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Tracheoesophageal fistula after lye ingestion
Tracheoesophageal By Raymond
A. Amoury,
Fistula After Lye Ingestion
Ellen E. Hrabovsky,
John C. Leonidas,
and Thomas
M. Holder
F
ISTULOUS COMMUNICATIONS between the esophagus and tracheobronchial tree as a consequence of lye ingestion are very rare and may occur as a direct result of the caustic, or later, after dilatation of a resulting stricture.’ The experimental production and evolution of caustic burns of the esophagus have been well described.2*3 The depth of the injury correlates with the concentration of lye both experimentally,4 and clinically.5 The virtually instantaneous, devastating, and fatal effects of concentrated lye have been emphasized recently.3 The following report is that of a child who developed a tracheoesophageal fistula secondary to caustic ingestion which resulted in his death. The patient is presented to indicate the severity of the injury and the radiographic and operative findings. CASE
REPORT
This 2-yr-old boy was admitted 3 hr after ingesting a handful of lye crystals. His mouth, lips, and tongue appeared charred, and he was in moderate respiratory distress. After being successfully intubated, a tracheostomy was performed. Endoscopy was deferred in view of the acuteness and severity of the oropharyngeal burns and he was started on a course of steroids and antibiotics. Four and one-half days after the caustic ingestion an esophagram was obtained (Fig. IA). Because of aspiration of oral barium, a tube was used to instill the contrast material into the upper esophagus. There was no communication between the esophagus and trachea. The mucosal pattern of the esophagus appeared intact; however, there was no change in appearance of the esophagus on sequential films indicating a lack of peristaltic activity. On the sixth hospital day the patient underwent laryngoscopy, esophagoscopy, and gastrostomy. The vocal cords showed no evidence lof burns. The epiglottis was intact but pale white. The surface of the posterior pharyngeal wall appeared necrotic as did the inside of his mouth and tongue. Inspection was limited to the upper esophagus and revealed that the entire esophageal mucosa was gray and necrotic. At gastrostomy the gastric mucosa appeared congested but not necrotic. A string was passed from the nose to the stomach to maintain an esophageal channel. Tracheal secretions were persistently heavy and began to show milk formula which had been administered per gastrostomy. A second barium study done via the gastrostomy tube on the ninth postburn day showed reflux of barium into the esophagus to the level of the third thoracic vertebral body where the esophagus communicated with the trachea via a tistula approximately 1 cm above the carina. The esophagus otherwise appeared intact and was not narrowed (Fig. I B). A right extrapleural thoractomy was done the next day. The findings are shown diagrammatically in Fig. 2. There was no recognizable esophagus in the posterior mediastinum but in its place there was a large grayish tubular cavity containing pus and the string previously placed through the esophagus. This string was helpful in marking the position of the esophagus before its dissolution. A I x IS-cm triangular-shaped hole was seen in the back wall of the trachea extending down the posterior wall of the left main bronchus. The defect was closed with an intercostal muscle bundle (the fifth) after which his air leak was controlled. After the placement of an extrapleural tube a laparotomy was done and no external damage to the stomach was seen. The esophagus was dissected free up into the mediastinum
From the Departments of Surgery and Radiology, The Children’s Mercy Hospital, Kansas City. MO. 64108 and The University of Missouri-Kansas City School of Medicine. Address for reprint requests: Raymond A. Amoury, M.D., Surgeon-in-Chief. The Children’s Mercy Hospital, 24th and Gillham Road, Kansas City. MO. 64108. Journal of Pediatric Surgery, Vol. 10. No. 2 (April), 1975
273
AMOURY
ET AL.
Fig. l(A) Lateral esophagram 4’3 days postingestion showing what appeared to be an intact esophageal mucosa. (B) Lateral esophagram, 9; 2 days postingestion which shows the tracheoesophageal communication (arrow).
ESOPHAGEAL SKELETON
-
--TRACHEA
MEDIASTINAL CAVITY
__ :HUS
SlLK STRING-
Fig. 2. ings.
Diagram
of operative
find-
TRACHEOESOPHAGEAL
FISTULA
AFTER
LYE INGESTION
275
to the point where it lost its integrity. The distal esophagus was oversewn and since the vagus nerves were destroyed with the esophagus, a pyloroplasty was done. The postoperative course was characterized by fever, copious tracheal secretions, and a progressive air leak. It was obvious that the tracheal closure had separated. His condition progressively deteriorated and he died I7 days after the thoracotomy. Postmortem examination showed only a rim of necrotic esophagus attached to the trachea at the posterior ends of the tracheal cartilages. The epiglottis was partly destroyed, and the membranous portion of the trachea was not viable. The original tracheoesophageal fistula, had enlarged and there were two smaller ones, There was a large gastric ulcer which had gone on to a localized perforation. (This was felt to be a delayed manifestation of the original caustic injury).
