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The burned trachea
Chest Surg Clin N Am 13 (2003) 343 – 348
The burned trachea Subroto Paul, MDa, Raphael Bueno, MDa,b,* a
Division of Thoracic Surgery, Department of Surgery, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA b Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA
Inhalation injury remains a challenging medical problem in terms of diagnosis and treatment. Burn injuries continue to be a major health problem in the United States, with an estimated 2.2 million burns reported each year of which 60,000 require hospitalization [1]. Some inhalation injury accompanies cutaneous burn injury in 50% to 75% of patients [2,3]. The degree of inhalation injury is reported to be the single most important factor that directly correlates with the incidence of death from burns in the first 24 to 48 hours after injury [2,3]. Despite major advances in the understanding and treatment of cutaneous burn injuries over the past 25 years, similar significant advances have not been made in the treatment of inhalation injury. Inhalation injury has been classified into three categories, with injuries occurring in the following anatomic sequence: (1) upper airways to the level of the true vocal cords, (2) trachea and major bronchi, and (3) parenchymal lung tissue [3]. In this article the authors review tracheal burns with respect to diagnosis, pathophysiology, treatment, and complications in the acute and chronic intervals.
Diagnosis and pathophysiology The possibility of burn injury to the trachea must be entertained by the treating medical team in the evaluation of all burn patients. Facial and chest cutaneous burns, singed nasal hairs, and carbonaceous sputum are suggestive of concomitant inhalation injury. Thermal injury occurring secondary to fire is the most common mechanism of burn injury; however, other mechanisms of inhalation injury are possible, including chemical burn injuries from exposure to toxic gases during industrial acid/base spills, suicide attempts by toxic ingestion and resultant
* Corresponding author. Raphael Bueno, MD, Division of Thoracic Surgery, Department of Surgery, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115. 1052-3359/03/$ – see front matter D 2003, Elsevier Inc. All rights reserved. doi:10.1016/S1052-3359(03)00003-6
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S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
aspiration and exposure to acid, and sulfur fumes produced from burning polyvinylchloride. Tracheal burn injury can also occur as a consequence of direct injury during tracheostomy, from electrocautery-induced combustion of volatile anesthetic gases during tracheolaryngeal surgery, or (as more recently reported in the literature) from injury sustained from fires induced by therapeutic lasers, including the commonly used carbon dioxide and KTP/YAG laser devices [4,5]. Without regard to the mechanism of injury, symptomatic patients usually complain of a range of symptoms from shortness of breath, hoarseness, stridor, and wheezing to frank respiratory collapse caused by extreme hypoxia or upper airway obstruction requiring intubation and ventilatory support [3,6 –8]. The key to diagnosis of tracheal burns lies in careful screening of all potential patients and early identification of patients who will likely progress to complete respiratory collapse despite an initial mild presentation. Many tests have been proposed for optimal evaluation and screening of patients at risk. Arterial blood tests to measure the PaO2 and carboxyhemoglobin levels can give an indication of the degree of smoke inhalation, but these tests provide no information of the degree of tracheal injury per se [3,9]. In the absence of severe pulmonary and tracheal injury, chest radiographs provide little information and often appear normal [9]. A CT of the chest might provide slightly more information about the extent of injury because tracheal edema is better visualized on CT; however, CT is not sufficiently accurate in the acute setting. Other studies such as pulmonary function tests and radioactive lung scans are not commonly used, nor are they informative in the diagnosis of tracheal injury [2,3,6]. The best diagnostic study in patients suspected to have tracheal burns remains fiberoptic bronchoscopy, which allows for direct visualization and assessment of the degree of injury. Fiberoptic bronchoscopy is the most sensitive and specific way to diagnose tracheal injury [3,6,8,10]. Rigid bronchoscopy should be available if mandated by the clinical scenario. Bronchoscopic findings of early tracheal injury include hyperemic mucosa, edema, carbon deposits, charring of tissue, and easy bruising. In severe cases, one can visualize either early or progressive mucosal sloughing or frank necrosis of airway tissue. Either of these findings makes imminent airway obstruction more likely and supports the decision for early intubation. The severity of the bronchoscopic findings often correlates with the overall degree of severity of the symptoms and findings in the patient. Patients