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Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients
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Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients
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Literature review current through: Sep 2017. | This topic last updated: Aug 21, 2017.

INTRODUCTION — Many complications associated with oral endotracheal tubes (ETTs) occur during initial placement. However, ETTs are also associated with complications following placement that can occur during the ensuing days to weeks of intensive care unit (ICU) admission.

This topic reviews basic aspects of prevention and treatment of complications associated with oral ETTs pertinent to the adult ICU patient. Intubation techniques, checking ETT position after initial placement, and immediate complications of ETT as well as complications associated with placement of supraglottic airway devices are discussed separately. (See "Overview of tracheostomy" and "Direct laryngoscopy and endotracheal intubation in adults" and "Rapid sequence intubation for adults outside the operating room" and "Induction agents for rapid sequence intubation in adults outside the operating room" and "Neuromuscular blocking agents (NMBAs) for rapid sequence intubation in adults outside of the operating room" and "Supraglottic devices (including laryngeal mask airways) for airway management for anesthesia in adults".)

INTUBATION IN THE INENSIVE CARE UNIT

Direct versus video laryngoscopy — Direct laryngoscopy is the traditional method used to intubate patients in the intensive care unit (ICU). However, video laryngoscopy is being increasingly used [1-3]. Choosing among these options and role of video laryngoscopy for endotracheal tube exchange in the ICU are discussed separately. (See "Approach to the difficult airway in adults outside the operating room" and "Video laryngoscopes and optical stylets for airway management for anesthesia in adults" and 'Exchanging the endotracheal tube' below.)

Immediate complications — This topic review discusses complications that occur in the intensive care unit following appropriate ETT placement. Complications that occur during or following intubation and ETT placement are discussed in detail separately. (See "Direct laryngoscopy and endotracheal intubation in adults".)

PREVENTION OF COMPLICATIONS IN THE ICU — Daily endotracheal tube care should be provided to avoid complications associated with ETTs. Daily care includes monitoring ETT cuff pressure, oral and endotracheal suctioning of secretions, and vigilant inspection to ensure that the ETT is rotated regularly and its position maintained. These preventative measures are especially important in those identified as having a difficult airway since reintubation is particularly risky and challenging in this population.  

Maintain optimal cuff pressure — The ETT cuff provides a seal between the ETT and the tracheal wall to ensure accurate delivery of tidal volumes during mechanical ventilation. Overinflation of the cuff can result in tissue ischemia, ulceration, and necrosis of the tracheal wall (image 1) while underinflation results in the leak of air and oropharyngeal secretions around the ETT cuff which predisposes the patient to inadequate ventilation, de-recruitment, and aspiration pneumonia, respectively [4]. Thus, setting a cuff pressure that ensures adequate ventilation while concurrently avoiding leak requires careful balance. (See 'Laryngeal injury' below and 'Endotracheal cuff leaks' below.)

Cuff pressures should be monitored routinely in patients who are intubated. The frequency of cuff pressure checks is institution-specific but typically performed daily, at minimum. There are several factors that can affect cuff pressure including tracheal size, ETT size, ventilatory pressures and patient position [5]. Thus, there is no single cuff pressure that is ideal for every patient. However, as a general guideline, the cuff pressure should be maintained between 20 and 30 cm H2O [6].

Occasionally, individual adjustment within these parameters is needed. As an example, a lower pressure may be sufficient in patients with a small airway diameter who have a large ETT in place. In contrast, higher cuff pressure is sometimes required to prevent significant air leak that can occur in patients with high peak airway pressures [7]; however, a small air leak at high ventilatory pressures may be tolerated without a need to increase cuff pressure beyond the set limit, provided gas exchange is acceptable.

Special caution is necessary when a patient is transported to a different altitude. Cuff pressure will increase when the patient is moved to a higher altitude because air expands within the cuff. The change of cuff pressure can be large; in one study, the mean rise in cuff pressure was 23 cm H2O when patients moved from sea level to a height of at least 3000 feet above sea level [8]. Thus, it is prudent to measure cuff pressure after transport to a different altitude and adjust cuff volume accordingly.

ETT cuffs are categorized as being high volume, low pressure (HVLP) cuffs or low volume, low pressure (LVLP) cuffs. Most ICUs use ETTs with HVLP cuffs. ETTs with HVLP cuffs that can automatically set the cuff pressure are commercially available but have not been shown to be associated with a significant clinical benefit when compared with manual measurement, such that they are not generally used [9,10]. Similarly, although leaks from the subglottic space to the tracheobronchial tree may be lower with LVLP cuffs [11], clinical trials demonstrating convincing improvement in important clinical outcomes (eg, rate of ventilator-associated pneumonia [VAP]) are necessary before ETTs with LVLP cuffs can become routinely used.

Suctioning and oral care — Suctioning and oral care is an important part of preventing ETT-associated infections and mucus plugging:

ETT suctioning – Since patients who are intubated cannot cough and clear their own lower airway secretions, patients should be suctioned regularly via the ETT using a sterile technique which has a sealed system that minimizes nosocomial contamination ("in-line" suctioning) [12]. The optimal frequency of suctioning depends on the quantity of secretions. The cross sectional area of the ETT will inevitably decrease over time because secretions and cellular debris collect within the lumen despite suctioning [13,14].

Oropharyngeal suctioning – Since oral and nasal secretions collect posteriorly in supine patients in whom the swallowing and cough reflex is impaired due to the ETT, regular oropharyngeal suctioning is also required. This is generally done manually with a Yankauer oral suction catheter. ETTs that provide continuous subglottic secretion drainage via an in-line port located just above the upper level of the cuff are also commercially available (figure 1). Although they have been shown in small trials to possibly decrease the incidence of VAP, methodologic flaws in many of the studies prevent definitive conclusions such that their routine use has not become widespread. These data are discussed separately. (See "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Subglottic drainage'.)

Oral decontamination – Oral decontamination, usually with antiseptics (eg, chlorhexidine), is a widespread practice used to reduce the risk of ETT-associated infections, including VAP. The role of oral decontamination in the prevention of VAP is discussed separately. (See "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Decontamination of the digestive tract'.)

Rotation and stabilization — Medical adhesive tape is used to secure the ETT in position at the level of the lip (usually on one side of the mouth). Occasionally, the tape needs to be replaced when it loses its adhesive properties (eg, excessive sweating or drooling).

The ETT should also be rotated from side to side daily to avoid pressure-induced ulceration at the lip, face, and cheek; however, the constant re-taping can weaken the stability of the ETT and can also result in skin tears in those with fragile skin.

Some experts use commercially available securement devices (ETT "holders") (picture 1) that mechanically secure the ETT in place without the use of tape, although some ICUs use both tape and ETT holders in those considered high risk of displacement. With some of these devices, the ETT exits the mouth centrally while others have a mechanism that can facilitate side to side rotation without compromising the ETT position [15-18]. There is no convincing evidence that ETT holding devices lower the rate of displacement or pressure ulceration, further details of which are discussed below. (See 'Displacement and unplanned extubation' below.)

Reassessment of position — Although the ETT is typically secured in place with adhesive tape after the initial placement, ETT migration is an inevitable consequence of coughing, suctioning, transport, and movement. Thus, the ETT position should be reassessed regularly. This is typically achieved with daily clinical monitoring of the ETT position by healthcare staff and periodic surveillance chest radiography.

The position of the ETT at the level of the lip should be formally checked by healthcare staff during daily routine assessments as well as following periods of care that are high risk for ETT displacement (eg, turning and transport).

Daily chest radiographs on mechanically ventilated patients (to check ETT position as well as other endpoints) are routine in many clinical centers; however, we and others believe that this practice is not necessary and that it is appropriate that chest radiographs only be performed when a clinical change such as ETT migration is suspected [19]. In support, randomized trials indicate that a more restrictive approach (eg, chest radiographs only in response to a change in clinical condition) decreases the number of chest radiographs without worsening clinical outcomes, such as mortality, length of ICU stay, or duration of mechanical ventilation [20,21]. Comparison of the position of the distal tip of the ETT on chest radiography is optimal when the position of the patient's head is similar on each radiograph; specifically, neck flexion advances the endotracheal tube toward the carina, while neck extension moves the tube away from the carina (figure 2) [22-24]. The tip of the ETT should be in the trachea, approximately 3 to 5 cm from the carina.

