A more detailed description for these procedures is presented in a dedicated chapter of this book.

Since electrocautery is available in our center, it is our instrument of choice. The probe is directly applied to the tissue that needs to be removed, always in coagulation mode.

The observed damage produced by cautery to the tissue has a very good correlation with the histological damage. This is very important, and represents one of the main differences with laser therapy, where the immediate visualization does not correlate with histological damage, since laser acts much deeper (6 mm depth) than electrocautery whose action is superficial.

A ground plate has to be attached to the patient’s back to avoid electric injury to both the patient and the endoscopist. If the plate is not used, electric current can travel directly to the operator since the RB is not insulated. The best way to avoid this event is to utilize bipolar probes through insulated BF [9].

Acute respiratory failure developing from tracheal stenosis requires a different approach than when the failure is progressive. It usually presents in the setting of an elective extubation during weaning from mechanical ventilation.

The permanence of the ETT in the larynx may produce ulcers in the posterior aspect of the vocal cords, followed by edema, granulation tissue, and scar formation [25]. Similarly, its permanence inside the trachea produces, in the early phase, mucosal lesion and ulceration followed by cartilage destruction, granulation tissue, and scar formation, leading to the formation of a stenotic area. In severe cases, tracheal rings are exposed, infection takes place, and they soften, fragment, and disintegrate, leading to a variety of tracheal lesions. Later, they may be reabsorbed, and the tracheal mechanical support is lost, resulting in collapse of the compromised segment [22] and, as we will discuss later, ultimately ending up in tracheomalacia.

To minimize the injury produced by the endotracheal tube cuff, high-volume low-pressure cuffs have been replaced by low-pressure high-volume ones. These low-pressure cuffs have a large residual volume prior to inflation. When the cuff is inflated and the operator feels a resistance, an important overexpansion of it may already exist [23]. High inflation pressures interfere with the submucosal vascularization of the trachea, causing ischemia and necrosis. Infected secretions above the cuff contribute to tracheal damage (that is why it is so important to have a careful subglottic aspiration). When pressure generated by the ETT cuff exceeds the mucosal capillary perfusion pressure, usually 20–30 mmHg, tracheal injury occurs. It is very important to maintain a low pressure on the tracheal mucosa, so when a cuff pressure of 25 mmHg is reached and air leak persists, it is advisable to intubate the trachea with a bigger tube instead of inflating the cuff over that pressure [26].

The usual clinical scenario is a patient weaned from MV that develops acute respiratory distress with stridor and other signs of upper airway obstruction and must be re-intubated. After the emergency has been solved, the following inspection is advisable: the bronchoscopist, with the aid of an anesthesiologist if possible, introduces the BF through the ETT until reaching its distal end. Once in place, an assistant proceeds to slowly remove the ETT while the endoscopist is inspecting the airway as they go. Areas of malacia and other lesions may be observed. Careful must be taken no to overpass the vocal cords level with the BF, since it may be necessary to intubate again and that can be easily performed over the bronchoscope. It is also very important to make an inspection of the airway proximal to the vocal cords. Once inspection through the ETT is completed, the BF can be introduced again via nasal route, while the patient is connected to mechanical ventilation. Most of the times no injury is found in the airway and extubation fails for important edema of the supraglottic area. A plan to proceed can be outlined after finishing this evaluation.

When a stenotic area is found, dilatation, electrocautery, or laser may be necessary, alone or in combination. When the only finding is edema, a trial of steroids is advisable. More complex lesions require a planned procedure, taking into account the type and extension of the affected area.

One very common cause of tracheal stenosis is granuloma formation. They develop from persistent inflammation, and they do not compromise the tracheal wall. Weblike stenosis, in turn, represents a different form of stenosis developed from fibrous tissue that produces a subtotal stenosis, also sparing the tracheal wall. Bottleneck stenosis consists on a localized collapse of the tracheal wall less than 5 cm in length. Weblike and bottleneck are referred as simple stenosis.

Complex stenoses are large, affecting more than 5 cm in length or six tracheal rings or localized in more than one segment of the tracheobronchial tree. Usually, only the bottleneck and the complex type are responsible for severe obstructions. A detailed classification and therapeutic strategies of stenosis may be found in Dumon and Diaz-Jimenez [27], and tracheal stenosis is also discussed elsewhere in this book.

