Abstract

Methods: Articles published between November 1995 and February 2023 were searched by a thorough exploration of databases. Studies that addressed recipient-related risk factors for airway complications following adult lung transplantation, such as cohorts, case-control, or cross-sectional studies, were included. Fixed-effects or random-effects models were used to calculate the odds ratios (ORs) or mean differences (MDs) with 95% confidence interval (CI).

Results: Twenty-one studies including a total of 38,321 recipients fulfilled the inclusion criteria. Based on the pooled analyses, taller height (MD=5.98, 95% CI: 5.69-6.27, I2 = 57.32%), intraoperative mechanical ventilation (OR=1.83, 95% CI: 1.41-2.38, I2=0%), male sex (OR=1.52, 95% CI: 1.33-1.74, I2=15.91%), preoperative extracorporeal membrane oxygenation (OR=1.58, 95% CI: 1.1-2.26, I2 =41.47 %), and preoperative steroid use (OR=1.21, 95% CI: 1.04-1.41, I2 = 0%) elevated the risk of airway complications following lung transplantation.

Conclusion: Taller height, intraoperative mechanical ventilation, male sex, preoperative extracorporeal membrane oxygenation, and preoperative steroid use can increase the risk of airway complications after lung transplantation. Identifying high-risk recipients or riskless situations can support the advancement of selective treatments or prevent the unnecessary avoidance of certain interventions.

Lung transplantation is the only solid organ transplantation in which systemic arterial blood supply is not routinely anastomosed.[3] Traditionally, bronchial arteries have been severed during transplantation. This results in ischemia until pulmonary artery collaterals develop in the submucosal plexus; this frequently takes weeks or months to establish. By boosting arterial resistance and interfering with collateral development, postoperative interstitial edema and reperfusion injury may be more responsible for anastomotic ischemia consequences.[1] As a result, the bronchial anastomosis is allowed to repair while being ischemic.[4]

A variety of potential risk factors for the development of AC have been found. These risk factors can be associated with the donor or recipient, surgical techniques, infections, medications, or immunosuppression.[5] Numerous research have been conducted to identify these risk variables.[2,6-25] In this systematic review and meta-analysis, we identify the most significant preoperative risk factors for ACs among adult LTx recipients.

Methods

The meta-analysis included original studies comparing groups with and without ACs in terms of risk factors. Studies without a control group, those concentrating on pediatric LTx or re-LTx, or those managing ACs were not included. The rat or animal experiments were also excluded. Case reports, case series studies, image interests, comments, and full texts that could not be accessed were not considered. Studies from the same author, study group, or institution that were the longest or most recent series were included, while others were excluded.

Selection criteria
Cohort, case-control, and cross-sectional studies were included, if they investigated which recipient"s factors directly influencing the development of ACs after LTx. Variables included age, male sex, body mass index (BMI), height, ischemic cardiac disease, diabetes mellitus (DM), preoperative diagnoses (i.e., chronic obstructive pulmonary disease [COPD], cystic fibrosis, pulmonary fibrosis, pulmonary hypertension), prior thoracic surgery, cytomegalovirus (CMV) positivity, microbiological colonization, preoperative steroid use, intraoperative mechanical ventilation, and preoperative extracorporeal membrane oxygenation (ECMO). After obtaining the complete text of the papers, the authors separately assessed eligibility. After the differences between the two reviewers were resolved, they were able to agree on the final set of data by reviewing relevant papers.

Data extraction
Two researchers independently compiled summaries of the papers that met the inclusion criteria and extracted data using a common data sheet. The following data were extracted from each study: first author's name, study design, publication year, study date (initial and end), country, comparison groups, sample size, number of postoperative ACs, AC delineations, the Newcastle-Ottawa Scale (NOS) (Table 1).

