Authors Sarah Orfanos MD, Ibrahim El Husseini MD Division of Pulmonary and Critical Medicine, Rutgers Robert Wood Johnson University Hospital.
Case
A 25-year-old female presented to the intensive care unit for altered
mental status following a suicidal attempt and ingestion of an unknown
substance. Patient was intubated for airway protection and treated with
Fomepizole and hemodialysis and extubated within 24 hours. A few hours
post-extubation, she developed inspiratory and expiratory stridor
requiring reintubation. Computed tomography (CT) of the chest (Figure 1)
and flexible bronchoscopy (Video 1) were performed for further
evaluation.
Figure 1: Post-extubation coronal computed tomography of the chest (parenchymal window)Video 1: Diagnostic bronchoscopy with visualization of the trachea
Question
What is the etiology of the patient’s persistent stridor and respiratory distress?
A. Tracheomalacia B. Post-intubation tracheal granuloma C. Tracheal caustic injury D. Tracheal tumor E. Tracheo-esophageal fistula
Answer
C. Tracheal caustic injury
Discussion
Tracheomalacia (answer A) would show dynamic collapse of the anterior
wall of the trachea rather than extensive sloughing seen during
bronchoscopy. Tracheal granulomas (answer B) are not commonly seen
following brief intubation as with this patient and bronchoscopy would
demonstrate granulation tissue rather than extensive injury and mucosal
sloughing as seen here. A tracheal tumor (answer D) would manifest as a
growth without extensive sloughing. A trachea-esophageal fistula (TEF,
answer E), a connection between the trachea and esophagus, is generally
diagnosed with bronchoscopy, though can be seen on CT or with barium
swallow. TEF generally occurs in the setting of thoracic malignancy,
with aspiration being the most common symptom.
CT chest in our case demonstrated circumferential tracheal narrowing
on the coronal view (shown above), with a transverse band of tissue
extending across the tracheal lumen. The tracheal lumen measured 5mm at
its narrowest with audible stridor and respiratory distress, stressing
the urgency of therapeutic bronchoscopy. Flexible bronchoscopy showed
diffuse caustic tracheal injury, with extensive fibrin and necrotic
tissue and a false membrane almost completely obstructing the trachea.
We were able to remove the obstructing tissue using flexible forceps.
Balloon dilatation or Argon Plasma Coagulation were not performed due to
the high risk of tracheal perforation in the setting of caustic injury.
The patient was successfully extubated and discharged. In the following
months she underwent two flexible bronchoscopies with balloon
dilatation due to persistent tracheal stenosis (Figure 2).
Figure 2: Bronchoscopy performed 3 months post initial injury showing improvement of the necrosis but development of scar tissue with tracheal stenosis
Caustic airway injury is less commonly reported than GI tract caustic
injury, however, it can result in serious consequences, including
tracheal perforation, necrosis or long-term complications such as
tracheal stenosis. The pathophysiology of caustic injury varies
depending on the proprieties of the ingested substance (acidic or
alkaline). Alkaline agents cause tissue injury by liquefactive necrosis
through saponification of fat. Acidic substances cause coagulation
necrosis with denaturation of the superficial protein layer. These
patients frequently require multiple bronchoscopies for diagnostic and
therapeutic purposes. Acute therapeutic options include debridement (as
performed in this case) and balloon dilatation, though dilation in this
setting is associated with high risk of tracheal perforation(1).
Alternative therapies once the inflammatory response settles include
pulmonary patch repair (2), airway stenting, balloon dilation with or
without heated ablative therapies, and slide tracheoplasty (3).
References
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Necrosis With Perforation Secondary to Caustic Ingestion. Ann Thorac
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Yong MS, Konstantinov IE. Understanding the impact of slide
tracheoplasty in congenital tracheal stenosis. Transl Pediatr. 2019
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