Prevention and Management of lntubation Injury of the Larynx and Trachea ERNEST A. WEYMULLER,
JR, MD
ACUTE INTUBATION INJURY--LARYNX Mucosal tears as a result of intubation are relatively common. Usually these are superficial tears that are created by the blade of the laryngoscope injuring the vallecula or the supraglottic larynx. The endotracheal tube may cause a tear in the supraglottic larynx, the vocal cords, or the lateral wall of the pyriform sinus or the esophageal inlet. Arytenoid dislocation and bilateral vocal cord paralysis have been reported as a complication of intubation.
an endotracheal tube cuff that is inflated within the larynx have the potential to injure the larynx. Identification The treating physician should be suspicious of acute injury in the patient who demonstrates hemoptysis, either at the time of or in the first 24 hours after intubation. Acute perforation of the pharyngeal or esophageal wall will soon be manifested by subcutaneous crepitus, fever, difficulty in swallowing, hoarseness, and/or stridor.
Etiology Prevention There are a number of factors that often contribute in a compounding way to the ultimate event of laryngeal injury. The likelihood for laryngeal injury is increased when unfavorable anatomy exists. In particular, obesity, limited excursion of the jaw or neck, or previous surgical procedures distorting the anatomy of the upper airway may predispose to laryngeal injury. Patients with acute infection, trauma, or neoplasm that distorts the anatomy of the upper airway and creates an emergency situation by virtue of ongoing obstruction are particularly prone to intubation trauma. Poor technique can also contribute to laryngeal injury. This ranges from indelicate use of instruments, such as the laryngoscope and the stylette, to inadequate visualization and improper preparation of the patient, including incomplete relaxation during induction. Additionally, an oversized endotracheal tube or
From the Department of Otolaryngology-Head and Neck Surgery, University of Washington, RL-30, Seattle, WA 98195. Address reprint requests to the Department of Otolaryngology-Head and Neck Surgery, University of Washington, RL-30, Seattle, WA 98195. Copyright 0 1992 by W.B. Saunders Company 0196-0?09/92/1303-0003$5.00/O American
Journal
of Otolaryngology,
Anticipation and preparation are the greatest factors in preventing acute intubation injury. Identification of the patient with predisposing factors as mentioned above is essential. The treating physician must consult with the anesthesiologist and allow time for methodical preparation and consideration of alternatives in the management of the airway. In patients with abnormal anatomy numerous alternatives are available and must be considered. The options include: Perform the operative procedure with local anesthetic, avoiding general anesthesia and intubation. Perform a tracheostomy using local anesthesia at the outset of the procedure. Use the transnasal fiberoptic technique for intubation. Transtracheal jet ventilation. Transtracheal jet ventilation is a convenient and effective technique, but is infrequently used. This modality must be practiced in a nonemergent setting and the clinician and anesthesiologist must have a clear understanding of its capabilities and limitations.’ Vol 13, No 3 (May-June),
1992: pp 139-144
139
140
Management Once acute laryngeal injury is identified, the management includes careful evaluation of the injury and consideration of a range of therapeutic options. If the injury is discovered during the course of the anesthetic, direct laryngoscopy and pharyngoscopy for assessment of the injury is appropriate. After completion of a general anesthetic, if the suspicion of laryngeal injury exists, the patient should be examined with a mirror or flexible fiberoptic scope to assess the degree of injury. If a major tear of the vocal cord is identified, the patient should be returned to the operating room for complete endoscopy with consideration of tracheotomy and open laryngeal repair. Most injuries are minor mucosal lacerations and may be managed expectantly. The patient should be observed in a carefully monitored setting and treated with antibiotics, oxygen, and humidification. If airway edema is threatened, intravenous hydrocortisone may be helpful (loo-mg bolus and XI mg every 8 hours for 2 days]. If the injury involves the pharynx or esophagus and is identified in the early postoperative period, a decision must be made between open or closed management. Large tears with open salivary soilage in the neck should be managed by an open surgical procedure to attempt mucosal closure and provide drainage of the neck spaces. Superficial mucosal injuries that are identified within the first few hours may be managed with antibiotic coverage and expectant management. In the presence of subcutaneous emphysema the patient should be brought to the operating room for complete endoscopic evaluation to determine the necessity for open drainage. Postoperative management includes broad-spectrum antibiotics, the placement of a nasogastric tube, and allowing 5 to 7 days for mucosal closure. Arytenoid Dislocation This injury almost always will be identified after extubation and is indicated by persisting hoarseness. Indirect examination will demonstrate an immobile vocal cord with laryngeal asymmetry. The management of this uncommon injury is controversial and difficult. Al-
ERNEST A. WEYMULLER