Evidence of migration should prompt chest radiography and repositioning when necessary, the details of which are discussed below. (See 'Displacement and unplanned extubation' below.)

Identify difficult airway — A small proportion of patients in the ICU are classified as having a "difficult airway." These are often patients who have had a traumatic initial intubation, a known anatomic abnormality that is associated with a difficult airway (eg, patients with or at risk of cervical dislocation, patients with a retropharyngeal mass), and obese patients with a narrow oropharynx. We and other experts believe that clear identification of this group (eg, color-coded signs in the room) is prudent since it alerts care givers to being extra vigilant regarding ETT safety and prompt rapid consultation of an expert in difficult airway management in the event that it is needed for an ETT-related complication, thereby avoiding multiple failed attempts at reintubation. (See "Approach to the difficult airway in adults outside the operating room".)

PRESENTATION AND MANAGEMENT OF COMPLICATIONS IN THE ICU — Adverse events that are directly attributable to oral ETTs are discussed in this section. Complications that occur during mechanical ventilation (eg, barotrauma) are discussed separately. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults" and "Ventilator-associated lung injury" and "Physiologic and pathophysiologic consequences of mechanical ventilation".)

Laryngeal injury — Laryngeal injury is the most common complication associated with ETT placement. It encompasses several disorders including laryngeal inflammation and edema as well as vocal cord ulceration, granulomas, paralysis, and stenosis. The pathogenesis likely relates to direct pressure and inflammation induced by the ETT on the larynx and surrounding tissue. Direct visualization of the vocal cords is typically required for diagnosis (usually laryngoscopy or bronchoscopy) and should be prompted when symptoms don't resolve following extubation or in those in whom a suspected condition is responsible for extubation failure, or failure to wean from mechanical ventilation. Most conditions associated with laryngeal injury heal spontaneously and symptomatic therapy may be administered while recovery is pending (eg, corticosteroids for edema, vocal cord injection for paralysis, speech training for dysphonia). Others require targeted therapy (eg, granuloma resection) which is discussed in the individual sections below. (See 'Inflammation and edema' below and 'Mucosal ulceration' below and 'Granulomas' below and 'Vocal cord paralysis' below and 'Laryngotracheal stenosis' below and "Overview of tracheostomy", section on 'Complications'.)

Clinical manifestations — Most patients with laryngeal injury manifest as hoarseness/dysphonia immediately following extubation. Other injuries (eg, bilateral vocal cord paralysis, severe edema, severe laryngotracheal stenosis) can also be associated with extubation failure presenting with acute stridor or respiratory failure after extubation. As an example in a case series of 136 patients, 12 percent of the patients exhibited extubation failure within 48 hours, half of whom had stridor. However, only half of the patients with stridor required reintubation [25].

Others, usually those with a tracheostomy in place, may present prior to extubation with signs and symptoms consistent with failure to wean from mechanical ventilation exhibited by an inability to tolerate a speech valve or inability to undergo prolonged spontaneous breathing trials (eg, tracheal stenosis). (See "Management and prognosis of patients requiring prolonged mechanical ventilation", section on 'Weaning'.)

Risk factors — Risk factors for laryngeal injury that have been described include the following [25-27]:

Prolonged intubation (variably defined as ≥36 hours to ≥3 days)

Traumatic intubation

Not using a myorelaxant drug during intubation,

Large ETT (>8 mm in men, >7 mm in women)

Aspiration

Unplanned extubation

Presence of a nasogastric tube

Noteworthy, is that the duration of intubation and ETT size (including those with an additional suction port to evacuate retropharyngeal secretions) are not associated with the severity of the laryngeal injury [28]. Traumatic intubation may be related to abnormal laryngeal anatomy, difficult laryngoscopy, multiple attempts, or operator inexperience. There may be a trend towards higher risk of airway injury in patients with diabetes, hypertension, heart failure, kidney, and malnutrition [29,30].

Laryngeal injuries are more frequent in women than men [25,31-33].

Older patients ≥50 years may be at greater risk of developing vocal cord paralysis than younger patients [29].

Obesity does not appear to predict laryngeal complications, though it may be associated with difficult intubation [28,34].

Inflammation and edema — Evidence suggests that laryngeal inflammation and edema are detected after extubation in more than half of patients (picture 2) [25,27,35], although not every case is associated with significant symptomatology.

Following extubation, most patients complain of mild to moderate symptoms including sore throat, dysphonia, and dysphagia thought to be due to laryngeal inflammation from the ETT [27,36,37].

More severe symptoms include stridor (sometimes requiring reintubation), which may be due to coexistent impairment in vocal cord mobility [25]. As an example, one prospective study, clinically significant laryngeal edema occurred in approximately 5 to 13 percent of patients and required reintubation in approximately 1 percent [32].

Laryngeal edema may be suspected prior to extubation or following extubation failure and may be supported by the presence of a negative cuff leak test. (See "Extubation management", section on 'Cuff leak'.)

Once extubated, laryngeal inflammation and edema resolve spontaneously over 24 to 48 hours. Persistent symptoms that do not resolve should prompt investigation for more serious injuries that may have occurred during intubation (eg, laceration hematoma, avulsion) or from prolonged intubation (eg, vocal cord ulcers, granulomas, paralysis, adhesions). (See "Direct laryngoscopy and endotracheal intubation in adults", section on 'Complications'.)

Acute management strategies include nebulized racemic epinephrine, heliox, glucocorticoids, and reintubation. Glucocorticoid therapy may be indicated for laryngeal edema associated with extubation failure, the details of which are discussed separately. (See "Extubation management", section on 'Glucocorticoids'.)

Mucosal ulceration — Mucosal ulcerations usually occur along the posteromedial aspect of the vocal cords (picture 3) and can only be appreciated by direct endoscopic visualization. They are most common when endotracheal intubation lasts longer than four days and occur in about a third of patients (figure 3) [25,27,35]. Patients with ulcers may be clinically silent or present similarly to those with laryngeal edema. Ulcers typically resolve spontaneously but may progress to granuloma or nodule formation for unclear reasons. Rarely, ulcers may heal and result in interarytenoid adhesions. (See 'Laryngotracheal stenosis' below.)

Granulomas — Endotracheal intubation can induce vocal cord granuloma formation, presumed to be a sequela of inflammation and ulceration and may occur in up to 30 or 40 percent of patients intubated for longer than three or four days (picture 4 and image 2 and picture 5) but symptoms may not be apparent until a few weeks (eg, four weeks) after extubation [25,27]. The duration of intubation and severity of initial laryngeal injury do not appear to predict granuloma formation [38]. Hoarseness that persists longer than 7 to 10 days following extubation may indicate the presence of a laryngeal granuloma and should prompt fiberoptic laryngoscopy for diagnosis. Granulomas may also be appreciated on computed tomography. Laryngeal granulomas often require surgical removal but some resolve spontaneously; subspecialty consultation is usually necessary for management.

Vocal cord paralysis — Vocal cord paralysis is a rare complication of intubation (<1 percent of intubations), particularly prolonged intubation [27,39,40]. It is generally caused by compression (typically from the cuff) of the anterior branch of the recurrent laryngeal nerve between the ETT cuff and the thyroid cartilage in the subglottic larynx (ie, neurogenic vocal cord paralysis); however rare cases may be due to arytenoid dislocation, possibly from forceful intubation [39,41-43]. When paralyzed, abduction (opening) of the affected vocal cord is impaired so that it becomes fixed in the adducted (closed) position (picture 6). Paralysis can be unilateral or bilateral:

Unilateral vocal cord paralysis is more common and typically manifests as hoarseness, dysphonia, vocal fatigue, and occasionally dysphagia immediately after extubation. It may also be supported by variable airflow obstruction on pulmonary function testing. It generally resolves over days to months.

Bilateral vocal cord injury is less common, but its clinical manifestations are more severe (eg, extubation failure, stridor) and patients will likely need to be reintubated after extubation; many additionally require consideration of tracheostomy for long term management.

