- Email: [email protected]
Post-intubation pulmonary embolism and tracheal stenosis: A case report and review of the literature
Respiratory Medicine (2008) 102, 1208e1212 available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/rmed
CASE REPORT
Post-intubation pulmonary embolism and tracheal stenosis: A case report and review of the literature Argyris Tzouvelekis a,*, George Kouliatsis a, Anastasia Oikonomou b, Georgia Trakada a, Marios Froudarakis a, Paschalis Steiropoulos a, Demosthenes Bouros a a b
Department of Pneumonology, Medical School, Democritus University of Thrace, Greece Department of Radiology, Medical School, Democritus University of Thrace, Greece
Received 16 January 2008; accepted 8 February 2008 Available online 24 June 2008
KEYWORDS Post-intubation tracheal stenosis; Post-intubation pulmonary embolism; Anticoagulant therapy; Rigid bronchoscopy
Summary Tracheal stenosis may be attributed to several conditions including trauma, infection, tumour or congenital and collagen vascular diseases. Despite improvement in the design of tracheal tubes, however, tracheal stenosis following intubation still remains an important cause for tracheal obstruction, which may be life threatening and often misdiagnosed. On the other hand, studies have exerted the impact of mechanical ventilation as a risk factor for pulmonary embolism. Here, we describe for the first time, an otherwise healthy patient who was mechanically ventilated due to a labor accident and developed acute pulmonary embolism that was further complicated with post-intubation tracheal stenosis. The patient was treated with anticoagulant therapy and oral corticosteroids and was further referred to a specialist centre for consideration for non-surgical endoscopic treatment. ª 2008 Elsevier Ltd. All rights reserved.
Introduction The association between injury and venous thromboembolic events (VTE) that include deep venous thombosis and pulmonary embolism is well established and recognized.1,2 * Corresponding author. Clinical Research Fellow, Medical School, Democritus University of Thrace, Department of Pneumonology, University Hospital of Alexandroupolis, Alexandroupolis 68100, Greece. Tel./fax: þ30 25510 76106. E-mail address: [email protected] (A. Tzouvelekis).
The reported incidence of VTE after trauma varies from 7% to 58%, with that of symptomatic pulmonary embolism ranging from 1.3 to 2.0% and an associated mortality approaching in some centers 50% of cases, depending upon the demographics of patients, the nature of injuries and the type of VTE prophylaxis.1e3 In a large retrospective analysis including 1602 episodes of VTE, duration of ventilation greater than 3 days was recognized as an independent risk factor for VTE.4 On the other hand, tracheal stenosis is a multi-causal condition that can be attributed to several factors, such as
0954-6111/$ - see front matter ª 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.rmed.2008.02.018
Post-intubation pulmonary embolism and tracheal stenosis
1209
traumatic conditions, inflammatory diseases, benign and malignant lesions, collagen vascular and congenital diseases. Of these causes the leading cause of tracheal stenosis still continues to be endotracheal intubation, despite technological improvements such as the introduction of high-volume low pressure cuffs and better patient care. We report here the first case in the literature of a post-intubation pulmonary embolism followed by a postintubation tracheal stenosis in an otherwise healthy, multitraumatic young patient who sustained a labor accident and was mechanically ventilated through an oral tracheal tube. The patient was treated with anticoagulant therapy and referred to a specialist centre for consideration of nonsurgical endoscopic treatment with rigid bronchoscopy and stent placement or laser incision of the membranous-like stenosis.