ternatives include nonintervention, endoscopic assessment and repositioning, and open repair with attempted repositioning of the arytenoid. A tear of the cricoarytenoid joint capsule, which is a sine qua non after arytenoid dislocation, has a high probability of resulting in cricoarytenoid arthritis, and it is most likely that the joint will become fixed. Endoscopic repositioning of the arytenoid with minimal manipulation has some potential to allow reconstitution of joint function. If the dislocation is severe laryngo fissure, repositioning, and soft stent for 7 to 10 days may be necessary. Vocal Cord Paralysis Acute vocal cord paralysis after intubation probably relates to inflation of the endotracheal tube cuff at the level of the subglottic larynx. At this location fibers of the recurrent laryngeal nerve enter between the cricoid and thyroid cartilage to innervate the intrinsic muscles of the larynx. Vocal cord paralysis is thought to result from direct pressure by the cuff causing neural injury (neuropraxia). It is best managed through prevention by careful assessment of the cuff placement and close monitoring of the pressure within the cuff. The technique of minimal occlusal volume is appropriate at all times. In using this technique one inflates the intratracheal cuff to an amount just sufficient to minimize the leak around the cuff. This is tested by positive pressure after insertion of the endotracheal tube. Cuff pressure may be further monitored by placing a pressure transducer and a threeway stopcock on the inflation port of the endotracheal tube cuff. The maximum safe pressure is 25 to 30 mm Hg (tracheal capillary perfusion pressure). ’ Acute vocal cord paralysis creates a significant management decision problem. If one cord is paralyzed, it is reasonable to manage the patient with observation. If both cords are paralyzed, and the airway is compromised, a temporary tracheostomy should be considered. Trachea Acute injury of the trachea from intubation is an uncommon event, but mucosal tears and
PREVENTION
AND MANAGEMENT
OF INTUBATION
141
INJURY
perforation may potentially occur. Tears are typically the result of insertion of the endotracheal tube with a stylette protruding beyond its tip and are most easily prevented by proper technique. Symptoms suggestive of tracheal injury include cough, hemoptysis, and subcutaneous emphysema. These symptoms should precipitate endoscopic evaluation either with a flexible fiberoptic scope or rigid endoscopy. For minor injuries the patient may be reintubated with the cuff placed below the injury allowing a short period of time for the wound to seal. If there is concern for more severe injury, the trachea may be explored via tracheal fissure and managed by the insertion of an indwelling Montgomery t-tube stent. CHRONIC INTUBATION INJURY-LARYNX There is a wide range of lesions that may result from the chronic presence of an endotracheal tube in the larynx. The minimal injury consists of mucosal erosion in the region of the vocal process of the arytenoid. This injury is symmetrical and predictably will exist after even a few days of intubation.3 Mucosal erosion may lead to the formation of a granuloma if reepithelialization after removal of the endotracheal tube fails to cover the mucosal ulcer. The process of mucosal ulceration over the arytenoid cartilage may invade the cricoarytenoid joint causing an active arthritis with ultimate fusion of the cricoarytenoid joint. The erosive process may also involve the posterior commissure exposing the interarytenoid muscle and even the cricoid cartilage. This sets the stage for the formation of glottic stenosis and rarely abscess formation involving the cricoid cartilage. Etiology The primary active agent of injury is the endotracheal tube itself. During prolonged intubation the endotracheal tube sits between the vocal cords, and by its physical presence exerts pressure in a lateral and posterior direction. This pressure exceeds mucosal capillary perfusion pressure causing ischemic necrosis in the area of the tube contact with the laryngeal surface. During the first few days, mucosal degeneration occurs allowing exposure
to airway bacteria and setting the stage for a range of potential outcomes that are often determined by a number of secondary factors. It is likely that compromised host defenses (diabetes, poor nutrition, and general immune suppression) are factors that promote progression of the initial injury. Additional factors include the presence of a nasogastric tube that may trap the posterior larynx between the endotracheal tube and the nasogastric tube.4 The size of the endotracheal tube in relation to the patient’s anatomy may also be a factor. It appears that females are more likely to develop laryngeal stenosis; this is felt most likely to relate to the smaller size of the female larynx, which sets the stage for placement of an endotracheal tube that is relatively too large and more likely to cause injury. Intubation injury in the pediatric age group, and in particular in the neonatal intensive care unit, is most likely to occur at the level of the subglottic larynx because the cricoid ring is relatively smaller than the glottis at this stage of human development. Identification Some degree of laryngeal injury after prolonged intubation is noted in virtually every patient examined after extubation. After 7 or more days of intubation, all patients can be expected to have erythema of the laryngeal mucosa and 70% or more will be noted to have ulceration.5 Fortunately, the vast majority of these injuries are self-limited and will resolve with time. The laryngeal injury associated with intubation evolves through two recognizable phases. During the first 24 to 96 hours, the larynx reacts to the presence of the tube with acute mucosal inflammatory infiltrate and submucosal edema. The edema resolves within the first few days of intubation, and then the injury becomes primarily localized to the mucosal erosion in the posterolat. era1 larynx and progressive involvement of the immediately underlying structures. An indication of the degree of edema within the larynx may be accomplished before extubation by deflating the cuff of the endotracheal tube and assessing the degree of “blow by.” If the cuff is taken down and free passage of air during ventilator cycles or mechanical ventila-
142