with superficial injury that is limited to the mucosa will likely heal with supportive therapy. Patients with deeper partial- or full-thickness injury will likely develop chronic complications, including strictures, and they will need long-term medical management. Bronchoscopy can be used as a therapeutic modality because it can be used to clear sloughed mucosa and carbonaceous or chemical irritants or facilitate the intubation of airways that are obstructed by reactive edema [6]. Bronchoscopy should also be performed for toilet or evaluation whenever an intubated patient with tracheal burn develops respiratory deterioration. The bronchoscopic findings described in this section are uniform regardless of the etiology of the original insult. Thermal and chemical injury to the trachea and
S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
345
bronchi can create hyperemia, edema, ulcerations, or necrosis of the mucosa. Both types of injury also destroy the mucociliary clearance ability of the columnar epithelium of the tracheal mucosa [3]. The difference between these insults lies in their distribution and pattern of injury. Inhaled toxic chemicals are evenly distributed throughout the respiratory tree, and thus they can result in extensive injury of the tracheobronchial tree. Chemical tracheal injury is usually the result of reactions between the mucosa and the chemicals inhaled, be it hydrogen cyanide or sulfur fumes, and it is a continuous process until the reaction ceases or the chemical is cleared. Chemical injury can produce all of the bronchoscopic findings mentioned previously; however, it is thought not to produce the same degree of mucosal ulceration as thermal injury [3,10,11]. The pattern of thermal injury differs from the pattern caused by chemical injury because of the modifying effect of the nasopharynx. The nasopharynx modulates the heat energy of the inhaled gases and influences the extent of heat injury below the vocal cords. The nasopharynx and upper airways are an efficient air conditioning system and serve to cool the inhaled gases to a large degree before tracheal exposure. This, combined with the reflex ability of the glottis to close when exposed to heat, leads to the relatively low frequency of tracheal thermal injury in patients with cutaneous burns (about 2 –5% of all cutaneous burns) [3,11]. Nevertheless, when the nasopharynx is overwhelmed by intensely heated vapors, the resulting thermal injury in the upper airways can lead to larygneal spasm and the need for immediate intubation and ventilatory support. Hence, patients with suspected inhalation injury should undergo immediate bronchoscopy in a highly monitored setting to initiate early diagnosis of tracheal injury and treatment of this potentially fatal condition.
Treatment Acute Initial treatment of tracheal burn injury depends on the degree of injury discovered on evaluation, the seriousness of other competing injuries, and the overall condition of the patient. Fluid resuscitation is initiated in the burned patient with the aid of the Parkland formula and guided by urine output. In patients with a large degree of parenchymal injury, fluid resuscitation should be carefully titrated so as not to induce fluid overload in a patient population that is susceptible to noncardiogenic pulmonary edema from increased capillary permeability. In such situations, pulmonary arterial wedge determinations through the aid of a Swan-Ganz catheter can be useful for guiding therapy [3,7,12,13]. Humidified oxygen should be administered to all patients in whom tracheal burn injury is suspected. Bronchodilators in the form of nebulizers or aerosols are indicated to treat bronchospasm accompanying respiratory injury. Humidification is helpful, especially in patients who have lost the ability to humidify their airway through their oropharynx as a result of burn injury. Any signs of respiratory
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S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
distress, including frank airway obstruction, increasing stridor or hoarseness, tachypnea, or severe abnormalities on bronchoscopy warrant intubation. Although some authors prefer nasotracheal intubation for any patient with signs of inhalation injury [3,14], there are no conclusive data to support this approach— nor would this approach be of any use in patients with signs of tracheal occlusion secondary to edema or mucosal sloughing. Tracheostomy can and should be performed, if necessary, in cases of severe upper laryngeal damage or in cases in which oral intubation is impossible. In general, tracheostomy should be avoided secondary to its associated possible complications such as tracheal stenosis, tracheoinnominate or tracheobronchial fistula. Tracheostomy might complicate further tracheal surgery in the future if it is needed for stenosis [2,3,10]. If tracheostomy is contemplated, it should be performed in a location on the trachea that is least likely to complicate further surgery. The best location for a tracheostomy might be in the most damaged area, which will likely require future