Case report A 23-year-old male was administered in the emergency department of our hospital due to acute dyspnea and mild chest pain. Three weeks earlier he had sustained a labor accident with a truck and had been mechanically ventilated through an oral tracheal tube for 5 days. Subsequently he had been transferred as a multi-traumatic patient with bilateral pneumothorax, hemithorax and rib fractures (data not shown) to a surgery department of our hospital from where he was discharged two weeks later with prophylactic anticoagulant and antibiotic treatment, in generally good condition. He was a lifetime non-smoker, his previous medical history was unremarkable and he was not taking any medication. On admission he was in extremis and had tachypnea (respiratory rate 32/min), a respiratory sound reduction in the upper left and right hemithorax, tachycardia (heart rate 130 bpm) and hypoxaemia (partial pressure of oxygen 65 mmHg) on arterial blood gas analysis. The rest of physical examinations and routine laboratory tests, including white blood cell count and differential, red blood cell count, erythrocyte sedimentation rate, liver and renal function, serum C-reactive protein were normal, while ECG revealed a sinoatrial tachycardia. Chest radiograph was taken and revealed a small unilateral left pleural effusion blunting the costophrenic angle (Fig. 1). D-dimers blood test was elevated (1280 ng/ml). Following diagnostic algorithm a helical computed tomography (CT) scan of the chest was then performed which demonstrated a central filling defect in the descending branch of the right pulmonary artery indicative of acute pulmonary embolism (Fig. 2). Patient was started on low-molecular weight heparin and acenocoumarol resulting in clinical, laboratory and radiological improvement 13 days after treatment, indicated by symptoms withdrawal, reduction of blood d-dimers concentration (280 ng/ml) and helical CT scan of the chest. However, on hospital day 14, patient started complaining on exertional dyspnoea and wheeze. On physical examination, tachypnea (respiratory rate 30/min) and use of accessory respiratory muscles were noticed, while inspiratory stridor was documented on auscultation. Systemic corticosteroids and inhaled bronchodilators were administered; however, the patient exhibited poor
Figure 1 Chest radiograph: posteroanterior chest radiograph showing a small unilateral left pleural effusion blunting the costophrenic angle; evidence that is attributed to the traumatic accident of the patient.
responsiveness. Therefore, we performed a new CT scan of the chest which showed significant narrowing of the trachea at the level of the thyroid gland (Fig. 3a and b). Pulmonary functional test was also supportive of a stable stenosis illustrating significant reduction in peak expiratory flow affecting both inspiratory and expiratory flowevolume curves (Fig. 4). Finally our patient underwent flexible bronchoscopy which revealed a membranous web-like stenosis of the tracheal mucosal, of 1.5 mm diameter that did not exceed 1 cm in length (Fig. 5). The patient continued his prophylactic anticoagulant therapy (acenocoumarol) and was released with systematic (methylprednisolone) and inhaled corticosteroids (beclomethasone). Three weeks later he presented with a slight clinical and functional improvement, however, he was still
Figure 2 Helical computed tomography (CT) of the chest (mediastinal window): contrast enhanced helical CT of the chest (mediastinal windowing) shows a central filling defect in the descending branch of the right pulmonary artery (white arrow) representing acute pulmonary embolism.
1210
A. Tzouvelekis et al.
Figure 3 Helical computed tomography (CT) of the chest (pulmonary window): helical CT of the chest (pulmonary windowing): sequential CT scans at the level of the lower neck e thoracic inlet, shows significant narrowing of the trachea at the level of the thyroid gland (a), compared to the scan three weeks earlier (b).
complaining on exertional dyspnoea and his spirometry was indicative on stable tracheal stenosis (data not shown). Therefore, after consultation with the patient, we referred him to a specialist centre for consideration of non-surgical endoscopic treatment with rigid bronchoscopy and stent placement or laser incision of the membranous-like stenosis.
Discussion To the best of our knowledge this is the first case in the literature of a post-traumatic pulmonary embolism followed by a post-intubation tracheal stenosis in an otherwise healthy, multi-traumatic young patient who sustained a labor accident and was mechanically ventilated through an oral tracheal tube. The association between injury and venous thromboembolic events (VTE) that include deep venous thrombosis and pulmonary embolism is well established and recognized.1,2 The reported incidence of VTE after trauma varies from 7%
to 58%, with that of symptomatic pulmonary embolism ranging from 1.3 to 2.0% and an associated mortality approaching in some centers 50% of cases, depending upon the demographics of patients, the nature of injuries and the type of VTE prophylaxis.1e3 In a large retrospective analysis of the American College of Surgeons of 1602 episodes of VTE, authors identified 9 risk factors that were independently associated with VTE. Intriguingly, among them, with an oddsratio of 10.62, was duration of ventilation greater than 3 days. In the present case, our patient was mechanically ventilated for 5 days; therefore the episode of pulmonary embolism that he experienced can be attributed to the ventilator days.4 Local inflammation and ischemia caused by endotracheal tube resulting in upregulation of tissue factor and inhibition of physiological fibrinolytic system, including proteins C and S, have been proposed as major pathogenetic mediators.5 In the present case, although contribution of lung parenchyma injuries and rib fractures cannot be excluded, in most series of patients, they are more related to complications such as hemothorax, pneumothorax and flail chest rather than pulmonary embolism.6
Figure 4 Pulmonary function test: the figure shows a characteristic reduction in peak expiratory flow indicating a stable thoracic tracheal stenosis affecting both inspiratory and expiratory flowevolume curves (A) compared to the normal predicted one (B).
