611-615.6. Sigalet D, Lees G. Tracheoesophageal injury secondary to disc battery ingestion. Journal of

Pediatric Surgery 1988; 23: 996-998.7. Shabino CL, Feinberg AN. Esophageal perforation secondary to alkaline battery ingestion.

Journal of the American College of Emergency Physicians 1979; 8(9): 360-362.8. Hamilton JM, Schraff SA, Notrica DM. Severe injuries from coin cell battery ingestions: 2 case

reports. Journal of Pediatric Surgery 2009; 44: 644-647.9. Samad L, Ali M, Ramzi H. Button battery ingestion: hazards of esophageal impaction. Journal of

Pediatric Surgery 1999; 34: 1527-1531.10. Gordon AC, Gough MH. Oesophageal perforation after button battery ingestion. Annals of the

Royal College of Surgeons of England 1993; 75: 362-364.11. Kay M, Wyllie R. Pediatric Foreign Bodies and Their Management. Current Gastroenterology

Reports 2005; 7: 212-218.12. Bernstein JM, Burrows SA, Saunders MW. Lodged oesophageal button battery masquerading as

a coin: an unusual cause of bilateral vocal cord paralysis. Emergency Medicine Journal 2007; 24: e15

13. Yoshikawa T, Asai S, Takekawa Y, Kida A, Ishikawa K. Experimental investigation of battery-induced esophageal burn injury in rabbits. Critical Care Medicine 1997; 25: 2039-2044.

14. Virgilis D, Weinberger JM, Fisher D, Goldberg S, Picard E, Kerem E. Vocal Cord Paralysis Secondary to Impacted Esophageal Foreign Bodies in Young Children. Pediatrics 2001; 107(6): e101.6

David H. Burstein, MD1; Mark J. Burstein, MD2; Jason Mouzakes, MD2; Perminder S. Parmar, MD1; and Sydney C. Butts, MD1

1SUNY Downstate Medical Center, Brooklyn, NY; 2Albany Medical Center, Albany, NY

Bilateral Vocal Cord Paralysis After Disc Battery IngestionBilateral Vocal Cord Paralysis After Disc Battery Ingestion

Figure 5. Attempts to ablate posterior glottic scar tissue using a CO2 laser in Patient 2 also failed.

Figure 3. At 6-month follow up, Patient 1 had regained limited

function of her left vocal fold, as seen on fiberoptic laryngoscopy.

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