Laryngotracheal stenosis is a challenging problem in the field of laryngology. In the majority of patients, acquired stenosis of the larynx and trachea is due to accidental trauma, prolonged intubations, or tracheostomy. Congenital stenosis, caustic injury, and granulomatous diseases are also etiological factors in laryngotracheal stenosis (Grenier PA et al, 2009). Tracheal stenosis can occur following tracheostomy or endotracheal intubation with inappropriate cuff pressure. It is due to pressure necrosis at the site of the cuff. Initially, there is inflammation of the damaged mucosa with increased secretion and secondary infection. Prolonged ischemia and secondary infection cause necrosis of the tracheal wall and exposure and sequestration of the cartilaginous rings. This damage results in the formation of granulation tissue and collapse of the tracheal wall (Satish Nair et al, 2014). The tracheal stenosis is classified as simple, which is a soft, short segment web-like narrowing often limited to the mucosa only or complex stenosis, which is a hard, long-segment stricture with destruction of tracheal cartilages and fibrosis. Post tracheostomy stenosis occurs most commonly at the stoma site or less commonly at the site where the tip of the tube has impinged on the tracheal mucosa (Liu J et al, 2015). The symptoms are generally insidious. Most arise 1 to 6 weeks after extubation, and early symptoms are often not recognized. The most common symptoms include shortness of breath, cough, recurrent pneumonia, wheezing, stridor, and cyanosis over time. Dyspnea is often the symptom until the tracheal diameter is 50% smaller than normal. When the tracheal diameter is 25% of its normal size, dyspnea and stridor may occur even at rest. These symptoms can be confused with other respiratory diseases (Rubikas R et al, 2014).