Post-intubation pulmonary embolism and tracheal stenosis
Figure 5 Flexible bronchoscopy: the figure shows a membranous web-like stenosis of the tracheal mucosal, of 1.5 mm diameter that does not exceed 1 cm in length.
There are several factors that may cause tracheal stenosis, including traumatic conditions (i.e. endotracheal intubation, endotracheal burns, traumatic rupture of the trachea etc), inflammatory diseases (tuberculosis, sarcoidosis, amyloidosis), benign and malignant lesions, collagen vascular diseases (i.e Wegener’s granulomatosis) and congenital conditions. Of these causes the leading cause of tracheal stenosis still continues to be endotracheal intubation, despite technological improvements such as the introduction of high-volume low pressure cuffs and better patient care. Although, in our case one could easily speculate that tracheal stenosis was caused by traumatic rupture of the trachea, however, the nature, the length and the progressive development of stenosis that led to symptoms almost a month after intubation, rule out this possibility. Autopsy studies in patients who died while under mechanical ventilation elucidated the primary cause of this complication and reported that a cuff pressure greater than 30 mmHg exceeds a critical point in the mucosal capillary perfusion pressure, causing mucosal ischemia leading to ulceration, chondritis of the tracheal cartilages and ultimately, development of irreversible fibrotic tissue.7,8 The endotracheal tube cuff causes circumferential erosion of the mucosa, which heals with a concentric (web-like) stenosis, like in our case. Based on the length of tracheal stenosis, the depth of the tracheal wall involvement and the presence or not of tracheomalacia, post-intubation tracheal stenosis falls into three categories, including short, ‘‘complex’’ and ‘‘pseudoglottic’’ stenosis.9 The few available prospective studies document an incidence of post-intubation and/or post-tracheostomy tracheal stenosis from 10 to 19%. However, symptomatic stenoses, affecting pulmonary function do not exceed 1% of the cases.10 Apart from cuff pressure and direct tracheal trauma during intubation, duration of intubation has also been proposed as a critical pathogenetic endpoint. However, data referring to this issue is still controversial, since there have been several reports of tracheal stenosis after only few days of intubation, evidence that was further extended by experimental data. In addition, the incidence
1211 of tracheal stenosis does not seem to be related to repeated intubations, the route of intubation or the emergency character of the procedure.10 Typically, post-intubation tracheal stenosis is diagnosed based on a combination of presenting airway obstruction signs and symptoms with a recent history of tracheal intubation. Airway obstruction usually presents as shortness of breath and either or both inspiratory stridor and expiratory wheeze. Symptoms do not usually occur until tracheal stenosis exceeds a critical point of greater than 20e30% of its original size, and it may take as long as 3 months time before most stenoses can be documented by a physician.7,8 Although, simple spirometry typically shows a reduction in peak expiratory flow and depending on the level of stenosis a characteristic flowevolume loop, however, is difficult to perform due to the severity of respiratory failure or cannot be interpreted reliably due to underlying lung disease, mostly chronic obstructive pulmonary disease (COPD). Chest radiograph is usually normal; as a result of the latter and the aforementioned clinical and functional findings, post-intubation tracheal stenosis is often misdiagnosed as asthma8 with a great proportion of these patients to be receiving large doses of systemic and/or inhaled corticosteroids for months.7,8 The diagnosis may be confirmed with plain radiography, computed and tracheal linear tomography or endoscopy. Despite the recent introduction