resection. The use of steroids in the treatment of tracheal burn injury remains a controversial issue. Proponents argue that steroids might be useful for laryngospasm and edema postinjury; hence they might prevent the need for intubation. Furthermore, it is postulated that steroids delay or prevent subsequent hypertrophic scar formation, and therefore prevent future tracheal stenosis, offering a survival benefit [3,15]. Others argue that steroids delay wound healing and hypertrophic scar production predisposing patients to infection. This issue has not yet been resolved. Whether they are intubated or not, patients who are being treated for tracheal burn injury should receive excellent pulmonary toilet with chest physiotherapy, nebulizers, humidification, and bronchoscopy (if needed) to maintain good airway clearance and avoid infection [3,16]. Chronic Chronic injuries resulting from tracheal burns largely manifest as tracheal stenosis. The incidence of this complication is relatively low, but varies from series to series (0.37% of burn patients in one series). Most patients who develop chronic tracheal stenosis have been intubated at some point during their treatment, and they likely had deep tracheal burns [10,11]. It is difficult to determine which components lead to the development of tracheal stenosis because there might be a complex interplay between the damaged epithelium and presence of the endotracheal tube [8,10,11]. In addition, patients with the worst burns are ventilated, and the degree of burn might contribute to the rate of chronic complications. Mucosal ischemia and a hypertrophic repair response seen in the altered hormonal milieu of the burn patient are also thought to play a part. Many cytokines are upregulated in this environment, including endothelin, HB-EGF, and others whose interplay likely contributes to the pathogenesis of subsequent burn-associated complications [17,18]. In terms of evaluating patients with suspected chronic injuries caused by tracheal burns, chest radiographs and chest CTs can provide some measure of the
S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
347
degree and extent of stenosis; however, bronchoscopy and laryngoscopy are required to fully evaluate patients [10]. Bronchoscopy in chronic injury typically shows hyperemic mucosa with friable bleeding granulation tissue in addition to the areas of stenosis [10,11]. Treatment options are varied and depend on the degree and extent of tracheal stenosis. Grillo and colleagues have reported on a large collective experience in the treatment of this late complication of tracheal burns. Treatment options include tracheal dilatation as a temporizing measure to allow for bronchoscopy or Montgomery T-tube (Boston Medical Products, Inc., Waltham, MA) placement. Occasionally, in less severe cases, dilation alone can be curative. For more severe degrees of stenosis, tracheal resection and reconstruction techniques with temporary or permanent T-tube stenting (as described by Gaissert et al) might be required [8,10]. It is recommended that surgery be delayed until inflammation in the trachea is resolved. In some circumstances, resectional surgery is not possible because of the length of the damaged portion of the airway or to recurrent stenosis after resection. These patients are best treated with long-term T-tubes. Such stenting can be applied from the level of the mainstem bronchi to the subglottic area. Subsequent tracheal resection can be offered to amenable candidates, whereas in others T-tube placement alone for a period of 2 to 3 years can be sufficient to treat the stenosis. In other patients, the T-tube becomes permanent, lifelong therapy, and it is well tolerated. T-tubes require some patient care with respect to suction, humidification, and (occasionally) bronchoscopic replacement and evaluation of the airways. Tracheostomy might be needed in some of these patients for upper airway obstruction; when needed they are placed in the region of greatest tracheal damage, which will be resected at some future date if possible [8,10]. Another therapeutic modality reported in the literature includes stenting of lower tracheal stenosis with silicone rubber stents after resection of a higher subglottic stenosis. Success rates are variable in terms of complete decannulation, and reported rates vary and are limited to small series. A completely normal airway is not achieved, but a functional patent airway is possible for many afflicted patients [19].
Summary Tracheal burns caused by thermal or chemical injuries are uncommon, but they can be difficult to manage. A high index of suspicion is required for early detection of these injuries. Acutely, they are often life threatening unless they are diagnosed quickly and managed properly. Tracheal burn injuries can lead to longterm stenoses, which require specialized surgical techniques and chronic therapy—often with Montgomery T-tubes—for their proper management.
References [1] Allson JS. The primary care manangement of burns. Nurse Pract 1995;20:77 – 9. [2] Moylan JA. Inhalation injury. J Trauma 1981;21:720 – 1.