tion is easily evident, one may anticipate potentially successful and uncomplicated extubation. If after deflation of the cuff there is impeded flow of air past the tube, one may expect to find laryngeal edema and anticipate the possibility of a complicated extubation. In this author’s experience, the use of flexible laryngoscopy has been limited in its ability to predict laryngeal competence and airway patency at the time of extubation. Examination of the patient before extubation may give additional indications of pathology if there is pain, tenderness, or swelling in the region of the larynx. Abnormal laryngeal function after extubation will be obvious through hoarseness, stridor, and respiratory obstruction requiring urgent reintubation. Extubation after resolution of the acute edematous phase is less likely to result in respiratory obstruction. At this time symptoms of laryngeal dysfunction include hoarseness, aspiration, and poor cough. Prevention Careful management of the endotracheal tube may help to minimize laryngeal injury. The smallest tube compatible with adequate respiratory management for the individual patient should be selected. In females a 7.0 tube should be considered. In males a 7.5 tube would usually be adequate. Another consideration in tube selection is the choice of biocompatible materials. Polyvinylchloride is inexpensive and thus most endotracheal tubes are made of this material, but numerous chemical additives are used to modify polyvinylchloride and these may be leached into surrounding tissues. A better selection for prolonged intubation would be silicone due to its less reactive nature and its reduced bacterial adherence. As mentioned previously, a rigid nasogastric tube may compress the posterior larynx against an endotracheal tube. In the setting of prolonged intubation, a soft, small nasogastric tube should be selected if at all possible.* Additionally, it appears that gastric reflux is a contributing factor to granuloma formation and other forms of laryngeal injury related to intubation. If possible, the patient should be placed with the head elevated and administered HZ-blockers to control
ERNEST A. WEYMULLER
acidity.’ When the probability for prolonged intubation is high, laryngeal injury may also be prevented by performing a tracheotomy. This decision should be made as early as possible in order to avoid the unfavorable scenario of performing a tracheotomy after laryngeal injury has been created by the prolonged presence of an endotracheal tube.6 Management The ideal form of management for the laryngeal injuries after prolonged intubation consists of early and aggressive intervention. The lesion may be visualized with indirect methods using laryngeal mirror or fiberoptic laryngoscope. During that examination if it is noted that the vocal cords move well and the lesion is limited to mucosal ulceration and limited amounts of granulation tissue, expectant management with inhaled steroids and broadspectrum antibiotics usually results in resolution of the problem. A more aggressive intervention should be considered if examination shows exuberant granulation tissue and limitation of laryngeal motion. Direct laryngoscopy for more complete examination and palpation of the arytenoid joints is appropriate. Granulation tissue should be removed with cupped forceps and submitted for culture and sensitivity evaluation. Examination should include assessment of the interarytenoid space. If erosion includes or involves both arytenoids and the interarytenoid space, the potential for a stenotic outcome is significantly increased. This author feels that injection of steroids in the submucosa of the interarytenoid and immediate crycoarytenoid regions is helpful. The sequence of surgical procedure consists of direct laryngoscopic examination and then submucosal injection of steroids before removal of granulation tissue. This improves the retention of the injected material submucosally. Granulation tissues are then thoroughly cleaned down to the level of adjacent mucosa. The patient should be carefully followed, and in 7 to 10 days, if granulation tissue and laryngeal function have not improved significantly, the procedure may be repeated. Antibiotic coverage guided by culture and sensitivity information is essential. If the otolaryngologist-head and neck sur-
PREVENTION
AND MANAGEMENT
OF INTUBATION
143
INJURY
geon is called to consider a tracheotomy in a patient who has already been intubated for 1 week or more, laryngeal pathology should be anticipated. After performing the tracheotomy, the endotracheal tube should be removed and direct laryngoscopy performed. At this time thorough removal of granulation tissue and injection of steroids should be considered based on findings during the examination. These patients should be monitored with a repeat examination 7 to 10 days after performance of the tracheotomy. The combination of a tracheotomy and laryngeal injury from prolonged intubation is dangerous, and aggressive early management of the evolving laryngeal injury usually will bring about a favorable outcome. It is additionally important to manage the tracheotomy wound with antibacterial dressings to prevent local infection and aggravation of the laryngeal injury. The natural history of adult laryngeal injury after chronic intubation is usually characterized by resolution of the injury. Ten percent or less will evolve to some form of laryngeal stenosis.7 Stenosis assumes a variety of forms and management may include dilatation, laser resection, “trapdoor flaps,” or an open procedure including laryngo fissure with keel or anterior-posterior cricoid split with laryngeal stents. In neonates a different injury is more likely. The small size of the cricoid ring relative to the remaining larynx predisposes to circumferential subglottic mucosal injury. Stridor after extubation is managed by reinsertion of the endotracheal tube, and consideration should then be given to performing an anterior cricoid split.* CHRONIC INTUBATION INJURY-TRACHEA As in the larynx, minor injury such as mucosal erosion is common. The more advanced form of injury includes submucosal damage to the tracheal cartilage, which is initially manifest as tracheal dilatation and later as tracheal stenosis when scarring causes circumferential tracheal contracture. When full thickness mucosal injury occurs in the posterior trachea, a tracheoesophageal fistula may occur.