of ‘‘virtual’’ bronchoscopy using reconstructed digital signals to depict the level of stenosis, flexible bronchoscopy represents the diagnostic technique of choice that both provides a definitive diagnosis and determines the type, location and severity of stenosis. In addition, it is easy to perform and directs the clinician to the selection of the appropriate type and duration of treatment. Regarding the latter, although there have been few reports of an effective therapeutic approach of tracheal stenosis with systematic and/or inhaled steroid regimens,11,12 the hallmark of treatment for symptomatic lesions is endoscopic and surgical.10 Rigid bronchoscopy and tracheal dilation possibly by laser or placement of special stents may be the only treatment required for less serious lesions.13 In recurrence or in case of more extensive stenosis, a definitive tracheal reconstructive surgery should be considered, with a mortality ranging from 1.8 to 5%.14 In summary, we conclude that endotracheal intubation may cause local inflammation and ischemia resulting in activation of platelet microaggregates,15 inhibition of fibrinolysis and ultimately development of fibrotic scar tissue leading to complications such as pulmonary embolism and tracheal stenosis. Post-intubation tracheal stenosis is an iatrogenic complication that should be considered in the differential diagnosis of any patient who has a recent history of intubation and who presents with exertional dyspnoea and wheeze, unresponsive to bronchodilators. Should it occur, timely diagnosis and effective management are crucial. In life-threatening situations, such patients require immediate transfer to specialist centres for definitive tracheal reconstructive surgery.
Conflict of interest statement The authors have no conflict of interest to declare.
1212
References 1. Geerts WH. Thromboembolism in trauma: the problem and its prevention. Semin Thromb Hemost 1996;22(Suppl. 2):19e24. 2. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP. A prospective study of venous thromboembolism after major trauma. N Engl J Med 1994;331(24):1601e6. 3. Geerts WH. Prevention of venous thromboembolism in high-risk patients. Hematology (Am Soc Hematol Educ Program); 2006: 462e6. 4. Knudson MM, Ikossi DG, Khaw L, Morabito D, Speetzen LS. Thromboembolism after trauma: an analysis of 1602 episodes from the American College of Surgeons National Trauma Data Bank. Ann Surg 2004;240(3):490e6. 5. Knudson MM, Ikossi DG. Venous thromboembolism after trauma. Curr Opin Crit Care 2004;10(6):539e48. 6. Ullman EA, Donley LP, Brady WJ. Pulmonary trauma emergency department evaluation and management. Emerg Med Clin North Am 2003;21(2):291e313. 7. Spittle CS, Beavis SE. Post-intubation tracheal stenosis. Hosp Med 2001;62(1):54.
A. Tzouvelekis et al. 8. Spittle N, McCluskey A. Lesson of the week: tracheal stenosis after intubation. BMJ 2000;321(7267):1000e2. 9. Bisson A, Bonnette P, el Kadi NB, et al. Tracheal sleeve resection for iatrogenic stenoses (subglottic laryngeal and tracheal). J Thorac Cardiovasc Surg 1992;104(4):882e7. 10. Brichet A, Verkindre C, Dupont J, et al. Multidisciplinary approach to management of postintubation tracheal stenoses. Eur Respir J 1999;13(4):888e93. 11. Braidy J, Breton G, Clement L. Effect of corticosteroids on postintubation tracheal stenosis. Thorax 1989;44(9):753e5. 12. Croft CB, Zub K, Borowiecki B. Therapy of iatrogenic subglottic stenosis: a steroid/antibiotic regimen. Laryngoscope 1979; 89(3):482e9. 13. Vergnon JM, Costes F, Polio JC. Efficacy and tolerance of a new silicone stent for the treatment of benign tracheal stenosis: preliminary results. Chest 2000;118(2):422e6. 14. Bonnette P, Colchen A, Leroy M, Bisson A. Tracheal resectionanastomosis for iatrogenic stenosis. Experience in 340 cases. Rev Mal Respir 1998;15(5):627e32. 15. Hyers TM. Management of venous thromboembolism: past, present, and future. Arch Intern Med 2003;163(7):759e68.