DISCUSSION
Of 93 cases of acquired nonmalignant esophagotracheobronchial fistulas collected by Coleman6 there were 31 in which the etiology of the fistula was considered traumatic and three of these were listed as being due to lye. In 36 cases of acquired nonmalignant esophagotracheobronchial fistulas reported from the Mayo Clinic, an esophagorespiratory fistula developed after lye ingestion in six patients. In three of these cases the fistulas followed the caustic injury and in three the fistulas occurred after dilatation of an esophageal stricture.’ Imre and Kopp8 presented 32 patients with late complications after corrosive burns of the esophagus. In 11 of these patients there was a chronic mediastinal abscess or an esophagorespiratory fistula due to perforation of the esophagus. Borjag reported on 90 cases of confirmed lye ingestion with one case of complete dissolution of the esophagus and an esophagotracheal fistula and one case of an esophagotracheoaortic fistula. The latter complication has been described in detail.‘O The signs and symptoms of esophagopulmonary fistulas in the chronic cases after lye ingestion are similar to those described in patients with congenital esophagopulmonary fistulas and the diagnostic approaches are similar.” In the early postinjury phase the esophagram is relied upon to detect a possible tracheoesophageal fistula as endoscopy carries with it the risk of perforation of a necrotic esophagus. Generally, there is a very poor correlation of the radiographic studies with the extent of the esophageal injury. In our patient, contrast studies showed a paralyzed but intact-appearing esophagus with the barium contained in an inflammatory fibrous sheath which was the remnant of the destroyed esophagus. None of the features of corrosive esophagitis as recently describedI were present. Perhaps an important sign is the lack of esophageal peristalsis noted in this case, and related to the destruction of the muscle layers. In this patient, complete dissolution of the esophagus and a portion of the membranous trachea occurred. The outlook was very likely hopeless from the onset. It is obvious that prevention of these injuries is crucial and Ashcraft and Padula13 have summarized the current status of caustic agents on the market. The authors indicate that “childproof” packaging is incomplete protection and that for the sake of the toddler these hazardous agents (including those in less than 10% concentration) are probably best banned from sale on the open market.
276
AMOURY
ET AL.
ACKNOWLEDGMENT We thank Dr. Eugene C. Beatty for his assistance Keith W. Ashcraft for reviewing the manuscript.
in evaluation
of the pathologic
material
and Dr.
REFERENCES 1. Wesselhoeft CW, Keshishian JM: Acquired nonmalignant esophagotracheal and esophagobronchial fistulas. Ann Thorac Surg 6: 187, 1968 2. Hailer JA Jr, Bachman K: The comparative effect of current therapy on experimental caustic burns of the esophagus. Pediatrics 34:236, 1964 3. Leape LL, Ashcraft KW, Scarpelli DG, et al: Hazard to health-Liquid lye. N Engl J Med 284578,197 1 4. Krey H: On the treatment of corrosive lesions in the oesophagus, an experimental study. Acta Otolaryngol (Suppl) 102:1, 1952 5. Daly JF: The early management of corrosive burns of the esophagus. Surg Clin North Am 34:343, 1954 6. Coleman FP: Acquired non-malignant esophagorespiratory fistula. Am J Surg 93:321, 1957 7. Wychulis AR, Ellis FH Jr, Andersen HA: Acquired nonmalignant esophagotracheobronchial fistula. Report of 36 cases. JAMA 196:117, 1966
8. Imre J, Kopp M: Arguments against longterm conservative treatment of esophageal strictures due to corrosive burns. Thorax 27:594, 1972 9. Borja AR, Ransdell HT, Thomas TV, et al: Lye injuries of the esophagus. Analysis of ninety cases of lye ingestion. J Thorac Cardiovasc Surg 57:533, 1969 10. McCabe RE, Scott JR, Knox WC: Fistulization between the esophagus, aorta and trachea as a complication of acute corrosive esophagitis: Report of a case. Am Surg 35:450, 1969 11. Blackburn WR, Amoury RA: Congenital esophago-pulmonary fistulas without esophageal atresia. An analysis of 260 fistulas in infants, children and adults. Rev Surg 23: 153, 1966 12. Martel W: Radiologic features of esophagogastritis secondary to extremely caustic agents. Radiology 103:31, 1972 13. Ashcraft KW, Padula RT: The effect of dilute corrosives on the esophagus. Pediatrics 53~226, 1974
A. Amoury,
Fistula After Lye Ingestion
Ellen E. Hrabovsky,
John C. Leonidas,
and Thomas
M. Holder
F