The diagnosis of vocal cord paralysis is generally made on direct laryngoscopy. However, vocal cord paralysis due to dislocation of the cricoarytenoid joint, can be distinguished from neurogenic paralysis by joint palpation and/or imaging [40].

While some may resolve spontaneously (eg, those that are paretic rather than paralyzed), if no resolution is seen by 6 to 12 months then recovery is unlikely [44]. Intervention is usually not required for unilateral paralysis, although occasionally, temporary injection of the affected vocal cord can augment the voice while recovery is pending. If vocal cord paralysis is due to arytenoid dislocation (image 3), it is generally treated by surgical reduction of the joint.  

Laryngotracheal stenosis — Stenosis of the larynx and/or trachea is a late complication of ETT placement taking weeks to months to develop after the initial intubation. The risk of developing stenosis is increased in those with prolonged intubation >7 days, and is rare in those intubated for short periods (eg, <3 days) [25,45]. The incidence is unknown but reports range from 1 to 21 percent [46,47].

Glottic (laryngeal) stenosis is thought to be due to pressure from the ETT itself, resulting in local tissue ischemia, inflammation, necrosis, and scarring. In support of this mechanism, inflammatory changes are seen in this region in as few as two to five days after intubation and most cases are located in the posterior glottis and interarytenoid regions, where the ETT rests [45].  

Tracheal stenosis is caused by high ETT cuff pressure (picture 7 and image 4). When the ETT cuff pressure exceeds the mean capillary pressure in the tracheal mucosa (approximately 20 cm H2O), obstruction of capillary blood flow causes ischemia, inflammation, and erosion of the mucosa. This leads to necrosis, destruction of the tracheal architecture, and scarring.

Patients who are extubated may develop subacute or progressive dyspnea and/or or stridor while those who remain intubated (usually tracheostomized) may present with failure to wean from mechanical ventilation. Tracheal stenosis usually becomes symptomatic within five weeks after extubation, sometimes longer (eg, months), and symptoms may become progressive over time. Stenosis may remain occult in a sedentary or deconditioned individual who is physically inactive. Pulmonary function testing may demonstrate fixed upper airway obstruction. If the patient remains intubated, a negative cuff leak test may support the diagnosis. Definitive diagnosis requires bronchoscopy or laryngoscopy, although emerging data suggests that spiral computed tomography (CT) with virtual bronchoscopy may be equally effective [48]. (See "Overview of pulmonary function testing in adults" and "Extubation management", section on 'Cuff leak'.)

Tracheal stenosis may require endoscopic stenting, balloon dilations, laser resection, or an alternative endoscopic intervention. Rates of success with endoscopic procedures are variable and restenosis is not infrequent. Mitomycin C (an antineoplastic agent) and steroids have been used anecdotally to prevent tracheal restenosis after local endoscopic therapies (eg, laser resection or balloon dilatation), although randomized studies are lacking [49,50]. Surgical resection is usually reserved for those with symptoms from extensive stenosis or those who fail endoscopic procedures. In contrast, stenotic lesions that involve the larynx are typically less amenable to endoscopic procedures and subspecialty consultation is advised. (See "Clinical presentation, diagnostic evaluation, and management of central airway obstruction in adults" and "Flexible bronchoscopy balloon dilation" and "Airway stents".)

More rarely, an obstructive fibrinous tracheal pseudomembrane may cause tracheal obstruction and be responsible for extubation failure [51]. In such cases, fiberoptic bronchoscopy reveals a thick, circular, rubber-like membrane adhering to the tracheal wall at the site of the endotracheal tube cuff. Rigid bronchoscopy is usually required for the removal of the pseudomembrane.

Displacement and unplanned extubation — ETTs may migrate caudally or distally and patients may self-extubate. Commercial tube holders (ETT with securement devices) are available and being increasingly used but no studies have proven definitive superiority over standard adhesive tape in preventing ETT migration or UE [52-54]. However, they may be preferred in those where tape is not desirable (eg, allergy, burns).  

Displacement — ETT displacement may be detected on routine monitoring (see 'Reassessment of position' above), or patients may develop symptoms associated with caudal or distal migration. Unless the ETT is suspected to be in the oropharynx, chest radiography should be immediately performed.

Caudal migration may manifest as a sizeable airway leak (ie, the exhaled tidal volume is lower than that delivered mechanically via the ventilator). Patients may develop respiratory distress, tachypnea, or agitation. This is frequently misinterpreted as cuff rupture, leading to unnecessary ETT replacement. In a series of 18 patients whose ETT was replaced due to a large airway leak, only 38 percent actually had a mechanical fault in the cuff [55].

When caudal migration is suspected and the balloon of the ETT is estimated to be located below the vocal cords and intact, a chest radiograph should be performed. Once confirmed, the ETT can be moved distally.

If the tip or balloon of the ETT is suspected to be in the oropharynx, then prompt reintubation with direct laryngoscopy should be performed without performing a chest radiograph. Although not always necessary, a new ETT is typically placed under these circumstances. The rationale for this approach is based upon the avoidance of a third attempt at reintubation if the displacement was originally due to a significant cuff leak/rupture (ie, a mechanical fault with the ETT). (See 'Endotracheal cuff leaks' below and "Direct laryngoscopy and endotracheal intubation in adults".)

Distal migration will result on impingement of the tip at the carina or mainstem intubation (usually right mainstem). Manifestations include respiratory distress, tachypnea, hypoxemia, elevated peak pressures, and unilateral breath sounds, and when severe, may result in tension pneumothorax. When suspected, a chest radiograph should be performed and once confirmed the ETT can be moved caudally. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)  

Repositioning the ETT should be performed by deflating the cuff and moving the ETT for a preselected distance that is estimated to place the ETT back to an appropriate position (eg 21 cm at the lip); the level at the lip is recorded, the cuff is reinflated, and the new position checked on chest radiography.

Unplanned extubation — Unplanned extubation (UE) can occur in 3 to 12 percent of intubated patients and is a quality marker utilized by many ICUs [56-58]. Most patients (over half) who undergo unplanned extubation should be promptly reintubated, although a select proportion may be monitored and supported (eg, noninvasive ventilation, high flow or low flow nasal oxygen) for a short period. Complications of UE include aspiration, respiratory distress, laryngeal edema, and death. Further details regarding UE are provided separately. (See "Extubation management", section on 'Unplanned extubation'.)

Endotracheal cuff leaks — The incidence of endotracheal cuff leaks in patients admitted to the ICU is 6 to 11 percent [59,60].

A cuff leak is diagnosed by hearing an audible leak (often a bubbling sound due to air escaping through the glottis) and the demonstration of a loss of tidal volume with failure to achieve set minute ventilation (ie, the recorded expired volume is lower than the set tidal volume). The clinical consequences vary from trivial to emergent respiratory compromise depending upon patient characteristics and the degree of leak. For example a small leak (eg, 25 mL) may not be tolerated well in a patient with severe acute respiratory distress syndrome on high ventilatory pressures and high fraction of inspired oxygen, while larger volumes may be tolerated in patients with normal underlying lung function who are intubated for airway protection.

The causes of endotracheal cuff leaks can be classified into two categories [61]:

Leaks due to a defective cuff/inflation system – Structural cuff/inflation system defects may be due to punctured pilot balloon, inflation line, or cuff. A defective inflation system may be suggested by an inability to retain cuff volume or pressure. When the cuff/inflation system is compromised, definitive management is replacement of the ETT. (See 'Exchanging the endotracheal tube' below.)

Leaks around an intact cuff/inflation system ─ Leaks around an intact cuff/inflation system are caused by cuff under-inflation, cephalad migration of the ETT, tracheal misplacement of oro/nasogastric tubes, discrepancy between ETT and tracheal diameter (occasionally the balloon will "soften" over time, or some patients have tracheomalacia), and high peak airway pressures. Demonstrating that the inflation system is intact involves obtaining a chest radiograph as well as checking the cuff inflation volume and pressure with a manual syringe and manometer, respectively) and assessing ventilator settings/readings (for peak and plateau pressures). When cephalad migration of the ETT is suspected, the ETT position should be checked, by direct inspection (laryngoscopy or bronchoscopy when balloon is suspected to be above the vocal cords) or chest radiography (when balloon is suspected to be above the vocal cords. If the cuff/inflation system is intact, the ETT may need an adjustment (eg, ETT repositioning, increased cuff volume, reducing peak pressures); the ETT typically does not have to be replaced with a new tube, unless a larger ETT is needed.