journal homepage: www.elsevier.com/locate/rmed
CASE REPORT
Post-intubation pulmonary embolism and tracheal stenosis: A case report and review of the literature Argyris Tzouvelekis a,*, George Kouliatsis a, Anastasia Oikonomou b, Georgia Trakada a, Marios Froudarakis a, Paschalis Steiropoulos a, Demosthenes Bouros a a b
Department of Pneumonology, Medical School, Democritus University of Thrace, Greece Department of Radiology, Medical School, Democritus University of Thrace, Greece
Received 16 January 2008; accepted 8 February 2008 Available online 24 June 2008
KEYWORDS Post-intubation tracheal stenosis; Post-intubation pulmonary embolism; Anticoagulant therapy; Rigid bronchoscopy
Summary Tracheal stenosis may be attributed to several conditions including trauma, infection, tumour or congenital and collagen vascular diseases. Despite improvement in the design of tracheal tubes, however, tracheal stenosis following intubation still remains an important cause for tracheal obstruction, which may be life threatening and often misdiagnosed. On the other hand, studies have exerted the impact of mechanical ventilation as a risk factor for pulmonary embolism. Here, we describe for the first time, an otherwise healthy patient who was mechanically ventilated due to a labor accident and developed acute pulmonary embolism that was further complicated with post-intubation tracheal stenosis. The patient was treated with anticoagulant therapy and oral corticosteroids and was further referred to a specialist centre for consideration for non-surgical endoscopic treatment. ª 2008 Elsevier Ltd. All rights reserved.
Introduction The association between injury and venous thromboembolic events (VTE) that include deep venous thombosis and pulmonary embolism is well established and recognized.1,2 * Corresponding author. Clinical Research Fellow, Medical School, Democritus University of Thrace, Department of Pneumonology, University Hospital of Alexandroupolis, Alexandroupolis 68100, Greece. Tel./fax: þ30 25510 76106. E-mail address: [email protected] (A. Tzouvelekis).
The reported incidence of VTE after trauma varies from 7% to 58%, with that of symptomatic pulmonary embolism ranging from 1.3 to 2.0% and an associated mortality approaching in some centers 50% of cases, depending upon the demographics of patients, the nature of injuries and the type of VTE prophylaxis.1e3 In a large retrospective analysis including 1602 episodes of VTE, duration of ventilation greater than 3 days was recognized as an independent risk factor for VTE.4 On the other hand, tracheal stenosis is a multi-causal condition that can be attributed to several factors, such as
0954-6111/$ - see front matter ª 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.rmed.2008.02.018
Post-intubation pulmonary embolism and tracheal stenosis
1209
traumatic conditions, inflammatory diseases, benign and malignant lesions, collagen vascular and congenital diseases. Of these causes the leading cause of tracheal stenosis still continues to be endotracheal intubation, despite technological improvements such as the introduction of high-volume low pressure cuffs and better patient care. We report here the first case in the literature of a post-intubation pulmonary embolism followed by a postintubation tracheal stenosis in an otherwise healthy, multitraumatic young patient who sustained a labor accident and was mechanically ventilated through an oral tracheal tube. The patient was treated with anticoagulant therapy and referred to a specialist centre for consideration of nonsurgical endoscopic treatment with rigid bronchoscopy and stent placement or laser incision of the membranous-like stenosis.