ISTULOUS COMMUNICATIONS between the esophagus and tracheobronchial tree as a consequence of lye ingestion are very rare and may occur as a direct result of the caustic, or later, after dilatation of a resulting stricture.’ The experimental production and evolution of caustic burns of the esophagus have been well described.2*3 The depth of the injury correlates with the concentration of lye both experimentally,4 and clinically.5 The virtually instantaneous, devastating, and fatal effects of concentrated lye have been emphasized recently.3 The following report is that of a child who developed a tracheoesophageal fistula secondary to caustic ingestion which resulted in his death. The patient is presented to indicate the severity of the injury and the radiographic and operative findings. CASE
REPORT
This 2-yr-old boy was admitted 3 hr after ingesting a handful of lye crystals. His mouth, lips, and tongue appeared charred, and he was in moderate respiratory distress. After being successfully intubated, a tracheostomy was performed. Endoscopy was deferred in view of the acuteness and severity of the oropharyngeal burns and he was started on a course of steroids and antibiotics. Four and one-half days after the caustic ingestion an esophagram was obtained (Fig. IA). Because of aspiration of oral barium, a tube was used to instill the contrast material into the upper esophagus. There was no communication between the esophagus and trachea. The mucosal pattern of the esophagus appeared intact; however, there was no change in appearance of the esophagus on sequential films indicating a lack of peristaltic activity. On the sixth hospital day the patient underwent laryngoscopy, esophagoscopy, and gastrostomy. The vocal cords showed no evidence lof burns. The epiglottis was intact but pale white. The surface of the posterior pharyngeal wall appeared necrotic as did the inside of his mouth and tongue. Inspection was limited to the upper esophagus and revealed that the entire esophageal mucosa was gray and necrotic. At gastrostomy the gastric mucosa appeared congested but not necrotic. A string was passed from the nose to the stomach to maintain an esophageal channel. Tracheal secretions were persistently heavy and began to show milk formula which had been administered per gastrostomy. A second barium study done via the gastrostomy tube on the ninth postburn day showed reflux of barium into the esophagus to the level of the third thoracic vertebral body where the esophagus communicated with the trachea via a tistula approximately 1 cm above the carina. The esophagus otherwise appeared intact and was not narrowed (Fig. I B). A right extrapleural thoractomy was done the next day. The findings are shown diagrammatically in Fig. 2. There was no recognizable esophagus in the posterior mediastinum but in its place there was a large grayish tubular cavity containing pus and the string previously placed through the esophagus. This string was helpful in marking the position of the esophagus before its dissolution. A I x IS-cm triangular-shaped hole was seen in the back wall of the trachea extending down the posterior wall of the left main bronchus. The defect was closed with an intercostal muscle bundle (the fifth) after which his air leak was controlled. After the placement of an extrapleural tube a laparotomy was done and no external damage to the stomach was seen. The esophagus was dissected free up into the mediastinum
From the Departments of Surgery and Radiology, The Children’s Mercy Hospital, Kansas City. MO. 64108 and The University of Missouri-Kansas City School of Medicine. Address for reprint requests: Raymond A. Amoury, M.D., Surgeon-in-Chief. The Children’s Mercy Hospital, 24th and Gillham Road, Kansas City. MO. 64108. Journal of Pediatric Surgery, Vol. 10. No. 2 (April), 1975
273
AMOURY
ET AL.
Fig. l(A) Lateral esophagram 4’3 days postingestion showing what appeared to be an intact esophageal mucosa. (B) Lateral esophagram, 9; 2 days postingestion which shows the tracheoesophageal communication (arrow).
ESOPHAGEAL SKELETON
-
--TRACHEA
MEDIASTINAL CAVITY
__ :HUS
SlLK STRING-
Fig. 2. ings.
Diagram
of operative
find-
TRACHEOESOPHAGEAL
FISTULA
AFTER
LYE INGESTION
275
to the point where it lost its integrity. The distal esophagus was oversewn and since the vagus nerves were destroyed with the esophagus, a pyloroplasty was done. The postoperative course was characterized by fever, copious tracheal secretions, and a progressive air leak. It was obvious that the tracheal closure had separated. His condition progressively deteriorated and he died I7 days after the thoracotomy. Postmortem examination showed only a rim of necrotic esophagus attached to the trachea at the posterior ends of the tracheal cartilages. The epiglottis was partly destroyed, and the membranous portion of the trachea was not viable. The original tracheoesophageal fistula, had enlarged and there were two smaller ones, There was a large gastric ulcer which had gone on to a localized perforation. (This was felt to be a delayed manifestation of the original caustic injury).