Etiology Injury to the trachea during chronic intubation is the result of pressure necrosis from the cuff of the endotracheal tube. The sequence of injury begins with inflation of the endotracheal tube cuff to pressures in excess of mucosal perfusion pressure. Once mucosal necrosis occurs, the immediate underlying cartilage is exposed to airway bacteria and a destructive inflammatory/infectious process is initiated. In many instances this process is unavoidable because cuff pressure must be maintained at a level sufficient to support high-pressure mechanical ventilation. Identification of Injury Careful attention to pressure within the endotracheal tube cuff during prolonged intubation is helpful. When pressures exceed 25 to XI mm Hg, mucosal injury can be predicted. Ventilator management should include selection of the lowest cuff pressure that allows adequate ventilation. Once this pressure exceeds 30 mm Hg, tracheal damage may be anticipated. The volume of air necessary to inflate the endotracheal cuff is another indication of progressive dilatation of the trachea, which may also be identified by chest x-ray. Tracheal esophageal fistula as a result of pressure necrosis from the cuff is an uncommon event, but may be identified or suspected when gastric distention occurs as a result of direct air leak from the trachea into the proximal esophagus. More commonly, the tracheal lesion created by cuff injury is not identified in the acute setting and only becomes apparent as a gradually progressive limitation of airway in the post-intensive care unit recovery phase. In this instance the lesion is pernicious and often not recognized for long periods of time, The slow progression of stenosis allows accommodation by the patient and its significance is usually not evident until >50% narrowing of the tracheal airway has occurred. Identification of the lesion is usually best accomplished with anterior and lateral radiographs of the trachea.
144
Prevention Careful monitoring of tracheal cuff pressure is essential to the prevention of tracheal stenosis. Once the scenario of increasing volumes to sustain adequate ventilatory pressure occurs, management becomes difficult. The options are limited and not always successful. In the setting of progressive tracheal dilatation, this author recommends performance of a tracheostomy and use of an endotracheal tube rather than a tracheotomy tube for ventilation. With careful monitoring, the endotracheal tube cuff may be placed at different levels within the trachea on an alternating basis every 12 to 24 hours. In this method sustained pressure at any one site in the trachea is minimized. It must be recognized that this method is a temporizing maneuver. The hope being that the underlying illness of the patient will resolve and the need for high-pressure ventilation eliminated. In the presence of tracheal esophageal fistula as a result of intubation, a decision must be made to undertake surgical closure. Usually these patients are extremely ill with multiple management problems. Aspiration of
ERNEST A. WEYMULLER
gastric contents in the acute setting may be controlled by placing the endotracheal balloon at the level of the fistula. Open surgical repair with three-layer closure should be accomplished as soon as possible. REFERENCES 1. Weymuller EA, Pavlin EG, Paugh D, et al: Management of difficult airway problems with transtracheal jet ventilation. Ann Otol Rhino1 Laryngol 96:34-37, 1987 2. Nordin U, Lindholm C-E, Wolgast M: Blood flow in the rabbit tracheal mucosa under normal conditions and the influence of tracheal intubation. Acta Anaesthesiol Stand 21:81-94, 1977 3. Lindholm C-E: Prolonged endotracheal intubation. Acta Anaesthesiol Stand Suppl 33:1-131,1969 4. Sofferman RA, Hubbell RN: Laryngeal complications of nasogastric tubes. Ann Otol Rhino1 Laryngol 90:465-468, 1981 5. Santos PM, Afrassiabi A, Weymuller EA: Prospective studies evaluating the standard endotracheal tube and a prototype endotracheal tube. Ann Otol Rhino1 Laryngol 95:935-940, 1989 6. Sasaki CT, Horiuchi M, Koss N: Tracheostomyrelated subglottic stenosis. Bacteriologic pathogenesis. Laryngoscope 89:857-865, 1979 7. Whited RE: Posterior commissure stenosis post longterm intubation. Laryngoscope 93:1314-1318, 1983 8. Cotton RT, Seid AB: Management of the extubation problem in the premature child-Anterior cricoid split as an alternative to tracheotomy. Ann Otol Rhino1 Laryngol 89:508-511, 1980
JR, MD
ACUTE INTUBATION INJURY--LARYNX Mucosal tears as a result of intubation are relatively common. Usually these are superficial tears that are created by the blade of the laryngoscope injuring the vallecula or the supraglottic larynx. The endotracheal tube may cause a tear in the supraglottic larynx, the vocal cords, or the lateral wall of the pyriform sinus or the esophageal inlet. Arytenoid dislocation and bilateral vocal cord paralysis have been reported as a complication of intubation.