Table 1: Baseline characteristics of the included studies

Table 1: Continued

Study quality evaluation
Based on the following nine questions, the NOS was used to rate the excellence of observational studies: The following criteria must be met: (i) representativeness of the exposed cohort; (ii) choice of the non-exposed cohort; (iii) determination of exposure; (iv) proof that the outcome was not present at the start of the study; (v) comparability; (vi) assessment of outcome; (vii) a dequate l ength o f follow-up; (viii) adequate participant follow-up; and (ix) total stars. There is a maximum score of 9 on this scale. A total score of 7 to 9 was considered "good," a score of 4-6 was considered "fair," and a score of 4 was considered "poor."

Statistical analysis
Statistical analysis was performed using the Medical Research Support (MedicReS E-PICOS Version 21.3, NY, United States) program. The odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the association between binary factors (age, male sex, BMI, height, ischemic cardiac disease, DM, COPD, cystic fibrosis, pulmonary fibrosis, pulmonary hypertension, prior thoracic surgery, CMV positivity, microbiological colonization, preoperative steroid use, intraoperative mechanical ventilation, and preoperative ECMO) and development of AC. We assessed the mean differences (MDs) for LTx subjects with and without AC, when the mean values and SDs for a specific risk factor were given. Fixed-effects models or random-effects models were used to produce the statistical estimates of effect based on I2. The I2 statistic was used to quantify heterogeneity. Using accepted guidelines, an I2 between 0 and 40% was considered to exclude heterogeneity, 30 and 60% moderate heterogeneity, 50 and 90% substantial heterogeneity, and 75 and 100% considerable heterogeneity. Publication bias was assessed with funnel plots.

Results

Figure 1: Flowchart of the meta-analysis.
* 216 papers on Web of Science and 218 on PubMed.

According to the NOS, all studies had excellent methodological quality (good or fair) (Table 1).

Age: S eventeen s tudies ( sample s ize=37,588) examined the impact of recipient age on the happening of AC following LTx.[2,6-11,13,15-21,24,25] The outcomes of this analysis displayed no significant difference in the mean age between patients who had AC (n=987) and those who did not (n=36,601) (MD=0.56, 95% CI: -0.72-1.84, p= 0.69). Heterogeneity was considerable (I2 = 95.81%, p<0.001) and random model and meta regression were used.

Male sex: N ineteen s tudies ( sample s ize=38,216) examined the impact of male sex on the happening of AC following LTx.[2,6-11,13-20,22-25] The outcomes of this analysis presented a significant difference in in the proportion of male sex between patients who had AC (n=1,112) and those who did not (n=37,104) (OR=1.52, 95% CI: 1.33-1.74, p<0.001). Populations were homogeneous (I2 = 15.91%, p=0.26) and fixed effect model was used (Figure 2).

Figure 2: The effect of recipient male sex on airway complications.
OR: Odds ratio; CI: Confidence interval.

BMI: Seven studies (sample size=17,681) examined the impact of recipient BMI on the happening of AC following LTx.[2,7-10,13,25] The outcomes of this analysis exhibited no significant difference in the mean BMI between patients who had AC (n=434) or and those who did not (n=17,247) (MD=0.72, 95% CI: -0.73-2.18, p = 0.33). Heterogeneity was considerable (I2 = 95.1%, p<0.001 ) and random model and meta regression were used.

Height: Three studies (sample size=674) examined the impact of recipient height on the happening of AC following LTx.[9,18,20] The outcomes of this analysis revealed a significant difference in the mean height between patients who had AC (n=75) or those who did not (n=599) (MD=5.98, 95% CI: 5.69-6.27, p<0.001). Heterogeneity was moderate (I2 = 57.32%, p=0.1) and fixed model was used (Figure 3).

Figure 3: The effect of recipient height on airway complications.
OR: Odds ratio; CI: Confidence interval.

Ischemic cardiac disease: Four studies (sample size=854) examined the impact of ischemic cardiac disease on the happening of AC following LTx.[6,9,16,20] The outcomes of this analysis indicated no significant difference in the proportion of ischemic cardiac disease between patients who had AC (n=141) and those who did not (n=713) (OR=0.74, 95% CI: 0.46-1.16, p=0.19). Heterogeneity was moderate (I2 = 30.27%, p=0.24) and fixed effect model was used.