If the stenosis is limited exclusively to the subglottic area, dilatation is the procedure of choice since subglottic stents, in our experience, are not useful. Sometimes the obstruction is produced by pure tracheo- or tracheobronchial malacia, and in these cases a stent may be deployed. We will discuss this entity in the next section.

TBM can be a cause of CAO in the ICU. The most usual clinical setting is a patient that is already extubated and develops signs and symptoms of acute upper airway obstruction and requires reintubation, and during endoscopic inspection, TBM is found.

TBM is a confuse term, of unclear meaning for healthcare professionals, where a variety of different pathologies have been included [28]. Briefly, we will refer to the correct utilization of these different terms.

TBM is an expiratory collapse of the central airway due to softening of the airway cartilage. The airway lumen at bronchoscopic examination acquires a saber-sheath shape or the crescent-type shape. The first is produced by a collapse of the lateral walls of the trachea, and the second one by the collapse of the anterior wall [29]. Tracheal cartilages are always compromised. When the anterior and lateral walls are involved, it is called circumferential type.

Expiratory collapse of the airway (ECA) refers to the collapse of some part of the tracheal wall. It is generally produced by the anterior bulging of the posterior membranous tracheal wall during expiration that decreases tracheal lumen. This is entirely due to the laxity of the membranous portion. The cartilages are intact, and in this specific case, the ECA is called dynamic airway collapse (DAC) . It may be normal when the reduction of the lumen is less than 50% at forced expiration. However some authors, including me, prefer the limit of 70% instead 50% TBM is also an ECA, but in this case the expiratory collapse is not produced by the laxity of the membranous wall of the trachea, but due to the softening of the tracheal cartilages [28, 29].

By consensus, when expiratory collapse is less than 50% of the tracheal lumen, it is considered normal. If it is 50% or higher, it is considered abnormal. As it was already referred it seems that a limit of 70% may be better.

DAC is frequently found in COPD and asthma patients. Some authors refer this normal collapse as DAC and reserve the term excessive dynamic airway collapse (EDAC) when it exceeds this value. We resume these terms in Table 37.4.

Upon bronchoscopic examination, the pathologic findings may be of pure TBM, pure EDAC, or both. Stent placement can be indicated, with or without previous dilatation. A tracheobronchial or a tracheal stent may be deployed depending on the location of the lesion. These entities are usually diagnosed after patients are extubated since the ETT functions like a stent, precluding airway collapse.

If the patient has a tracheostomy in place, we prefer to use TRACOE tracheostomy tubes , which are available in different sizes and lengths. They have the advantage of producing a good sealing of the trachea, and migration is uncommon.

Prior to a stent placement, a conservative management can be tried applying NIPPV in the form of continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP) ventilation. There are no comparative studies showing which of the two assisted ventilation modes is better (CPAP or BiPAP); however, we adhere to Murgu SD, who argues that CPAP is preferable, since in patients with high respiratory rates and small tidal volumes, the different inspiratory and expiratory trigger sensitivities of BiPAP could result in patient-ventilator asynchrony [30].

Recently high-flow nasal therapy was proposed as a form to replace continuous positive airway pressure ventilation (high flow about 30 L/m). Some reports in recent literature emphasize this approach [31].

Sometimes, the affection is limited to a bronchus or a segment, and stenting it can solve the problem. It is possible that the same degree of collapse in health condition does not interfere with a normal life. Once surpassed the acute event, the stent can be removed [32].

In cases of pure tracheal compromise, referred as tracheomalacia (TM) or EDAC limited to the trachea, the distal tip of the tracheostomy tube needs to lie above the carina, in order to stent all the tracheal length. Appropriate placement can be assessed by BF.

In summary:

In addition to bronchoscopy, there are other diagnostic procedures that can help to evaluate these patients, but they are difficult to apply in the ICU (e.g., paired inspiratory/expiratory dynamic computed tomography or cine magnetic resonance imaging) [35, 36].

Another frequent consultation from the ICU is the evaluation of bleeding through a tracheostomy. Most of the times, bleeding is scant and represents mucosal injury produced by the tip of the tracheostomy tube, forceful aspirations, or tracheobronchitis and has no consequences.