an endotracheal tube cuff that is inflated within the larynx have the potential to injure the larynx. Identification The treating physician should be suspicious of acute injury in the patient who demonstrates hemoptysis, either at the time of or in the first 24 hours after intubation. Acute perforation of the pharyngeal or esophageal wall will soon be manifested by subcutaneous crepitus, fever, difficulty in swallowing, hoarseness, and/or stridor.
Etiology Prevention There are a number of factors that often contribute in a compounding way to the ultimate event of laryngeal injury. The likelihood for laryngeal injury is increased when unfavorable anatomy exists. In particular, obesity, limited excursion of the jaw or neck, or previous surgical procedures distorting the anatomy of the upper airway may predispose to laryngeal injury. Patients with acute infection, trauma, or neoplasm that distorts the anatomy of the upper airway and creates an emergency situation by virtue of ongoing obstruction are particularly prone to intubation trauma. Poor technique can also contribute to laryngeal injury. This ranges from indelicate use of instruments, such as the laryngoscope and the stylette, to inadequate visualization and improper preparation of the patient, including incomplete relaxation during induction. Additionally, an oversized endotracheal tube or
From the Department of Otolaryngology-Head and Neck Surgery, University of Washington, RL-30, Seattle, WA 98195. Address reprint requests to the Department of Otolaryngology-Head and Neck Surgery, University of Washington, RL-30, Seattle, WA 98195. Copyright 0 1992 by W.B. Saunders Company 0196-0?09/92/1303-0003$5.00/O American
Journal
of Otolaryngology,
Anticipation and preparation are the greatest factors in preventing acute intubation injury. Identification of the patient with predisposing factors as mentioned above is essential. The treating physician must consult with the anesthesiologist and allow time for methodical preparation and consideration of alternatives in the management of the airway. In patients with abnormal anatomy numerous alternatives are available and must be considered. The options include: Perform the operative procedure with local anesthetic, avoiding general anesthesia and intubation. Perform a tracheostomy using local anesthesia at the outset of the procedure. Use the transnasal fiberoptic technique for intubation. Transtracheal jet ventilation. Transtracheal jet ventilation is a convenient and effective technique, but is infrequently used. This modality must be practiced in a nonemergent setting and the clinician and anesthesiologist must have a clear understanding of its capabilities and limitations.’ Vol 13, No 3 (May-June),
1992: pp 139-144
139
140
Management Once acute laryngeal injury is identified, the management includes careful evaluation of the injury and consideration of a range of therapeutic options. If the injury is discovered during the course of the anesthetic, direct laryngoscopy and pharyngoscopy for assessment of the injury is appropriate. After completion of a general anesthetic, if the suspicion of laryngeal injury exists, the patient should be examined with a mirror or flexible fiberoptic scope to assess the degree of injury. If a major tear of the vocal cord is identified, the patient should be returned to the operating room for complete endoscopy with consideration of tracheotomy and open laryngeal repair. Most injuries are minor mucosal lacerations and may be managed expectantly. The patient should be observed in a carefully monitored setting and treated with antibiotics, oxygen, and humidification. If airway edema is threatened, intravenous hydrocortisone may be helpful (loo-mg bolus and XI mg every 8 hours for 2 days]. If the injury involves the pharynx or esophagus and is identified in the early postoperative period, a decision must be made between open or closed management. Large tears with open salivary soilage in the neck should be managed by an open surgical procedure to attempt mucosal closure and provide drainage of the neck spaces. Superficial mucosal injuries that are identified within the first few hours may be managed with antibiotic coverage and expectant management. In the presence of subcutaneous emphysema the patient should be brought to the operating room for complete endoscopic evaluation to determine the necessity for open drainage. Postoperative management includes broad-spectrum antibiotics, the placement of a nasogastric tube, and allowing 5 to 7 days for mucosal closure. Arytenoid Dislocation This injury almost always will be identified after extubation and is indicated by persisting hoarseness. Indirect examination will demonstrate an immobile vocal cord with laryngeal asymmetry. The management of this uncommon injury is controversial and difficult. Al-
ERNEST A. WEYMULLER
ternatives include nonintervention, endoscopic assessment and repositioning, and open repair with attempted repositioning of the arytenoid. A tear of the cricoarytenoid joint capsule, which is a sine qua non after arytenoid dislocation, has a high probability of resulting in cricoarytenoid arthritis, and it is most likely that the joint will become fixed. Endoscopic repositioning of the arytenoid with minimal manipulation has some potential to allow reconstitution of joint function. If the dislocation is severe laryngo fissure, repositioning, and soft stent for 7 to 10 days may be necessary. Vocal Cord Paralysis Acute vocal cord paralysis after intubation probably relates to inflation of the endotracheal tube cuff at the level of the subglottic larynx. At this location fibers of the recurrent laryngeal nerve enter between the cricoid and thyroid cartilage to innervate the intrinsic muscles of the larynx. Vocal cord paralysis is thought to result from direct pressure by the cuff causing neural injury (neuropraxia). It