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S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
[3] Mosley S. Inhalation injury: a review of the literature. Heart Lung 1988;17:3 – 9. [4] Awan MS, Ahmed I. Endotracheal tube fire during tracheostomy: a case report. Ear Nose Throat J 2002;81:90 – 2. [5] Ilgner J, Fakter F, Westhofen M. Long-term follow-up after laser-induced endotracheal fire. J Laryngol Otol 2002;116:213 – 5. [6] Evans GA. Awake fiberoptic intubation for airway burns. J R Army Med Corps 1998;144:105 – 6. [7] Harvey JS, Watkins GS, Sherman RT. Emergent burn care. South Med J 1984;77:204 – 14. [8] Grillo HC, Mathisen DJ. Surgical management of tracheal strictures. Surg Clin N Am 1988;68: 511 – 24. [9] Horvitz J. Diagnostic tools for use in smoke inhalation. J Trauma 1981;21:958 – 61. [10] Gaissert HA, Lofren RH, Grillo HC. Upper airway compromise after inhalation injury. Complex strictures of the larynx and trachea and their manangement. Ann Surg 1993;218:672 – 8. [11] Colice GL, Munster AM, Haponik EF. Tracheal stenosis complicating cutaneous burns: an underestimated problem. Am Rev Respir Dis 1986;34:1315 – 8. [12] Nyhus LM. Current treatment of the extensively burned patient. Surg Ann 1983;15:331 – 64. [13] Whitelock-Jones L, Bass DH, Millar AJ, et al. Inhalation burns in children. Pediatr Surg Int 1999;15:50 – 5. [14] Venus B, Matsuda T, Copiozo JB, et al. Prophylatic intubation and continuous airway pressure in the management of inhalation injury in burn victims. Crit Care Med 1981;9:519 – 23. [15] Head JM. Inhalation injury in burns. Am J Surg 1980;139:508 – 12. [16] Bartlett RH. Types of respiratory injury. J Trauma 1979;19:18 – 9. [17] Cribbs RK, Harding PA, Luquette MH, et al. Endogenous production of heparin-binding EGF-like growth factor during murine partial-thickness burn wound healing. J Burn Care Rehabil 2002;23:116 – 25. [18] McMillen MA. Endothelin plasma levels in burn patients. Arch Surg 2001;136:1084. [19] Timon CI, McShane D, McGovern E, et al. Treatment of combined subglottic and critically low tracheal stenoses secondary to burn inhalation injury. J Laryngol Otol 1989;103:1083 – 6.
The burned trachea Subroto Paul, MDa, Raphael Bueno, MDa,b,* a
Division of Thoracic Surgery, Department of Surgery, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA b Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA
Inhalation injury remains a challenging medical problem in terms of diagnosis and treatment. Burn injuries continue to be a major health problem in the United States, with an estimated 2.2 million burns reported each year of which 60,000 require hospitalization [1]. Some inhalation injury accompanies cutaneous burn injury in 50% to 75% of patients [2,3]. The degree of inhalation injury is reported to be the single most important factor that directly correlates with the incidence of death from burns in the first 24 to 48 hours after injury [2,3]. Despite major advances in the understanding and treatment of cutaneous burn injuries over the past 25 years, similar significant advances have not been made in the treatment of inhalation injury. Inhalation injury has been classified into three categories, with injuries occurring in the following anatomic sequence: (1) upper airways to the level of the true vocal cords, (2) trachea and major bronchi, and (3) parenchymal lung tissue [3]. In this article the authors review tracheal burns with respect to diagnosis, pathophysiology, treatment, and complications in the acute and chronic intervals.