Occasionally, when a cause for a substantial air leak cannot be determined, many clinicians opt to replace the ETT. (See 'Exchanging the endotracheal tube' below.)

Infections — Bacteria enmeshed in a biofilm can adhere to the inner surface of the ETT within hours of intubation which may contribute to both ventilator-associated pneumonia (VAP [ie, infection-related ventilator associated complication; iVAC]) and ventilator-associated tracheobronchitis (VAT) [13,62-65]. In addition, the ETT can impair sinus drainage leading to an increased risk of sinusitis. Evidence supporting specific strategies regarding the management of ETT-associated infections is best described for VAP but similar principles are used for managing VAT and sinusitis.

Ventilator-associated pneumonia/events — VAP (ie, iVAC) is an important complication of intubation and mechanical ventilation. The ETT is one risk factor among others for VAP. The role of silver-coated endotracheal tubes in biofilm development and further details regarding VAP are discussed separately [63-65]. (See "The ventilator circuit and ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults" and "Clinical presentation and diagnosis of ventilator-associated pneumonia" and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults" and "Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults".)

Tracheobronchitis — The estimated incidence of VAT (also called nosocomial tracheobronchitis) ranges from 1.4 to 11 percent [66-69]. As an example, in a prospective cohort of 1889 intubated patients, VAT developed in 11 percent of patients. VAT was associated with a longer duration of mechanical ventilation (24 versus 9 days) and an increased length of ICU stay (32 versus 13 days) when compared to cases without VAT [68]; a nonsignificant increase in mortality was also reported (36 versus 32).

VAT may be an intermediate condition between lower respiratory tract colonization and VAP (ie, iVAC). It is unclear whether VAT is a precursor or risk factor for VAP. Some believe VAT may represent a disease continuum with VAP [70]. Some studies have demonstrated an increased risk of VAP in patients with VAT [68] or decreased risk of VAP with treatment for VAT [71]. In contrast, other studies have reported similar rates of ICU and hospital stay, duration of mechanical ventilation, survival, tracheostomy, and antibiotic use in patients with VAT and VAP, suggesting no relationship between these entities [69].

Although there is no consensus definition, VAT is generally considered present if the following criteria are met [72]:

Fever (>38ºC)

No other recognizable cause of fever

New or increased sputum production

Positive culture of tracheal aspirates

No radiographic infiltrate or evidence of pneumonia

From a practical perspective VAT is a hard diagnosis to make since many patients intubated in the ICU have abnormal radiographs and positive sputum cultures and it is frequently challenging to effectively rule out all the potential causes for fever. Thus, clinical judgement and other clinical features (eg, history of bronchiectasis, chronic bronchitis, wheezing, endoscopic evidence of severe tracheitis or bronchitis) may facilitate the diagnosis.

Commonly implicated bacteria include Pseudomonas aeruginosa, Staphylococcus aureus, and Acinetobacter baumannii. Multidrug resistant bacteria, polymicrobial infections, and viral organisms including herpes simplex can also be pathogenic [69,73].

The management of VAT is virtually identical to the management of VAP. Suspected cases of VAT should be treated with systemic antimicrobial therapy while cultures are pending and be modified, once cultures return. In support of this approach, one trial randomly assigned 58 patients with VAT to receive intravenous antibiotics or placebo for eight days [71]. VAT was defined by the criteria described above, plus an endotracheal aspirate culture of >1,000,000 colony forming units (cfu)/mL. Serial endotracheal aspirates facilitated targeted antibiotic therapy. The patients who received antibiotic therapy had significantly fewer episodes of VAP (13 versus 47 percent), reduced ICU mortality (18 versus 47 percent), and more ventilator-free days. There was no difference in the duration of mechanical ventilation or the length of ICU stay. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

Aerosolized antibiotics may expedite the resolution of clinical signs of VAT, according to one randomized trial [74]. Despite these results, the value of aerosolized antibiotics is best considered unproven since most of the patients enrolled in the trial also had pneumonia.

Sinusitis — The ETT can impair sinus drainage, leading to collections of uninfected fluid within the sinuses. Infection of these sinus collections causes nosocomial sinusitis.

The reported incidence of sinusitis in mechanically ventilated patients ranges from 8 to 70 percent, the wide range likely reflecting differences in diagnostic methods used [75,76]. While the incidence of sinus opacification is common in intubated patients [77], the incidence of infection is probably lower than originally thought. Increased awareness of the role of nasogastric tubes and their avoidance may have contributed to a potential decrease in incidence of nosocomial sinusitis over time, although this is unproven.

Although a nasal alpha-adrenergic agonist plus a nasal glucocorticoid may decrease the incidence of nosocomial sinusitis [78], larger controlled clinical trials are necessary before this approach is suggested for the routine prevention of sinusitis in mechanically ventilated patients.

Risk factors in ICU patients for nosocomial sinusitis include endotracheal intubation, nasal colonization with Gram negative organisms, and enteral feeding via a nasogastric tube (table 1) [75]. Sedation and a Glasgow coma score <7 may be additional risk factors. Although nasotracheally intubated patients are more susceptible to noninfectious sinus opacification, the incidence of nosocomial sinusitis appears to be similar among patients who are nasotracheally intubated and those who are orotracheally intubated [76,79,80].

Nosocomial sinusitis should be suspected in all intubated patients who have a fever without an obvious source, especially if there is purulent nasal drainage. When suspected, computed tomography (CT) is the preferred modality because it is more sensitive than plain radiography [81]. Sinus ultrasonography can also detect sinus opacification, although expertise with this technique is not widespread [11,82]. For those with sinus opacification on imaging, culture of sinus fluid is the gold standard for diagnosis. Endoscopic-guided middle meatal aspiration is a well-tolerated method of obtaining sinus fluid, although other approaches exist (eg, maxillary aspiration). Secretions collected from the nares or oral cavity are unreliable.

Quantitative culture of sinus fluid identifies a likely pathogen in 60 to 70 percent of patients who are strongly suspected of having nosocomial sinusitis (ie, have fever without an alternative cause, sinus opacification on CT, purulent nasal drainage) [76,83,84]. A common threshold used to declare a quantitative culture positive is 103 cfu/mL.

Pathogens that cause nosocomial sinusitis are similar to those that cause VAP and include Staphylococcus aureus, Streptococcus species, Pseudomonas species, and other gram-negative bacilli [75,79,85,86]. Gram-negative bacilli may be responsible for approximately half of cases of nosocomial sinusitis [75,79]. Anaerobic bacteria and yeast (especially Candida albicans) have also been cultured from sinus aspirates of patients with nosocomial sinusitis [87]. However, it is uncertain how often the anaerobic bacteria are pathogens rather than oral contaminants [88]. (See "Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Microbiology' and "Fungal rhinosinusitis".)

Treatment is typically systemic antibiotics together with local therapies:

Antimicrobial therapy should target pathogens identified by the sinus fluid culture. When therapy is empiric or the culture data are ambiguous, initial antimicrobial therapy should target common nosocomial pathogens. This approach is virtually identical to choosing an initial antibiotic regimen for VAP, which is discussed separately. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Empiric therapy'.)

Additional therapies include saline irrigation and removal of tubes from the nose (ie, replacing a nasogastric tube with an orogastric tube), nasal decongestants, and occasionally and intranasal glucocorticoids. (See "Uncomplicated acute sinusitis and rhinosinusitis in adults: Treatment", section on 'Symptomatic therapies'.)

Antimicrobial therapy may not be sufficient for some patients [83]. Patients who do not improve with antimicrobial therapy or who develop nosocomial sinusitis while receiving antimicrobial therapy may require sinus drainage.

All patients with nosocomial sinusitis should be assessed for concurrent VAP. (See "Clinical presentation and diagnosis of ventilator-associated pneumonia".)