is best managed through prevention by careful assessment of the cuff placement and close monitoring of the pressure within the cuff. The technique of minimal occlusal volume is appropriate at all times. In using this technique one inflates the intratracheal cuff to an amount just sufficient to minimize the leak around the cuff. This is tested by positive pressure after insertion of the endotracheal tube. Cuff pressure may be further monitored by placing a pressure transducer and a threeway stopcock on the inflation port of the endotracheal tube cuff. The maximum safe pressure is 25 to 30 mm Hg (tracheal capillary perfusion pressure). ’ Acute vocal cord paralysis creates a significant management decision problem. If one cord is paralyzed, it is reasonable to manage the patient with observation. If both cords are paralyzed, and the airway is compromised, a temporary tracheostomy should be considered. Trachea Acute injury of the trachea from intubation is an uncommon event, but mucosal tears and
PREVENTION
AND MANAGEMENT
OF INTUBATION
141
INJURY
perforation may potentially occur. Tears are typically the result of insertion of the endotracheal tube with a stylette protruding beyond its tip and are most easily prevented by proper technique. Symptoms suggestive of tracheal injury include cough, hemoptysis, and subcutaneous emphysema. These symptoms should precipitate endoscopic evaluation either with a flexible fiberoptic scope or rigid endoscopy. For minor injuries the patient may be reintubated with the cuff placed below the injury allowing a short period of time for the wound to seal. If there is concern for more severe injury, the trachea may be explored via tracheal fissure and managed by the insertion of an indwelling Montgomery t-tube stent. CHRONIC INTUBATION INJURY-LARYNX There is a wide range of lesions that may result from the chronic presence of an endotracheal tube in the larynx. The minimal injury consists of mucosal erosion in the region of the vocal process of the arytenoid. This injury is symmetrical and predictably will exist after even a few days of intubation.3 Mucosal erosion may lead to the formation of a granuloma if reepithelialization after removal of the endotracheal tube fails to cover the mucosal ulcer. The process of mucosal ulceration over the arytenoid cartilage may invade the cricoarytenoid joint causing an active arthritis with ultimate fusion of the cricoarytenoid joint. The erosive process may also involve the posterior commissure exposing the interarytenoid muscle and even the cricoid cartilage. This sets the stage for the formation of glottic stenosis and rarely abscess formation involving the cricoid cartilage. Etiology The primary active agent of injury is the endotracheal tube itself. During prolonged intubation the endotracheal tube sits between the vocal cords, and by its physical presence exerts pressure in a lateral and posterior direction. This pressure exceeds mucosal capillary perfusion pressure causing ischemic necrosis in the area of the tube contact with the laryngeal surface. During the first few days, mucosal degeneration occurs allowing exposure
to airway bacteria and setting the stage for a range of potential outcomes that are often determined by a number of secondary factors. It is likely that compromised host defenses (diabetes, poor nutrition, and general immune suppression) are factors that promote progression of the initial injury. Additional factors include the presence of a nasogastric tube that may trap the posterior larynx between the endotracheal tube and the nasogastric tube.4 The size of the endotracheal tube in relation to the patient’s anatomy may also be a factor. It appears that females are more likely to develop laryngeal stenosis; this is felt most likely to relate to the smaller size of the female larynx, which sets the stage for placement of an endotracheal tube that is relatively too large and more likely to cause injury. Intubation injury in the pediatric age group, and in particular in the neonatal intensive care unit, is most likely to occur at the level of the subglottic larynx because the cricoid ring is relatively smaller than the glottis at this stage of human development. Identification Some degree of laryngeal injury after prolonged intubation is noted in virtually every patient examined after extubation. After 7 or more days of intubation, all patients can be expected to have erythema of the laryngeal mucosa and 70% or more will be noted to have ulceration.5 Fortunately, the vast majority of these injuries are self-limited and will resolve with time. The laryngeal injury associated with intubation evolves through two recognizable phases. During the first 24 to 96 hours, the larynx reacts to the presence of the tube with acute mucosal inflammatory infiltrate and submucosal edema. The edema resolves within the first few days of intubation, and then the injury becomes primarily localized to the mucosal erosion in the posterolat. era1 larynx and progressive involvement of the immediately underlying structures. An indication of the degree of edema within the larynx may be accomplished before extubation by deflating the cuff of the endotracheal tube and assessing the degree of “blow by.” If the cuff is taken down and free passage of air during ventilator cycles or mechanical ventila-
142