Case report A 23-year-old male was administered in the emergency department of our hospital due to acute dyspnea and mild chest pain. Three weeks earlier he had sustained a labor accident with a truck and had been mechanically ventilated through an oral tracheal tube for 5 days. Subsequently he had been transferred as a multi-traumatic patient with bilateral pneumothorax, hemithorax and rib fractures (data not shown) to a surgery department of our hospital from where he was discharged two weeks later with prophylactic anticoagulant and antibiotic treatment, in generally good condition. He was a lifetime non-smoker, his previous medical history was unremarkable and he was not taking any medication. On admission he was in extremis and had tachypnea (respiratory rate 32/min), a respiratory sound reduction in the upper left and right hemithorax, tachycardia (heart rate 130 bpm) and hypoxaemia (partial pressure of oxygen 65 mmHg) on arterial blood gas analysis. The rest of physical examinations and routine laboratory tests, including white blood cell count and differential, red blood cell count, erythrocyte sedimentation rate, liver and renal function, serum C-reactive protein were normal, while ECG revealed a sinoatrial tachycardia. Chest radiograph was taken and revealed a small unilateral left pleural effusion blunting the costophrenic angle (Fig. 1). D-dimers blood test was elevated (1280 ng/ml). Following diagnostic algorithm a helical computed tomography (CT) scan of the chest was then performed which demonstrated a central filling defect in the descending branch of the right pulmonary artery indicative of acute pulmonary embolism (Fig. 2). Patient was started on low-molecular weight heparin and acenocoumarol resulting in clinical, laboratory and radiological improvement 13 days after treatment, indicated by symptoms withdrawal, reduction of blood d-dimers concentration (280 ng/ml) and helical CT scan of the chest. However, on hospital day 14, patient started complaining on exertional dyspnoea and wheeze. On physical examination, tachypnea (respiratory rate 30/min) and use of accessory respiratory muscles were noticed, while inspiratory stridor was documented on auscultation. Systemic corticosteroids and inhaled bronchodilators were administered; however, the patient exhibited poor
Figure 1 Chest radiograph: posteroanterior chest radiograph showing a small unilateral left pleural effusion blunting the costophrenic angle; evidence that is attributed to the traumatic accident of the patient.
responsiveness. Therefore, we performed a new CT scan of the chest which showed significant narrowing of the trachea at the level of the thyroid gland (Fig. 3a and b). Pulmonary functional test was also supportive of a stable stenosis illustrating significant reduction in peak expiratory flow affecting both inspiratory and expiratory flowevolume curves (Fig. 4). Finally our patient underwent flexible bronchoscopy which revealed a membranous web-like stenosis of the tracheal mucosal, of 1.5 mm diameter that did not exceed 1 cm in length (Fig. 5). The patient continued his prophylactic anticoagulant therapy (acenocoumarol) and was released with systematic (methylprednisolone) and inhaled corticosteroids (beclomethasone). Three weeks later he presented with a slight clinical and functional improvement, however, he was still
Figure 2 Helical computed tomography (CT) of the chest (mediastinal window): contrast enhanced helical CT of the chest (mediastinal windowing) shows a central filling defect in the descending branch of the right pulmonary artery (white arrow) representing acute pulmonary embolism.
1210
A. Tzouvelekis et al.
Figure 3 Helical computed tomography (CT) of the chest (pulmonary window): helical CT of the chest (pulmonary windowing): sequential CT scans at the level of the lower neck e thoracic inlet, shows significant narrowing of the trachea at the level of the thyroid gland (a), compared to the scan three weeks earlier (b).
complaining on exertional dyspnoea and his spirometry was indicative on stable tracheal stenosis (data not shown). Therefore, after consultation with the patient, we referred him to a specialist centre for consideration of non-surgical endoscopic treatment with rigid bronchoscopy and stent placement or laser incision of the membranous-like stenosis.
Discussion To the best of our knowledge this is the first case in the literature of a post-traumatic pulmonary embolism followed by a post-intubation tracheal stenosis in an otherwise healthy, multi-traumatic young patient who sustained a labor accident and was mechanically ventilated through an oral tracheal tube. The association between injury and venous thromboembolic events (VTE) that include deep venous thrombosis and pulmonary embolism is well established and recognized.1,2 The reported incidence of VTE after trauma varies from 7%
to 58%, with that of symptomatic pulmonary embolism ranging from 1.3 to 2.0% and an associated mortality approaching in some centers 50% of cases, depending upon the demographics of patients, the nature of injuries and the type of VTE prophylaxis.1e3 In a large retrospective analysis of the American College of Surgeons of 1602 episodes of VTE, authors identified 9 risk factors that were independently associated with VTE. Intriguingly, among them, with an oddsratio of 10.62, was duration of ventilation greater than 3 days. In the present case, our patient was mechanically ventilated for 5 days; therefore the episode of pulmonary embolism that he experienced can be attributed to the ventilator days.4 Local inflammation and ischemia caused by endotracheal tube resulting in upregulation of tissue factor and inhibition of physiological fibrinolytic system, including proteins C and S, have been proposed as major pathogenetic mediators.5 In the present case, although contribution of lung parenchyma injuries and rib fractures cannot be excluded, in most series of patients, they are more related to complications such as hemothorax, pneumothorax and flail chest rather than pulmonary embolism.6
Figure 4 Pulmonary function test: the figure shows a characteristic reduction in peak expiratory flow indicating a stable thoracic tracheal stenosis affecting both inspiratory and expiratory flowevolume curves (A) compared to the normal predicted one (B).