Swallowing and speech impairment — Swallowing is abnormal following extubation in approximately half of patients [89-91], although clinically significant aspiration is much less common (6 to 14 percent) [89]. This was illustrated by a series of 254 patients who were intubated endotracheally for >48 hours following cardiac surgery [90]. Fifty-one percent of the patients exhibited post-extubation dysphagia. In another study of patients discharged following intubation for acute respiratory distress syndrome, clinically important dysphagia was identified in one-third of patients, although it is likely that the true prevalence of dysphagia was underestimated since this was a questionnaire-based study [92]. Risk factors for post-extubation dysphagia include a prolonged duration of endotracheal intubation, perioperative cerebrovascular events, and perioperative sepsis. (See "Oropharyngeal dysphagia: Clinical features, diagnosis, and management".)

The cause of impaired swallowing following extubation is not well understood, but it usually resolves without intervention [92].

There are no data that predict clinically significant swallowing dysfunction that may predispose a patient to aspiration following extubation. The point at which patients can eat following extubation should be individualized and depends upon factors including duration of intubation, mental status, and underlying comorbidities (eg, neuromuscular disorders, critical care myopathy, poor level of consciousness) which may predispose patients to dysphagia and aspiration.

As a general rule, patients intubated for short periods (eg, less than one week) can generally eat within a few hours after extubation; swallowing is initially typically observed with small amounts of ice chips or water and if tolerated, a solid diet is slowly introduced over the ensuing few days.

However, many clinicians do not allow patients who have been intubated for a prolonged duration (eg, two weeks or longer) to eat for approximately 12 to 24 hours following extubation. In this population many experts request a bedside, and sometimes a formal radiographic and/or fiberoptic endoscopic evaluation of swallowing (FEES), before allowing the patient; although such evaluations are thought to minimize the risk of aspiration from swallowing impairment, they ultimately lead to a delay in receiving adequate nutrition. As an example, in one case series, only around a quarter of patients received adequate nutrition (defined as at least 75 percent of their predicted daily requirement) during the first week following extubation [93]. (See "Oropharyngeal dysphagia: Clinical features, diagnosis, and management".)

However, there is little evidence and no guidelines to support best practice. Thus, in our opinion, clinicians should weigh the benefits of feeding against the risk of aspiration in all cases and seek formal testing when patients are suspected to have a high risk of aspiration.

Speech impairment (eg, vocal fatigue) is a common complication of intubation, even for short periods, and is likely due to laryngeal injury. It generally resolves spontaneously but speech therapy may be required when dysphonia is profound or associated with vocal paralysis. (See 'Vocal cord paralysis' above.)

Tracheomalacia — Tracheomalacia is a well described long term complication of prolonged tracheal intubation. The pathophysiology is thought to relate to thinning and destruction of cartilaginous tissues due to elevated cuff pressures. Similar to tracheal stenosis, it occurs weeks to months after the initial intubation. Further details are described separately. (See "Tracheomalacia and tracheobronchomalacia in adults".)

Tracheoarterial fistula — Tracheoarterial fistula (most often tracheoinnominate artery fistula) is a rare but devastating complication that is more commonly encountered in patients with a tracheostomy but can occur in those with prolonged intubation with an ETT. Details regarding tracheoarterial fistula are provided separately. (See "Overview of tracheostomy", section on 'Complications'.)

Tracheoesophageal fistula — Formation of a tracheoesophageal fistula (TEF) in an intubated or tracheostomized patient is rare, but the consequences can be devastating (picture 8) [94-97]. TEFs are thought to be due to erosion from the tube tip or cuff into the posterior wall of the tracheal to result in a fistulous communication with the esophagus. Most cases of TEF are due to endotracheal intubation however, other etiologies include iatrogenic complication from endoscopic procedures (eg, endobronchial brachytherapy), infections, and malignancy [98].

TEF may present with recurrent aspiration pneumonia or recurrent hypoxemic events, which may, in turn, prolong the duration of mechanical ventilation. TEF may also present with acute respiratory distress, evidence of enteral feed in ETT aspirate during suctioning, positive air leak, and gastric distension. Presenting signs and symptoms may occur when the ETT or tracheostomy is in place or following extubation or decannulation. (See 'Endotracheal cuff leaks' above.)

High ETT cuff pressure is the dominant risk factor. Other risk factors include high airway pressures, excessive motion of the ETT, prolonged duration of mechanical ventilation, and possibly, diabetes, infection, steroids, and the presence of a nasogastric tube [99,100].

Evaluation of suspected TEF generally involves an esophagram using water-soluble contrast (eg, gastrografin), computed tomography, esophagoscopy, and/or bronchoscopy (picture 8 and image 5). Conservative care is indicated until the patient is stable enough to undergo surgical correction (may take weeks to months). This consists of positioning the ETT cuff distal to the fistula, elevating the head of the bed, and frequent suctioning. Insertion of a jejunostomy tube for feeding plus a gastrostomy tube to suction gastric contents may help reduce gastroesophageal reflux while others including the authors of this topic rest the bowel completely and administer total parenteral nutrition. (See "Nutrition support in critically ill patients: An overview".)

Spontaneous closure is rare. Surgical correction is the definitive procedure of choice for TEF closure, although endoscopic closure using cardiac septal defect occluders, silicon rings, or vascular plugs has been reported with partial success in a small number of cases [101-103]. Surgical repair is a complicated procedure that uses a cervicotomy or cervicosternotomy approach to obtain esophageal closure and tracheal resection or reconstruction. It is not infrequently complicated by wound dehiscence, recurrent TEF, and tracheal stenosis and has a reported operative mortality of 11 percent [98,104]. Endoscopic intervention with a combination of esophageal and/or tracheal stenting has been used for palliation and for transient medical management [105].

NASAL INTUBATION AND TRACHEOSTOMY — Although nasal intubation is typically temporary, occasionally they are placed for prolonged periods. In contrast, tracheostomy is generally placed for those in whom mechanical ventilation is prolonged. Long term complications can occur with both of these modes of intubation and include all of the conditions described in this topic. (See "Overview of tracheostomy" and "Flexible scope intubation for anesthesia", section on 'Nasal intubation' and "Direct laryngoscopy and endotracheal intubation in adults", section on 'Nasal intubation using direct laryngoscopy'.)

EXCHANGING THE ENDOTRACHEAL TUBE — ETT exchange in ICU patients may be required, most often due to a cuff leak. Other less common indications for ETT replacement include the need for a different ETT size (eg, smaller ETT in patients with severe vocal cord edema or to accommodate bronchoscopy which traditionally needs an ETT >7.5 mm in diameter) or for single lung ventilation (eg, massive hemoptysis). (See 'Presentation and management of complications in the ICU' above.)

However, exchanging the ETT may be life-threatening and lead to esophageal intubation, loss of the airway, severe hypoxia, or cardiac arrest. The risk may be greatest in those with a difficult airway or those with poor cardiopulmonary reserve such that information regarding underlying disorders and details regarding prior intubations are important. (See "Approach to the difficult airway in adults outside the operating room".)

The optimal method used to change the ETT is unstudied. When the ETT needs to be changed, experienced providers including an advanced airway team should be consulted prior to ETT replacement. Options include replacing the ETT under laryngoscopic guidance with or without the assistance of a bougie guidewire. Most experts perform the exchange using medications similar to those for intubation. Most experts first assess the airway using direct laryngoscopy and if deemed safe (ie, good view of the vocal cords and ETT), will proceed with ETT exchange; if direct laryngoscopy is not considered optimal, use of video laryngoscopy with or without a guidewire is considered appropriate. One prospective study examined an approach similar to this in 328 patients in whom the vocal cords were not easily visualized using direct laryngoscopy [106]. Compared with historical controls, video laryngoscopy reduced the number of attempts at ETT exchange (92 versus 68 percent first-pass success rate) and was associated with fewer complications including hypoxemia, esophageal intubation, bradycardia, and need for rescue airway device intervention. (See "Direct laryngoscopy and endotracheal intubation in adults".)