Diagnosis and pathophysiology The possibility of burn injury to the trachea must be entertained by the treating medical team in the evaluation of all burn patients. Facial and chest cutaneous burns, singed nasal hairs, and carbonaceous sputum are suggestive of concomitant inhalation injury. Thermal injury occurring secondary to fire is the most common mechanism of burn injury; however, other mechanisms of inhalation injury are possible, including chemical burn injuries from exposure to toxic gases during industrial acid/base spills, suicide attempts by toxic ingestion and resultant
* Corresponding author. Raphael Bueno, MD, Division of Thoracic Surgery, Department of Surgery, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115. 1052-3359/03/$ – see front matter D 2003, Elsevier Inc. All rights reserved. doi:10.1016/S1052-3359(03)00003-6
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S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
aspiration and exposure to acid, and sulfur fumes produced from burning polyvinylchloride. Tracheal burn injury can also occur as a consequence of direct injury during tracheostomy, from electrocautery-induced combustion of volatile anesthetic gases during tracheolaryngeal surgery, or (as more recently reported in the literature) from injury sustained from fires induced by therapeutic lasers, including the commonly used carbon dioxide and KTP/YAG laser devices [4,5]. Without regard to the mechanism of injury, symptomatic patients usually complain of a range of symptoms from shortness of breath, hoarseness, stridor, and wheezing to frank respiratory collapse caused by extreme hypoxia or upper airway obstruction requiring intubation and ventilatory support [3,6 –8]. The key to diagnosis of tracheal burns lies in careful screening of all potential patients and early identification of patients who will likely progress to complete respiratory collapse despite an initial mild presentation. Many tests have been proposed for optimal evaluation and screening of patients at risk. Arterial blood tests to measure the PaO2 and carboxyhemoglobin levels can give an indication of the degree of smoke inhalation, but these tests provide no information of the degree of tracheal injury per se [3,9]. In the absence of severe pulmonary and tracheal injury, chest radiographs provide little information and often appear normal [9]. A CT of the chest might provide slightly more information about the extent of injury because tracheal edema is better visualized on CT; however, CT is not sufficiently accurate in the acute setting. Other studies such as pulmonary function tests and radioactive lung scans are not commonly used, nor are they informative in the diagnosis of tracheal injury [2,3,6]. The best diagnostic study in patients suspected to have tracheal burns remains fiberoptic bronchoscopy, which allows for direct visualization and assessment of the degree of injury. Fiberoptic bronchoscopy is the most sensitive and specific way to diagnose tracheal injury [3,6,8,10]. Rigid bronchoscopy should be available if mandated by the clinical scenario. Bronchoscopic findings of early tracheal injury include hyperemic mucosa, edema, carbon deposits, charring of tissue, and easy bruising. In severe cases, one can visualize either early or progressive mucosal sloughing or frank necrosis of airway tissue. Either of these findings makes imminent airway obstruction more likely and supports the decision for early intubation. The severity of the bronchoscopic findings often correlates with the overall degree of severity of the symptoms and findings in the patient. Patients with superficial injury that is limited to the mucosa will likely heal with supportive therapy. Patients with deeper partial- or full-thickness injury will likely develop chronic complications, including strictures, and they will need long-term medical management. Bronchoscopy can be used as a therapeutic modality because it can be used to clear sloughed mucosa and carbonaceous or chemical irritants or facilitate the intubation of airways that are obstructed by reactive edema [6]. Bronchoscopy should also be performed for toilet or evaluation whenever an intubated patient with tracheal burn develops respiratory deterioration. The bronchoscopic findings described in this section are uniform regardless of the etiology of the original insult. Thermal and chemical injury to the trachea and
S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
345
bronchi can create hyperemia, edema, ulcerations, or necrosis of the mucosa. Both types of injury also destroy the mucociliary clearance ability of the columnar epithelium of the tracheal mucosa [3]. The difference between these insults lies in their distribution and pattern of injury. Inhaled toxic chemicals are evenly distributed throughout the respiratory tree, and thus they can result in extensive injury of the tracheobronchial tree. Chemical tracheal injury is usually the result of reactions between the mucosa and the chemicals inhaled, be it hydrogen cyanide or sulfur fumes, and it is a continuous process until the reaction ceases or the chemical is cleared. Chemical injury can produce all of the bronchoscopic findings mentioned previously; however, it is thought not to produce the same degree of mucosal ulceration as thermal injury [3,10,11]. The pattern of thermal injury differs from the pattern caused by chemical injury because of the modifying effect of the nasopharynx. The nasopharynx modulates the heat energy of the inhaled gases and influences the extent of heat injury below the vocal cords. The nasopharynx and upper airways are an efficient air conditioning system and serve to cool the inhaled gases to a large degree before tracheal exposure. This, combined with the reflex ability of the glottis to close when exposed to heat, leads to the relatively low frequency of tracheal thermal injury in patients with cutaneous burns (about 2 –5% of all cutaneous burns) [3,11]. Nevertheless, when the nasopharynx is overwhelmed by intensely heated vapors, the resulting thermal injury in the upper airways can lead to larygneal spasm and the need for immediate intubation and ventilatory support. Hence, patients with suspected inhalation injury should undergo immediate bronchoscopy in a highly monitored setting to initiate early diagnosis of tracheal injury and treatment of this potentially fatal condition.