Post-intubation pulmonary embolism and tracheal stenosis
Figure 5 Flexible bronchoscopy: the figure shows a membranous web-like stenosis of the tracheal mucosal, of 1.5 mm diameter that does not exceed 1 cm in length.
There are several factors that may cause tracheal stenosis, including traumatic conditions (i.e. endotracheal intubation, endotracheal burns, traumatic rupture of the trachea etc), inflammatory diseases (tuberculosis, sarcoidosis, amyloidosis), benign and malignant lesions, collagen vascular diseases (i.e Wegener’s granulomatosis) and congenital conditions. Of these causes the leading cause of tracheal stenosis still continues to be endotracheal intubation, despite technological improvements such as the introduction of high-volume low pressure cuffs and better patient care. Although, in our case one could easily speculate that tracheal stenosis was caused by traumatic rupture of the trachea, however, the nature, the length and the progressive development of stenosis that led to symptoms almost a month after intubation, rule out this possibility. Autopsy studies in patients who died while under mechanical ventilation elucidated the primary cause of this complication and reported that a cuff pressure greater than 30 mmHg exceeds a critical point in the mucosal capillary perfusion pressure, causing mucosal ischemia leading to ulceration, chondritis of the tracheal cartilages and ultimately, development of irreversible fibrotic tissue.7,8 The endotracheal tube cuff causes circumferential erosion of the mucosa, which heals with a concentric (web-like) stenosis, like in our case. Based on the length of tracheal stenosis, the depth of the tracheal wall involvement and the presence or not of tracheomalacia, post-intubation tracheal stenosis falls into three categories, including short, ‘‘complex’’ and ‘‘pseudoglottic’’ stenosis.9 The few available prospective studies document an incidence of post-intubation and/or post-tracheostomy tracheal stenosis from 10 to 19%. However, symptomatic stenoses, affecting pulmonary function do not exceed 1% of the cases.10 Apart from cuff pressure and direct tracheal trauma during intubation, duration of intubation has also been proposed as a critical pathogenetic endpoint. However, data referring to this issue is still controversial, since there have been several reports of tracheal stenosis after only few days of intubation, evidence that was further extended by experimental data. In addition, the incidence
1211 of tracheal stenosis does not seem to be related to repeated intubations, the route of intubation or the emergency character of the procedure.10 Typically, post-intubation tracheal stenosis is diagnosed based on a combination of presenting airway obstruction signs and symptoms with a recent history of tracheal intubation. Airway obstruction usually presents as shortness of breath and either or both inspiratory stridor and expiratory wheeze. Symptoms do not usually occur until tracheal stenosis exceeds a critical point of greater than 20e30% of its original size, and it may take as long as 3 months time before most stenoses can be documented by a physician.7,8 Although, simple spirometry typically shows a reduction in peak expiratory flow and depending on the level of stenosis a characteristic flowevolume loop, however, is difficult to perform due to the severity of respiratory failure or cannot be interpreted reliably due to underlying lung disease, mostly chronic obstructive pulmonary disease (COPD). Chest radiograph is usually normal; as a result of the latter and the aforementioned clinical and functional findings, post-intubation tracheal stenosis is often misdiagnosed as asthma8 with a great proportion of these patients to be receiving large doses of systemic and/or inhaled corticosteroids for months.7,8 The diagnosis may be confirmed with plain radiography, computed and tracheal linear tomography or endoscopy. Despite the recent introduction