When the decision is made to proceed with exchanging the ETT, selecting a different size, length, and type of ETT should be individualized and decided in advance. ETT selection depends upon the reason for reintubation and may be influenced by additional factors including infection (eg, silicone-covered ETT may be appropriate), tracheal size (eg, smaller ETT may be indicated for a small airway), difficulty weaning (smaller ETT may increase resistance and contribute to difficulty weaning), and secretions (ETT with subglottic drainage may be appropriate). (See "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Subglottic drainage' and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Silver-coated endotracheal tube' and "Weaning from mechanical ventilation: Readiness testing".)

TRAINING AND COMPETENCY — There is general consensus that ETTs should be placed by experienced personnel, although this may not be pragmatic in regions with minimal staffing. Evidence suggests that more than two failed attempts at intubation increases the risk of complications and death [107]. Despite their increasing use, whether or not video laryngoscopes should be used to reduce this risk is unknown. Institutions should create policies with regards to training and placement of ETT in emergent settings.

SUMMARY AND RECOMMENDATIONS

Following initial placement, complications of oral endotracheal tubes (ETTs) can occur during the first few days and weeks of intensive care unit (ICU) admission that need to be recognized and managed. (See 'Introduction' above.)

Daily ETT care includes monitoring and maintaining ETT cuff pressure (ideally at 20 to 30 cm H2O) to avoid under- or over-inflation, oral and endotracheal suctioning of secretions, and vigilant inspection to ensure that the ETT is rotated regularly and its position maintained. These preventative measures are especially important in those identified as having a difficult airway since reintubation for complications is particularly risky and challenging in this population. (See 'Prevention of complications in the ICU' above.)

Laryngeal injury is the most common complication associated with ETT placement. It encompasses several disorders including laryngeal inflammation and edema as well as vocal cord ulceration, granulomas, paralysis, and laryngotracheal stenosis. Most conditions require direct visualization of the vocal cords for diagnosis (usually laryngoscopy or bronchoscopy). ETT-associated laryngeal injury lesions typically heal spontaneously and symptomatic therapy may be administered while recovery is pending (eg, corticosteroids for edema, vocal cord injection for paralysis, speech training for dysphonia). Others require targeted therapy (eg, granuloma resection). (See 'Laryngeal injury' above.)

If ETT migration is suspected, a chest radiograph should be performed and if confirmed, the ETT should be repositioned. The exception to this rule is when it is suspected that the ETT is in the oropharynx, in which case, direct laryngoscopy should be performed and the ETT repositioned or replaced. Following repositioning/replacement, chest radiography is indicated to confirm appropriate placement. (See 'Displacement and unplanned extubation' above and "Extubation management", section on 'Unplanned extubation'.)

ETT cuff leaks (ie, the recorded expired volume is lower than the set tidal volume) can be due to a defective cuff/inflation system or to a leak around the cuff. Distinguishing these from one another can be done by clinical and assessment of the patient, the ventilator, the ETT position and cuff/inflation system, and chest radiography. When the cuff/inflation system is compromised, definitive management is replacement of the ETT. If the cuff/inflation system is intact, the ETT may need an adjustment (eg, ETT repositioning, increased cuff volume, reducing peak pressures). (See 'Endotracheal cuff leaks' above.)

Bacteria enmeshed in a biofilm can adhere to the inner surface of the ETT within hours of intubation which may contribute to both ventilator-associated pneumonia (VAP; also known as infection-related ventilator associated complication [iVAC]) and ventilator-associated tracheobronchitis (VAT). The ETT can also impair sinus drainage leading to an increased risk of sinusitis. The management of ETT-associated infections is similar to that described for VAP. (See 'Infections' above and "Clinical presentation and diagnosis of ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults" and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults".)

Swallowing is abnormal following extubation in approximately half of patients, although clinically significant aspiration is much less common (6 to 14 percent). The point at which patients can eat following extubation should be individualized and depends upon factors including duration of intubation, mental status, and underlying comorbidities (eg, neuromuscular disorders, critical care myopathy, poor level of consciousness) which may predispose patients to dysphagia and aspiration. (See 'Swallowing and speech impairment' above.)

Additional uncommon complications include tracheomalacia and tracheoarterial and tracheoesophageal fistula formation. (See 'Tracheomalacia' above and 'Tracheoarterial fistula' above and 'Tracheoesophageal fistula' above.)

ETT exchange is potentially life-threatening and should only be done when absolutely indicated (eg, significant cuff leak), preferably by an experienced provider. (See 'Exchanging the endotracheal tube' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Kristy Bauman, MD, who contributed to an earlier version of this topic review.