Treatment Acute Initial treatment of tracheal burn injury depends on the degree of injury discovered on evaluation, the seriousness of other competing injuries, and the overall condition of the patient. Fluid resuscitation is initiated in the burned patient with the aid of the Parkland formula and guided by urine output. In patients with a large degree of parenchymal injury, fluid resuscitation should be carefully titrated so as not to induce fluid overload in a patient population that is susceptible to noncardiogenic pulmonary edema from increased capillary permeability. In such situations, pulmonary arterial wedge determinations through the aid of a Swan-Ganz catheter can be useful for guiding therapy [3,7,12,13]. Humidified oxygen should be administered to all patients in whom tracheal burn injury is suspected. Bronchodilators in the form of nebulizers or aerosols are indicated to treat bronchospasm accompanying respiratory injury. Humidification is helpful, especially in patients who have lost the ability to humidify their airway through their oropharynx as a result of burn injury. Any signs of respiratory
346
S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
distress, including frank airway obstruction, increasing stridor or hoarseness, tachypnea, or severe abnormalities on bronchoscopy warrant intubation. Although some authors prefer nasotracheal intubation for any patient with signs of inhalation injury [3,14], there are no conclusive data to support this approach— nor would this approach be of any use in patients with signs of tracheal occlusion secondary to edema or mucosal sloughing. Tracheostomy can and should be performed, if necessary, in cases of severe upper laryngeal damage or in cases in which oral intubation is impossible. In general, tracheostomy should be avoided secondary to its associated possible complications such as tracheal stenosis, tracheoinnominate or tracheobronchial fistula. Tracheostomy might complicate further tracheal surgery in the future if it is needed for stenosis [2,3,10]. If tracheostomy is contemplated, it should be performed in a location on the trachea that is least likely to complicate further surgery. The best location for a tracheostomy might be in the most damaged area, which will likely require future resection. The use of steroids in the treatment of tracheal burn injury remains a controversial issue. Proponents argue that steroids might be useful for laryngospasm and edema postinjury; hence they might prevent the need for intubation. Furthermore, it is postulated that steroids delay or prevent subsequent hypertrophic scar formation, and therefore prevent future tracheal stenosis, offering a survival benefit [3,15]. Others argue that steroids delay wound healing and hypertrophic scar production predisposing patients to infection. This issue has not yet been resolved. Whether they are intubated or not, patients who are being treated for tracheal burn injury should receive excellent pulmonary toilet with chest physiotherapy, nebulizers, humidification, and bronchoscopy (if needed) to maintain good airway clearance and avoid infection [3,16]. Chronic Chronic injuries resulting from tracheal burns largely manifest as tracheal stenosis. The incidence of this complication is relatively low, but varies from series to series (0.37% of burn patients in one series). Most patients who develop chronic tracheal stenosis have been intubated at some point during their treatment, and they likely had deep tracheal burns [10,11]. It is difficult to determine which components lead to the development of tracheal stenosis because there might be a complex interplay between the damaged epithelium and presence of the endotracheal tube [8,10,11]. In addition, patients with the worst burns are ventilated, and the degree of burn might contribute to the rate of chronic complications. Mucosal ischemia and a hypertrophic repair response seen in the altered hormonal milieu of the burn patient are also thought to play a part. Many cytokines are upregulated in this environment, including endothelin, HB-EGF, and others whose interplay likely contributes to the pathogenesis of subsequent burn-associated complications [17,18]. In terms of evaluating patients with suspected chronic injuries caused by tracheal burns, chest radiographs and chest CTs can provide some measure of the
S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
347
degree and extent of stenosis; however, bronchoscopy and laryngoscopy are required to fully evaluate patients [10]. Bronchoscopy in chronic injury typically shows hyperemic mucosa with friable bleeding granulation tissue in addition to the areas of stenosis [10,11]. Treatment options are varied and depend on the degree and extent of tracheal stenosis. Grillo and colleagues have reported on a large collective experience in the treatment of this late complication of tracheal burns. Treatment options include tracheal dilatation as a temporizing measure to allow for bronchoscopy or Montgomery T-tube (Boston Medical Products, Inc., Waltham, MA) placement. Occasionally, in less severe cases, dilation alone can be curative. For more severe degrees of stenosis, tracheal resection and reconstruction techniques with temporary or permanent T-tube stenting (as described by Gaissert et al) might be required [8,10]. It is recommended that surgery be delayed until inflammation in the trachea is resolved. In some circumstances, resectional surgery is not possible because of the length of the damaged portion of the airway or to recurrent stenosis after resection. These patients are best treated with long-term T-tubes. Such stenting can be applied from the level of the mainstem bronchi to the subglottic area. Subsequent tracheal resection can be offered to amenable candidates, whereas in others T-tube placement alone for a period of 2 to 3 years can be sufficient to treat the stenosis. In other patients, the T-tube becomes permanent, lifelong therapy, and it is well tolerated. T-tubes require some patient care with respect to suction, humidification, and (occasionally) bronchoscopic replacement and evaluation of the airways. Tracheostomy might be needed in some of these patients for upper airway obstruction; when needed they are placed in the region of greatest tracheal damage, which will be resected at some future date if possible [8,10]. Another therapeutic modality reported in the literature includes stenting of lower tracheal stenosis with silicone rubber stents after resection of a higher subglottic stenosis. Success rates are variable in terms of complete decannulation, and reported rates vary and are limited to small series. A completely normal airway is not achieved, but a functional patent airway is possible for many afflicted patients [19].