of ‘‘virtual’’ bronchoscopy using reconstructed digital signals to depict the level of stenosis, flexible bronchoscopy represents the diagnostic technique of choice that both provides a definitive diagnosis and determines the type, location and severity of stenosis. In addition, it is easy to perform and directs the clinician to the selection of the appropriate type and duration of treatment. Regarding the latter, although there have been few reports of an effective therapeutic approach of tracheal stenosis with systematic and/or inhaled steroid regimens,11,12 the hallmark of treatment for symptomatic lesions is endoscopic and surgical.10 Rigid bronchoscopy and tracheal dilation possibly by laser or placement of special stents may be the only treatment required for less serious lesions.13 In recurrence or in case of more extensive stenosis, a definitive tracheal reconstructive surgery should be considered, with a mortality ranging from 1.8 to 5%.14 In summary, we conclude that endotracheal intubation may cause local inflammation and ischemia resulting in activation of platelet microaggregates,15 inhibition of fibrinolysis and ultimately development of fibrotic scar tissue leading to complications such as pulmonary embolism and tracheal stenosis. Post-intubation tracheal stenosis is an iatrogenic complication that should be considered in the differential diagnosis of any patient who has a recent history of intubation and who presents with exertional dyspnoea and wheeze, unresponsive to bronchodilators. Should it occur, timely diagnosis and effective management are crucial. In life-threatening situations, such patients require immediate transfer to specialist centres for definitive tracheal reconstructive surgery.
Conflict of interest statement The authors have no conflict of interest to declare.
1212
References 1. Geerts WH. Thromboembolism in trauma: the problem and its prevention. Semin Thromb Hemost 1996;22(Suppl. 2):19e24. 2. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP. A prospective study of venous thromboembolism after major trauma. N Engl J Med 1994;331(24):1601e6. 3. Geerts WH. Prevention of venous thromboembolism in high-risk patients. Hematology (Am Soc Hematol Educ Program); 2006: 462e6. 4. Knudson MM, Ikossi DG, Khaw L, Morabito D, Speetzen LS. Thromboembolism after trauma: an analysis of 1602 episodes from the American College of Surgeons National Trauma Data Bank. Ann Surg 2004;240(3):490e6. 5. Knudson MM, Ikossi DG. Venous thromboembolism after trauma. Curr Opin Crit Care 2004;10(6):539e48. 6. Ullman EA, Donley LP, Brady WJ. Pulmonary trauma emergency department evaluation and management. Emerg Med Clin North Am 2003;21(2):291e313. 7. Spittle CS, Beavis SE. Post-intubation tracheal stenosis. Hosp Med 2001;62(1):54.
A. Tzouvelekis et al. 8. Spittle N, McCluskey A. Lesson of the week: tracheal stenosis after intubation. BMJ 2000;321(7267):1000e2. 9. Bisson A, Bonnette P, el Kadi NB, et al. Tracheal sleeve resection for iatrogenic stenoses (subglottic laryngeal and tracheal). J Thorac Cardiovasc Surg 1992;104(4):882e7. 10. Brichet A, Verkindre C, Dupont J, et al. Multidisciplinary approach to management of postintubation tracheal stenoses. Eur Respir J 1999;13(4):888e93. 11. Braidy J, Breton G, Clement L. Effect of corticosteroids on postintubation tracheal stenosis. Thorax 1989;44(9):753e5. 12. Croft CB, Zub K, Borowiecki B. Therapy of iatrogenic subglottic stenosis: a steroid/antibiotic regimen. Laryngoscope 1979; 89(3):482e9. 13. Vergnon JM, Costes F, Polio JC. Efficacy and tolerance of a new silicone stent for the treatment of benign tracheal stenosis: preliminary results. Chest 2000;118(2):422e6. 14. Bonnette P, Colchen A, Leroy M, Bisson A. Tracheal resectionanastomosis for iatrogenic stenosis. Experience in 340 cases. Rev Mal Respir 1998;15(5):627e32. 15. Hyers TM. Management of venous thromboembolism: past, present, and future. Arch Intern Med 2003;163(7):759e68.