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REFERENCES

  1. Silverberg MJ, Li N, Acquah SO, Kory PD. Comparison of video laryngoscopy versus direct laryngoscopy during urgent endotracheal intubation: a randomized controlled trial. Crit Care Med 2015; 43:636.
  2. Platts-Mills TF, Campagne D, Chinnock B, et al. A comparison of GlideScope video laryngoscopy versus direct laryngoscopy intubation in the emergency department. Acad Emerg Med 2009; 16:866.
  3. Lascarrou JB, Boisrame-Helms J, Bailly A, et al. Video Laryngoscopy vs Direct Laryngoscopy on Successful First-Pass Orotracheal Intubation Among ICU Patients: A Randomized Clinical Trial. JAMA 2017; 317:483.
  4. Rello J, Soñora R, Jubert P, et al. Pneumonia in intubated patients: role of respiratory airway care. Am J Respir Crit Care Med 1996; 154:111.
  5. Lizy C, Swinnen W, Labeau S, et al. Cuff pressure of endotracheal tubes after changes in body position in critically ill patients treated with mechanical ventilation. Am J Crit Care 2014; 23:e1.
  6. American Thoracic Society, Infectious Diseases Society of America. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005; 171:388.
  7. Guyton DC, Barlow MR, Besselievre TR. Influence of airway pressure on minimum occlusive endotracheal tube cuff pressure. Crit Care Med 1997; 25:91.
  8. Henning J, Sharley P, Young R. Pressures within air-filled tracheal cuffs at altitude--an in vivo study. Anaesthesia 2004; 59:252.
  9. Efrati S, Leonov Y, Oron A, et al. Optimization of endotracheal tube cuff filling by continuous upper airway carbon dioxide monitoring. Anesth Analg 2005; 101:1081.
  10. Valencia M, Ferrer M, Farre R, et al. Automatic control of tracheal tube cuff pressure in ventilated patients in semirecumbent position: a randomized trial. Crit Care Med 2007; 35:1543.
  11. Young PJ, Pakeerathan S, Blunt MC, Subramanya S. A low-volume, low-pressure tracheal tube cuff reduces pulmonary aspiration. Crit Care Med 2006; 34:632.
  12. Combes P, Fauvage B, Oleyer C. Nosocomial pneumonia in mechanically ventilated patients, a prospective randomised evaluation of the Stericath closed suctioning system. Intensive Care Med 2000; 26:878.
  13. Shah C, Kollef MH. Endotracheal tube intraluminal volume loss among mechanically ventilated patients. Crit Care Med 2004; 32:120.
  14. Glass C, Grap MJ, Sessler CN. Endotracheal tube narrowing after closed-system suctioning: prevalence and risk factors. Am J Crit Care 1999; 8:93.
  15. Barnason S, Graham J, Wild MC, et al. Comparison of two endotracheal tube securement techniques on unplanned extubation, oral mucosa, and facial skin integrity. Heart Lung 1998; 27:409.
  16. Buckley JC, Brown AP, Shin JS, et al. A Comparison of the Haider Tube-Guard® Endotracheal Tube Holder Versus Adhesive Tape to Determine if This Novel Device Can Reduce Endotracheal Tube Movement and Prevent Unplanned Extubation. Anesth Analg 2016; 122:1439.
  17. Rothaug O, Müller-Wolff A, Kaltwasser R, et al. [Methods for endotracheal tube fixation. Results of a survey of intensive care nurses]. Med Klin Intensivmed Notfmed 2013; 108:507.
  18. Choi YS, Chae YR. [Effects of rotated endotracheal tube fixation method on unplanned extubation, oral mucosa and facial skin integrity in ICU patients]. J Korean Acad Nurs 2012; 42:116.
  19. https://acsearch.acr.org/docs/69452/Narrative.
  20. Krivopal M, Shlobin OA, Schwartzstein RM. Utility of daily routine portable chest radiographs in mechanically ventilated patients in the medical ICU. Chest 2003; 123:1607.
  21. Hejblum G, Chalumeau-Lemoine L, Ioos V, et al. Comparison of routine and on-demand prescription of chest radiographs in mechanically ventilated adults: a multicentre, cluster-randomised, two-period crossover study. Lancet 2009; 374:1687.
  22. Olufolabi AJ, Charlton GA, Spargo PM. Effect of head posture on tracheal tube position in children. Anaesthesia 2004; 59:1069.
  23. Hartrey R, Kestin IG. Movement of oral and nasal tracheal tubes as a result of changes in head and neck position. Anaesthesia 1995; 50:682.
  24. Yap SJ, Morris RW, Pybus DA. Alterations in endotracheal tube position during general anaesthesia. Anaesth Intensive Care 1994; 22:586.
  25. Tadié JM, Behm E, Lecuyer L, et al. Post-intubation laryngeal injuries and extubation failure: a fiberoptic endoscopic study. Intensive Care Med 2010; 36:991.
  26. Friedman M, Baim H, Shelton V, et al. Laryngeal injuries secondary to nasogastric tubes. Ann Otol Rhinol Laryngol 1981; 90:469.
  27. Santos PM, Afrassiabi A, Weymuller EA Jr. Risk factors associated with prolonged intubation and laryngeal injury. Otolaryngol Head Neck Surg 1994; 111:453.
  28. Colton House J, Noordzij JP, Murgia B, Langmore S. Laryngeal injury from prolonged intubation: a prospective analysis of contributing factors. Laryngoscope 2011; 121:596.
  29. Kikura M, Suzuki K, Itagaki T, et al. Age and comorbidity as risk factors for vocal cord paralysis associated with tracheal intubation. Br J Anaesth 2007; 98:524.
  30. Walner DL, Stern Y, Gerber ME, et al. Gastroesophageal reflux in patients with subglottic stenosis. Arch Otolaryngol Head Neck Surg 1998; 124:551.
  31. Stone DJ, Bogdonoff DL. Airway considerations in the management of patients requiring long-term endotracheal intubation. Anesth Analg 1992; 74:276.
  32. Darmon JY, Rauss A, Dreyfuss D, et al. Evaluation of risk factors for laryngeal edema after tracheal extubation in adults and its prevention by dexamethasone. A placebo-controlled, double-blind, multicenter study. Anesthesiology 1992; 77:245.
  33. Poetker DM, Ettema SL, Blumin JH, et al. Association of airway abnormalities and risk factors in 37 subglottic stenosis patients. Otolaryngol Head Neck Surg 2006; 135:434.
  34. Dargin JM, Emlet LL, Guyette FX. The effect of body mass index on intubation success rates and complications during emergency airway management. Intern Emerg Med 2013; 8:75.
  35. Colice GL, Stukel TA, Dain B. Laryngeal complications of prolonged intubation. Chest 1989; 96:877.
  36. Hamdan AL, Sibai A, Rameh C, Kanazeh G. Short-term effects of endotracheal intubation on voice. J Voice 2007; 21:762.
  37. Kitahara S, Masuda Y, Kitagawa Y. Vocal fold injury following endotracheal intubation. J Laryngol Otol 2005; 119:825.
  38. Colice GL. Resolution of laryngeal injury following translaryngeal intubation. Am Rev Respir Dis 1992; 145:361.
  39. Sariego J. Vocal fold hypomobility secondary to elective endotracheal intubation: a general surgeon's perspective. J Voice 2010; 24:110.
  40. Sue RD, Susanto I. Long-term complications of artificial airways. Clin Chest Med 2003; 24:457.
  41. Weber S. Traumatic complications of airway management. Anesthesiol Clin North America 2002; 20:503.
  42. Myssiorek D. Recurrent laryngeal nerve paralysis: anatomy and etiology. Otolaryngol Clin North Am 2004; 37:25.
  43. Paulsen FP, Jungmann K, Tillmann BN. The cricoarytenoid joint capsule and its relevance to endotracheal intubation. Anesth Analg 2000; 90:180.
  44. Young VN, Smith LJ, Rosen C. Voice outcome following acute unilateral vocal fold paralysis. Ann Otol Rhinol Laryngol 2013; 122:197.
  45. Whited RE. A prospective study of laryngotracheal sequelae in long-term intubation. Laryngoscope 1984; 94:367.
  46. Koshkareva Y, Gaughan JP, Soliman AM. Risk factors for adult laryngotracheal stenosis: a review of 74 cases. Ann Otol Rhinol Laryngol 2007; 116:206.
  47. Anand VK, Alemar G, Warren ET. Surgical considerations in tracheal stenosis. Laryngoscope 1992; 102:237.
  48. Taha MS, Mostafa BE, Fahmy M, et al. Spiral CT virtual bronchoscopy with multiplanar reformatting in the evaluation of post-intubation tracheal stenosis: comparison between endoscopic, radiological and surgical findings. Eur Arch Otorhinolaryngol 2009; 266:863.
  49. Rahbar R, Shapshay SM, Healy GB. Mitomycin: effects on laryngeal and tracheal stenosis, benefits, and complications. Ann Otol Rhinol Laryngol 2001; 110:1.
  50. Shadmehr MB, Abbasidezfouli A, Farzanegan R, et al. The Role of Systemic Steroids in Postintubation Tracheal Stenosis: A Randomized Clinical Trial. Ann Thorac Surg 2017; 103:246.
  51. Lins M, Dobbeleir I, Germonpré P, et al. Postextubation obstructive pseudomembranes: a case series and review of a rare complication after endotracheal intubation. Lung 2011; 189:81.
  52. Kaplow R, Bookbinder M. A comparison of four endotracheal tube holders. Heart Lung 1994; 23:59.
  53. Carlson J, Mayrose J, Krause R, Jehle D. Extubation force: tape versus endotracheal tube holders. Ann Emerg Med 2007; 50:686.
  54. Gomaa D, Branson RD. Endotracheal tube holders and the prone position: a cause for concern. Respir Care 2015; 60:e41.
  55. Kearl RA, Hooper RG. Massive airway leaks: an analysis of the role of endotracheal tubes. Crit Care Med 1993; 21:518.