Summary Tracheal burns caused by thermal or chemical injuries are uncommon, but they can be difficult to manage. A high index of suspicion is required for early detection of these injuries. Acutely, they are often life threatening unless they are diagnosed quickly and managed properly. Tracheal burn injuries can lead to longterm stenoses, which require specialized surgical techniques and chronic therapy—often with Montgomery T-tubes—for their proper management.
References [1] Allson JS. The primary care manangement of burns. Nurse Pract 1995;20:77 – 9. [2] Moylan JA. Inhalation injury. J Trauma 1981;21:720 – 1.
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S. Paul, R. Bueno / Chest Surg Clin N Am 13 (2003) 343–348
[3] Mosley S. Inhalation injury: a review of the literature. Heart Lung 1988;17:3 – 9. [4] Awan MS, Ahmed I. Endotracheal tube fire during tracheostomy: a case report. Ear Nose Throat J 2002;81:90 – 2. [5] Ilgner J, Fakter F, Westhofen M. Long-term follow-up after laser-induced endotracheal fire. J Laryngol Otol 2002;116:213 – 5. [6] Evans GA. Awake fiberoptic intubation for airway burns. J R Army Med Corps 1998;144:105 – 6. [7] Harvey JS, Watkins GS, Sherman RT. Emergent burn care. South Med J 1984;77:204 – 14. [8] Grillo HC, Mathisen DJ. Surgical management of tracheal strictures. Surg Clin N Am 1988;68: 511 – 24. [9] Horvitz J. Diagnostic tools for use in smoke inhalation. J Trauma 1981;21:958 – 61. [10] Gaissert HA, Lofren RH, Grillo HC. Upper airway compromise after inhalation injury. Complex strictures of the larynx and trachea and their manangement. Ann Surg 1993;218:672 – 8. [11] Colice GL, Munster AM, Haponik EF. Tracheal stenosis complicating cutaneous burns: an underestimated problem. Am Rev Respir Dis 1986;34:1315 – 8. [12] Nyhus LM. Current treatment of the extensively burned patient. Surg Ann 1983;15:331 – 64. [13] Whitelock-Jones L, Bass DH, Millar AJ, et al. Inhalation burns in children. Pediatr Surg Int 1999;15:50 – 5. [14] Venus B, Matsuda T, Copiozo JB, et al. Prophylatic intubation and continuous airway pressure in the management of inhalation injury in burn victims. Crit Care Med 1981;9:519 – 23. [15] Head JM. Inhalation injury in burns. Am J Surg 1980;139:508 – 12. [16] Bartlett RH. Types of respiratory injury. J Trauma 1979;19:18 – 9. [17] Cribbs RK, Harding PA, Luquette MH, et al. Endogenous production of heparin-binding EGF-like growth factor during murine partial-thickness burn wound healing. J Burn Care Rehabil 2002;23:116 – 25. [18] McMillen MA. Endothelin plasma levels in burn patients. Arch Surg 2001;136:1084. [19] Timon CI, McShane D, McGovern E, et al. Treatment of combined subglottic and critically low tracheal stenoses secondary to burn inhalation injury. J Laryngol Otol 1989;103:1083 – 6.