DISCUSSION
Of 93 cases of acquired nonmalignant esophagotracheobronchial fistulas collected by Coleman6 there were 31 in which the etiology of the fistula was considered traumatic and three of these were listed as being due to lye. In 36 cases of acquired nonmalignant esophagotracheobronchial fistulas reported from the Mayo Clinic, an esophagorespiratory fistula developed after lye ingestion in six patients. In three of these cases the fistulas followed the caustic injury and in three the fistulas occurred after dilatation of an esophageal stricture.’ Imre and Kopp8 presented 32 patients with late complications after corrosive burns of the esophagus. In 11 of these patients there was a chronic mediastinal abscess or an esophagorespiratory fistula due to perforation of the esophagus. Borjag reported on 90 cases of confirmed lye ingestion with one case of complete dissolution of the esophagus and an esophagotracheal fistula and one case of an esophagotracheoaortic fistula. The latter complication has been described in detail.‘O The signs and symptoms of esophagopulmonary fistulas in the chronic cases after lye ingestion are similar to those described in patients with congenital esophagopulmonary fistulas and the diagnostic approaches are similar.” In the early postinjury phase the esophagram is relied upon to detect a possible tracheoesophageal fistula as endoscopy carries with it the risk of perforation of a necrotic esophagus. Generally, there is a very poor correlation of the radiographic studies with the extent of the esophageal injury. In our patient, contrast studies showed a paralyzed but intact-appearing esophagus with the barium contained in an inflammatory fibrous sheath which was the remnant of the destroyed esophagus. None of the features of corrosive esophagitis as recently describedI were present. Perhaps an important sign is the lack of esophageal peristalsis noted in this case, and related to the destruction of the muscle layers. In this patient, complete dissolution of the esophagus and a portion of the membranous trachea occurred. The outlook was very likely hopeless from the onset. It is obvious that prevention of these injuries is crucial and Ashcraft and Padula13 have summarized the current status of caustic agents on the market. The authors indicate that “childproof” packaging is incomplete protection and that for the sake of the toddler these hazardous agents (including those in less than 10% concentration) are probably best banned from sale on the open market.
276
AMOURY
ET AL.
ACKNOWLEDGMENT We thank Dr. Eugene C. Beatty for his assistance Keith W. Ashcraft for reviewing the manuscript.
in evaluation
of the pathologic
material
and Dr.
REFERENCES 1. Wesselhoeft CW, Keshishian JM: Acquired nonmalignant esophagotracheal and esophagobronchial fistulas. Ann Thorac Surg 6: 187, 1968 2. Hailer JA Jr, Bachman K: The comparative effect of current therapy on experimental caustic burns of the esophagus. Pediatrics 34:236, 1964 3. Leape LL, Ashcraft KW, Scarpelli DG, et al: Hazard to health-Liquid lye. N Engl J Med 284578,197 1 4. Krey H: On the treatment of corrosive lesions in the oesophagus, an experimental study. Acta Otolaryngol (Suppl) 102:1, 1952 5. Daly JF: The early management of corrosive burns of the esophagus. Surg Clin North Am 34:343, 1954 6. Coleman FP: Acquired non-malignant esophagorespiratory fistula. Am J Surg 93:321, 1957 7. Wychulis AR, Ellis FH Jr, Andersen HA: Acquired nonmalignant esophagotracheobronchial fistula. Report of 36 cases. JAMA 196:117, 1966
8. Imre J, Kopp M: Arguments against longterm conservative treatment of esophageal strictures due to corrosive burns. Thorax 27:594, 1972 9. Borja AR, Ransdell HT, Thomas TV, et al: Lye injuries of the esophagus. Analysis of ninety cases of lye ingestion. J Thorac Cardiovasc Surg 57:533, 1969 10. McCabe RE, Scott JR, Knox WC: Fistulization between the esophagus, aorta and trachea as a complication of acute corrosive esophagitis: Report of a case. Am Surg 35:450, 1969 11. Blackburn WR, Amoury RA: Congenital esophago-pulmonary fistulas without esophageal atresia. An analysis of 260 fistulas in infants, children and adults. Rev Surg 23: 153, 1966 12. Martel W: Radiologic features of esophagogastritis secondary to extremely caustic agents. Radiology 103:31, 1972 13. Ashcraft KW, Padula RT: The effect of dilute corrosives on the esophagus. Pediatrics 53~226, 1974