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Bronchoscopic Images

Caustic Tracheobronchitis

Represas, Cristina MD*; Fernández-Villar, Alberto PhD*; Leiro, Virginia MD*; Botana, Maribel MD*; Blanco, Montserrat PhD; Rodríguez, Carlos MD; Mallo, Rosa MD; Piñeiro, Luis MD*

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Ingestion of caustic substances can cause injuries from a little epithelial burn to a total necrosis of the wall of esophagus, stomach, duodenum, jejunum, or another organs.1,2 Fifty percent of caustic ingestion in adults is caused by suicide attempt in the context of psychiatric illness or sentimental problems.3 Alkaline substances cause necrosis by liquidization that penetrates quickly with a risk of perforation of stomach and esophagus. Acid substances cause necrosis by coagulation forming a protective eschar that limits airway injury and penetration of the caustic. Deep burns in esophagus and in the distal portion of stomach can produce fibrosis, with stenoses and obstruction. Moreover, aspiration of caustic substances can produce severe injuries in the pharynx and larynx causing problems in deglutition and speech. Aspiration of part of the ingested substance is possible and it could bring about injuries in tracheobronchial tree.1–7 However, there are few references in bibliography about lower airway affectation.

We report bronchoscopic findings in a patient with laryngotracheobronchitis secondary to chloric acid ingestion, and development of tracheal stenoses.


A 33-year-old man came to our hospital after hydrochloric acid ingestion as a suicide attempt. He presented with severe gastric necrosis and chemical peritonitis. He was operated, and a total gastrectomy, distal esophagostomy with Kehr tube placement, and alimentary jejunostomy were carried out. He was admitted in an intensive care unit for several months on parenteral nutrition.

A month after ingestion the patient developed productive cough and dysphonia. An esophagogram was performed revealing deglution dysfunction with aspiration of the contrast into the bronchial tree. Flexible bronchoscopy demonstrated an intense inflammation and edema of the epiglottis, vocal cords, trachea and both main bronchi. The mucosa was edematous with superficial inflammation and granulation tissue. No abnormalities in distal bronchi were seen (Fig. 1). Parenteral steroids were also added to the regimen.

Videobronchoscopy image 1 month after caustic ingestion. Lesions in epiglottis, vocal cords (left side), trachea, and main bronchi (central and right side) were seen.

A month later, another videobronchoscopy was carried out, as difficulty in swallowing persisted. Appearance of the epiglottis was unchanged. There was some repair involving glottis, vocal cords, and trachea. There was 25% narrowing of the upper of the trachea by granulation tissue and scar formation (Fig. 2).

Videobronchoscopy image 1 month after Figure 1. We observed injuries in glottis, vocal cords, and trachea (left and right side). Stenoses in 25% of the lumen in upper third of trachea were observed (central image).

In succeeding months the patient developed progressive dyspnea. Airways CT revealed a significative stenosis (Fig. 3). At that moment we decided moving the patient to a hospital specialized in rigid bronchoscopy for tracheal dilatation with balloon.

Airway CT revealed significative stenoses (left side: coronal image; right side: sagittal image).


Diagnosis was caustic laryngotracheobronchitis, probably from bronchoaspiration of part of the chloric acid ingested by the patient.

Although there are several papers about caustic ingestion injuries on the digestive tract only references of individual case reports or small series of cases about the respiratory finding of caustic aspiration exist in MEDLINE and ENBASE databases.1–10

Tracheobronchial necrosis is explained by 2 mechanisms6: direct aspiration and, more probably, necrotic extension from burned esophagus or mediastinum. These lesions are usually located on the left side of posterior wall of the trachea, on the carina, and on the first centimeters of the left main bronchus, just in the area of anatomic contact with the esophagus.6 Caustic aspirations are frequent because of vomiting and pharyngolaryngeal edema.6 In this case, tracheal lesions involved the entire mucosa and most of them were located on the right side. They were characterized by an inflammatory aspect that hide the underlying necrosis during the first days.6

According to Sarfati et al,6 tracheobronchial necrosis with perforation after ingestion of a caustic substance is the main cause of death in patients who have deep burns of the upper digestive tract. They reported a series of 679 patients admitted to their department because of ingestion of caustic substances; 87 presented severe caustic burns of the entire esophagus, together with panparietal necrosis. Twenty-one developed tracheobronchial necrosis with perforation. These authors believe that after caustic ingestion, initial evaluation should include tracheobronchial examination with a bronchoscopy when severe and necrotic digestive burns occur.6 If the trachea seems normal, the preventive act should be esophagectomy by stripping to avoid local extension of caustic burns and potential development of tracheobronchial necrosis.6

The fact that few cases of caustic ingestion required interventional respiratory support suggests that the protection afforded by the pharyngeal glottic mechanism to the lower airway is extremely efficient. In our case we think that tracheobronchial affectation was related to severe lesions in epiglottis, which produced an incomplete laryngeal protection with aspiration. This mechanism is reflected in other publications.8

Inflammatory and necrotic tracheal injuries evolved into fibrosis, with development of a partial stenosis in tracheal lumen. This process is widely described in esophagus and stomach,7,8 but not in respiratory tract.

Experimentally, tracheal stenoses can be produced through bronchoscopic application of a caustic agent causing progressive deep mucosal and submucosal injury in animal models.9

The question which is not answered is the long-term evolution, whether cicatrizial tracheal injuries can degenerate to malignancy, similar to malignant esophageal lesions that develop after caustic ingestion.10


Tracheobronchial aspiration leading to severe stenosis is possible after caustic ingestion. Airway direct observation by bronchoscopy is necessary for a correct evaluation of these patients and to prevent respiratory tract complications.


1. Bertket B, Castellani P, Brioche M, et al. Early operation for severe corrosive injury of the upper gastrointestinal tract. Eur J Surg. 1996;162:951–955.
2. Guth AA, Pachter HL, Albanese C, et al. Combined duodenal and colonic necrosis. An unusual sequela of caustic ingestion. J Clin Gastroenterol. 1994;87:303–305.
3. Christesen HB. Caustic Ingestion in adults. Epidemiology and Prevention. J Toxicol. 1994;32:557–568.
4. Friedman EM, Lovejoy FH Jr. The emergency management of caustic ingestions. Emerg Med Clin North Am. 1984;2:77.
5. Wason S. The emergency management of caustic ingestion. J Emerg Med. 1984;2:175.
6. Sarfati E, Jacob L, Servant JM, et al. Tracheobronchial necrosis after caustic ingestion. J Thorac Cardiovasc Surg. 1992;103:412–413.
7. Turner A, Robinson P. Respiratory and gastrointestinal complications of caustic ingestion in children. Emerg Med J. 2005;22:359–361.
8. Scott JC, Jones B, Eisele DW, et al. Caustic ingestion injuries of the upper aerodigestive tract. Laryngoscope. 1992;102:1–8.
9. Marquette CH, Mensier E, Copin MC, et al. Experimental models of tracheobronchial stenoses: a useful tool for evaluating airway stents. Ann Thorac Surg. 1995;60:651–656.
10. Kozarek RA, Sanowski RA. Caustic cicatrization of the pharynx associated with dysphagia and premalignant mucosal changes. Am J Gastroenterol. 1982;77:5–8.

caustic; tracheobronchitis; tracheal stenosis; bronchoscopy

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