  56. Kiekkas P, Aretha D, Panteli E, et al. Unplanned extubation in critically ill adults: clinical review. Nurs Crit Care 2013; 18:123.
  57. de Groot RI, Dekkers OM, Herold IH, et al. Risk factors and outcomes after unplanned extubations on the ICU: a case-control study. Crit Care 2011; 15:R19.
  58. Carrión MI, Ayuso D, Marcos M, et al. Accidental removal of endotracheal and nasogastric tubes and intravascular catheters. Crit Care Med 2000; 28:63.
  59. Stauffer JL, Olson DE, Petty TL. Complications and consequences of endotracheal intubation and tracheotomy. A prospective study of 150 critically ill adult patients. Am J Med 1981; 70:65.
  60. Zwillich CW, Pierson DJ, Creagh CE, et al. Complications of assisted ventilation. A prospective study of 354 consecutive episodes. Am J Med 1974; 57:161.
  61. El-Orbany M, Salem MR. Endotracheal tube cuff leaks: causes, consequences, and management. Anesth Analg 2013; 117:428.
  62. Adair CG, Gorman SP, Feron BM, et al. Implications of endotracheal tube biofilm for ventilator-associated pneumonia. Intensive Care Med 1999; 25:1072.
  63. Olson ME, Harmon BG, Kollef MH. Silver-coated endotracheal tubes associated with reduced bacterial burden in the lungs of mechanically ventilated dogs. Chest 2002; 121:863.
  64. Berra L, De Marchi L, Yu ZX, et al. Endotracheal tubes coated with antiseptics decrease bacterial colonization of the ventilator circuits, lungs, and endotracheal tube. Anesthesiology 2004; 100:1446.
  65. Rello J, Kollef M, Diaz E, et al. Reduced burden of bacterial airway colonization with a novel silver-coated endotracheal tube in a randomized multiple-center feasibility study. Crit Care Med 2006; 34:2766.
  66. Kampf G, Wischnewski N, Schulgen G, et al. Prevalence and risk factors for nosocomial lower respiratory tract infections in German hospitals. J Clin Epidemiol 1998; 51:495.
  67. Rello J, Ausina V, Castella J, et al. Nosocomial respiratory tract infections in multiple trauma patients. Influence of level of consciousness with implications for therapy. Chest 1992; 102:525.
  68. Nseir S, Di Pompeo C, Pronnier P, et al. Nosocomial tracheobronchitis in mechanically ventilated patients: incidence, aetiology and outcome. Eur Respir J 2002; 20:1483.
  69. Dallas J, Skrupky L, Abebe N, et al. Ventilator-associated tracheobronchitis in a mixed surgical and medical ICU population. Chest 2011; 139:513.
  70. Nseir S, Povoa P, Salluh J, et al. Is there a continuum between ventilator-associated tracheobronchitis and ventilator-associated pneumonia? Intensive Care Med 2016; 42:1190.
  71. Nseir S, Favory R, Jozefowicz E, et al. Antimicrobial treatment for ventilator-associated tracheobronchitis: a randomized, controlled, multicenter study. Crit Care 2008; 12:R62.
  72. Horan TC, Andrus M, Dudeck MA. CDC/NHSN surveillance definition of health care-associated infection and criteria for specific types of infections in the acute care setting. Am J Infect Control 2008; 36:309.
  73. Nseir S, Di Pompeo C, Soubrier S, et al. Outcomes of ventilated COPD patients with nosocomial tracheobronchitis: a case-control study. Infection 2004; 32:210.
  74. Palmer LB, Smaldone GC, Chen JJ, et al. Aerosolized antibiotics and ventilator-associated tracheobronchitis in the intensive care unit. Crit Care Med 2008; 36:2008.
  75. George DL, Falk PS, Umberto Meduri G, et al. Nosocomial sinusitis in patients in the medical intensive care unit: a prospective epidemiological study. Clin Infect Dis 1998; 27:463.
  76. Holzapfel L, Chevret S, Madinier G, et al. Influence of long-term oro- or nasotracheal intubation on nosocomial maxillary sinusitis and pneumonia: results of a prospective, randomized, clinical trial. Crit Care Med 1993; 21:1132.
  77. Huyett P, Lee S, Ferguson BJ, Wang EW. Sinus opacification in the intensive care unit patient. Laryngoscope 2016; 126:2433.
  78. Pneumatikos I, Konstantonis D, Tsagaris I, et al. Prevention of nosocomial maxillary sinusitis in the ICU: the effects of topically applied alpha-adrenergic agonists and corticosteroids. Intensive Care Med 2006; 32:532.
  79. Rouby JJ, Laurent P, Gosnach M, et al. Risk factors and clinical relevance of nosocomial maxillary sinusitis in the critically ill. Am J Respir Crit Care Med 1994; 150:776.
  80. Salord F, Gaussorgues P, Marti-Flich J, et al. Nosocomial maxillary sinusitis during mechanical ventilation: a prospective comparison of orotracheal versus the nasotracheal route for intubation. Intensive Care Med 1990; 16:390.
  81. Heffner JE. Nosocomial sinusitis. Den of multiresistant thieves? Am J Respir Crit Care Med 1994; 150:608.
  82. Hilbert G, Vargas F, Valentino R, et al. Comparison of B-mode ultrasound and computed tomography in the diagnosis of maxillary sinusitis in mechanically ventilated patients. Crit Care Med 2001; 29:1337.
  83. Souweine B, Mom T, Traore O, et al. Ventilator-associated sinusitis: microbiological results of sinus aspirates in patients on antibiotics. Anesthesiology 2000; 93:1255.
  84. Casiano RR, Cohn S, Villasuso E 3rd, et al. Comparison of antral tap with endoscopically directed nasal culture. Laryngoscope 2001; 111:1333.
  85. Talmor M, Li P, Barie PS. Acute paranasal sinusitis in critically ill patients: guidelines for prevention, diagnosis, and treatment. Clin Infect Dis 1997; 25:1441.
  86. Westergren V, Lundblad L, Hellquist HB, Forsum U. Ventilator-associated sinusitis: a review. Clin Infect Dis 1998; 27:851.
  87. Le Moal G, Lemerre D, Grollier G, et al. Nosocomial sinusitis with isolation of anaerobic bacteria in ICU patients. Intensive Care Med 1999; 25:1066.
  88. Geiss HK. Nosocomial sinusitis. Intensive Care Med 1999; 25:1037.
  89. Barquist E, Brown M, Cohn S, et al. Postextubation fiberoptic endoscopic evaluation of swallowing after prolonged endotracheal intubation: a randomized, prospective trial. Crit Care Med 2001; 29:1710.
  90. Barker J, Martino R, Reichardt B, et al. Incidence and impact of dysphagia in patients receiving prolonged endotracheal intubation after cardiac surgery. Can J Surg 2009; 52:119.
  91. Skoretz SA, Flowers HL, Martino R. The incidence of dysphagia following endotracheal intubation: a systematic review. Chest 2010; 137:665.
  92. Brodsky MB, Huang M, Shanholtz C, et al. Recovery from Dysphagia Symptoms after Oral Endotracheal Intubation in Acute Respiratory Distress Syndrome Survivors. A 5-Year Longitudinal Study. Ann Am Thorac Soc 2017; 14:376.
  93. Peterson SJ, Tsai AA, Scala CM, et al. Adequacy of oral intake in critically ill patients 1 week after extubation. J Am Diet Assoc 2010; 110:427.
  94. Payne DK, Anderson WM, Romero MD, et al. Tracheoesophageal fistula formation in intubated patients. Risk factors and treatment with high-frequency jet ventilation. Chest 1990; 98:161.
  95. Harley HR. Ulcerative tracheo-oesophageal fistula during treatment by tracheostomy and intermittent positive pressure ventilation. Thorax 1972; 27:338.
  96. Mooty RC, Rath P, Self M, et al. Review of tracheo-esophageal fistula associated with endotracheal intubation. J Surg Educ 2007; 64:237.
  97. Reed MF, Mathisen DJ. Tracheoesophageal fistula. Chest Surg Clin N Am 2003; 13:271.
  98. Bibas BJ, Guerreiro Cardoso PF, Minamoto H, et al. Surgical Management of Benign Acquired Tracheoesophageal Fistulas: A Ten-Year Experience. Ann Thorac Surg 2016; 102:1081.
  99. Dartevelle P, Macchiarini P. Management of acquired tracheoesophageal fistula. Chest Surg Clin N Am 1996; 6:819.
  100. Sanwal MK, Ganjoo P, Tandon MS. Posttracheostomy tracheoesophageal fistula. J Anaesthesiol Clin Pharmacol 2012; 28:140.
  101. Li J, Gao X, Chen J, et al. Endoscopic closure of acquired oesophagorespiratory fistulas with cardiac septal defect occluders or vascular plugs. Respir Med 2015; 109:1069.
  102. Erdim I, Sirin AA, Baykal B, et al. Treatment of large persistent tracheoesophageal peristomal fistulas using silicon rings. Braz J Otorhinolaryngol 2016.
  103. Hammoudeh ZS, Gursel E, Baciewicz FA Jr. Split latissimus dorsi muscle flap repair of acquired, nonmalignant, intrathoracic tracheoesophageal and bronchoesophageal fistulas. Heart Lung Circ 2015; 24:e75.
  104. Muniappan A, Wain JC, Wright CD, et al. Surgical treatment of nonmalignant tracheoesophageal fistula: a thirty-five year experience. Ann Thorac Surg 2013; 95:1141.
  105. Daniel SJ, Smith MM. Tracheoesophageal fistula: open versus endoscopic repair. Curr Opin Otolaryngol Head Neck Surg 2016; 24:510.
  106. Mort TC, Braffett BH. Conventional Versus Video Laryngoscopy for Tracheal Tube Exchange: Glottic Visualization, Success Rates, Complications, and Rescue Alternatives in the High-Risk Difficult Airway Patient. Anesth Analg 2015; 121:440.
  107. Buis ML, Maissan IM, Hoeks SE, et al. Defining the learning curve for endotracheal intubation using direct laryngoscopy: A systematic review. Resuscitation 2016; 99:63.
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