tion is easily evident, one may anticipate potentially successful and uncomplicated extubation. If after deflation of the cuff there is impeded flow of air past the tube, one may expect to find laryngeal edema and anticipate the possibility of a complicated extubation. In this author’s experience, the use of flexible laryngoscopy has been limited in its ability to predict laryngeal competence and airway patency at the time of extubation. Examination of the patient before extubation may give additional indications of pathology if there is pain, tenderness, or swelling in the region of the larynx. Abnormal laryngeal function after extubation will be obvious through hoarseness, stridor, and respiratory obstruction requiring urgent reintubation. Extubation after resolution of the acute edematous phase is less likely to result in respiratory obstruction. At this time symptoms of laryngeal dysfunction include hoarseness, aspiration, and poor cough. Prevention Careful management of the endotracheal tube may help to minimize laryngeal injury. The smallest tube compatible with adequate respiratory management for the individual patient should be selected. In females a 7.0 tube should be considered. In males a 7.5 tube would usually be adequate. Another consideration in tube selection is the choice of biocompatible materials. Polyvinylchloride is inexpensive and thus most endotracheal tubes are made of this material, but numerous chemical additives are used to modify polyvinylchloride and these may be leached into surrounding tissues. A better selection for prolonged intubation would be silicone due to its less reactive nature and its reduced bacterial adherence. As mentioned previously, a rigid nasogastric tube may compress the posterior larynx against an endotracheal tube. In the setting of prolonged intubation, a soft, small nasogastric tube should be selected if at all possible.* Additionally, it appears that gastric reflux is a contributing factor to granuloma formation and other forms of laryngeal injury related to intubation. If possible, the patient should be placed with the head elevated and administered HZ-blockers to control
ERNEST A. WEYMULLER
acidity.’ When the probability for prolonged intubation is high, laryngeal injury may also be prevented by performing a tracheotomy. This decision should be made as early as possible in order to avoid the unfavorable scenario of performing a tracheotomy after laryngeal injury has been created by the prolonged presence of an endotracheal tube.6 Management The ideal form of management for the laryngeal injuries after prolonged intubation consists of early and aggressive intervention. The lesion may be visualized with indirect methods using laryngeal mirror or fiberoptic laryngoscope. During that examination if it is noted that the vocal cords move well and the lesion is limited to mucosal ulceration and limited amounts of granulation tissue, expectant management with inhaled steroids and broadspectrum antibiotics usually results in resolution of the problem. A more aggressive intervention should be considered if examination shows exuberant granulation tissue and limitation of laryngeal motion. Direct laryngoscopy for more complete examination and palpation of the arytenoid joints is appropriate. Granulation tissue should be removed with cupped forceps and submitted for culture and sensitivity evaluation. Examination should include assessment of the interarytenoid space. If erosion includes or involves both arytenoids and the interarytenoid space, the potential for a stenotic outcome is significantly increased. This author feels that injection of steroids in the submucosa of the interarytenoid and immediate crycoarytenoid regions is helpful. The sequence of surgical procedure consists of direct laryngoscopic examination and then submucosal injection of steroids before removal of granulation tissue. This improves the retention of the injected material submucosally. Granulation tissues are then thoroughly cleaned down to the level of adjacent mucosa. The patient should be carefully followed, and in 7 to 10 days, if granulation tissue and laryngeal function have not improved significantly, the procedure may be repeated. Antibiotic coverage guided by culture and sensitivity information is essential. If the otolaryngologist-head and neck sur-
PREVENTION
AND MANAGEMENT
OF INTUBATION
143
INJURY
geon is called to consider a tracheotomy in a patient who has already been intubated for 1 week or more, laryngeal pathology should be anticipated. After performing the tracheotomy, the endotracheal tube should be removed and direct laryngoscopy performed. At this time thorough removal of granulation tissue and injection of steroids should be considered based on findings during the examination. These patients should be monitored with a repeat examination 7 to 10 days after performance of the tracheotomy. The combination of a tracheotomy and laryngeal injury from prolonged intubation is dangerous, and aggressive early management of the evolving laryngeal injury usually will bring about a favorable outcome. It is additionally important to manage the tracheotomy wound with antibacterial dressings to prevent local infection and aggravation of the laryngeal injury. The natural history of adult laryngeal injury after chronic intubation is usually characterized by resolution of the injury. Ten percent or less will evolve to some form of laryngeal stenosis.7 Stenosis assumes a variety of forms and management may include dilatation, laser resection, “trapdoor flaps,” or an open procedure including laryngo fissure with keel or anterior-posterior cricoid split with laryngeal stents. In neonates a different injury is more likely. The small size of the cricoid ring relative to the remaining larynx predisposes to circumferential subglottic mucosal injury. Stridor after extubation is managed by reinsertion of the endotracheal tube, and consideration should then be given to performing an anterior cricoid split.* CHRONIC INTUBATION INJURY-TRACHEA As in the larynx, minor injury such as mucosal erosion is common. The more advanced form of injury includes submucosal damage to the tracheal cartilage, which is initially manifest as tracheal dilatation and later as tracheal stenosis when scarring causes circumferential tracheal contracture. When full thickness mucosal injury occurs in the posterior trachea, a tracheoesophageal fistula may occur.
Etiology Injury to the trachea during chronic intubation is the result of pressure necrosis from the cuff of the endotracheal tube. The sequence of injury begins with inflation of the endotracheal tube cuff to pressures in excess of mucosal perfusion pressure. Once mucosal necrosis occurs, the immediate underlying cartilage is exposed to airway bacteria and a destructive inflammatory/infectious process is initiated. In many instances this process is unavoidable because cuff pressure must be maintained at a level sufficient to support high-pressure mechanical ventilation. Identification of Injury Careful attention to pressure within the endotracheal tube cuff during prolonged intubation is helpful. When pressures exceed 25 to XI mm Hg, mucosal injury can be predicted. Ventilator management should include selection of the lowest cuff pressure that allows adequate ventilation. Once this pressure exceeds 30 mm Hg, tracheal damage may be anticipated. The volume of air necessary to inflate the endotracheal cuff is another indication of progressive dilatation of the trachea, which may also be identified by chest x-ray. Tracheal esophageal fistula as a result of pressure necrosis from the cuff is an uncommon event, but may be identified or suspected when gastric distention occurs as a result of direct air leak from the trachea into the proximal esophagus. More commonly, the tracheal lesion created by cuff injury is not identified in the acute setting and only becomes apparent as a gradually progressive limitation of airway in the post-intensive care unit recovery phase. In this instance the lesion is pernicious and often not recognized for long periods of time, The slow progression of stenosis allows accommodation by the patient and its significance is usually not evident until >50% narrowing of the tracheal airway has occurred. Identification of the lesion is usually best accomplished with anterior and lateral radiographs of the trachea.
144
Prevention Careful monitoring of tracheal cuff pressure is essential to the prevention of tracheal stenosis. Once the scenario of increasing volumes to sustain adequate ventilatory pressure occurs, management becomes difficult. The options are limited and not always successful. In the setting of progressive tracheal dilatation, this author recommends performance of a tracheostomy and use of an endotracheal tube rather than a tracheotomy tube for ventilation. With careful monitoring, the endotracheal tube cuff may be placed at different levels within the trachea on an alternating basis every 12 to 24 hours. In this method sustained pressure at any one site in the trachea is minimized. It must be recognized that this method is a temporizing maneuver. The hope being that the underlying illness of the patient will resolve and the need for high-pressure ventilation eliminated. In the presence of tracheal esophageal fistula as a result of intubation, a decision must be made to undertake surgical closure. Usually these patients are extremely ill with multiple management problems. Aspiration of
ERNEST A. WEYMULLER
gastric contents in the acute setting may be controlled by placing the endotracheal balloon at the level of the fistula. Open surgical repair with three-layer closure should be accomplished as soon as possible. REFERENCES 1. Weymuller EA, Pavlin EG, Paugh D, et al: Management of difficult airway problems with transtracheal jet ventilation. Ann Otol Rhino1 Laryngol 96:34-37, 1987 2. Nordin U, Lindholm C-E, Wolgast M: Blood flow in the rabbit tracheal mucosa under normal conditions and the influence of tracheal intubation. Acta Anaesthesiol Stand 21:81-94, 1977 3. Lindholm C-E: Prolonged endotracheal intubation. Acta Anaesthesiol Stand Suppl 33:1-131,1969 4. Sofferman RA, Hubbell RN: Laryngeal complications of nasogastric tubes. Ann Otol Rhino1 Laryngol 90:465-468, 1981 5. Santos PM, Afrassiabi A, Weymuller EA: Prospective studies evaluating the standard endotracheal tube and a prototype endotracheal tube. Ann Otol Rhino1 Laryngol 95:935-940, 1989 6. Sasaki CT, Horiuchi M, Koss N: Tracheostomyrelated subglottic stenosis. Bacteriologic pathogenesis. Laryngoscope 89:857-865, 1979 7. Whited RE: Posterior commissure stenosis post longterm intubation. Laryngoscope 93:1314-1318, 1983 8. Cotton RT, Seid AB: Management of the extubation problem in the premature child-Anterior cricoid split as an alternative to tracheotomy. Ann Otol Rhino1 Laryngol 89:508-511, 1980