DM: Five studies (sample size=34,591) examined the impact of DM on the happening of AC following LTx.[2,6,9,11,13] The outcomes of this analysis showed no significant difference in the proportion of DM between patients who had AC (n=588) and those who did not (n=34,003) (OR=1.06, 95% CI: 0.86-1.31, p=0.6). Populations were homogeneous (I2 = 0%, p=0.52). Fixed effect model was used.

COPD: Fourteen studies (sample size=19,138) examined the impact of COPD on the happening of AC following LTx.[6,8-10,13,16-23,25] The outcomes of this analysis displayed no significant difference in the proportion of COPD between patients who had AC (n=645) or and those who did not (n=18,493) (OR=0.91, 95% CI: 0.76-1.1, p=0.33). Heterogeneity was moderate (I2 =37.18 %, p=0.08) and fixed effect model was used.

Cystic fibrosis: Ten studies (sample size=18,242) examined the impact of cystic fibrosis on the happening of AC following LTx.[9,10,13,14,16-21] The outcomes of this analysis presented no significant difference in the proportion of cystic fibrosis between patients who had AC (n=583) and those who did not (n=17,659) (OR=0.99, 95% CI: 0.78-1.25, p=0.92). Study populations were homogeneous (I2 = 9.08%, p=0.36) and fixed effect model was used.

Pulmonary fibrosis: Sixteen studies (sample size=19,863) examined the impact of pulmonary fibrosis on the happening of AC following LTx.[2,6-9,13-23] The outcomes of this analysis displayed no significant difference in the proportion of pulmonary fibrosis between patients who had AC (n=758) or and those who did not (n=19,105) (OR=1.06, 95% CI: 0.9-1.26, p=0.49). Heterogeneity was moderate (I2 =47.11%, p=0.02) and fixed effect model was used.

Pulmonary hypertension: Ten studies (sample size=19,013) examined the impact of pulmonary hypertension on the happening of AC following LTx.[2,6,8,10,13,14,17,18,20,23] The outcomes of this analysis showed no significant difference in the proportion of pulmonary hypertension between patients who had AC (n=649) and those who did not (n=18,364) (OR=1.04, 95% CI: 0.74-1.47, p=0.82). Heterogeneity was moderate (I2 = 34.2%, p=0.14) and fixed effect model was used.

Prior thoracic surgery: Three studies (sample size=18,378) examined the impact of prior thoracic surgery on the happening of AC following LTx.[2,8,11] The outcomes of this analysis indicated no significant difference in the proportion of prior thoracic surgery between patients who had AC (n=315) and those who did not (n=18,063) (OR=1.13, 95% CI: 0.77-1.65, p=0.54). Study populations were homogeneous (I2 = 0%, p=0.65) and fixed effect model was used.

Cytomegalovirus positivity: Three studies (sample size=757) examined the impact of CMV positivity on the happening of AC following LTx.[16,18,20] The outcomes of this a nalysis exhibited no significant difference in the proportion of CMV positivity between patients who had AC (n=99) and those who did not (n=658) (OR=0.95, 95% CI: 0.62-1.47, p=0.83). Study populations were homogeneous (I2 = 0%, p=0.98) and fixed effect model was used.

Microbiological colonization: Six studies examined (sample size=1,247) the impact of microbiological colonization on the happening of AC following LTx.[2,7,9,14,19,22] The outcomes of this analysis displayed no significant difference in the proportion of microbiological colonization between patients who had AC (n=224) and those who did not (n=1,023) (OR=0.87, 95% CI: 0.4-1.89, p=0.72). Heterogeneity was considerable (I2 = 82.47%, p<0.001) and random effect model was used.

Preoperative steroid use: Eleven studies (sample size=36,038) examined the impact of preoperative steroid use on the happening of AC following LTx.[2,8,11-13,18-23] The outcomes of this analysis revealed a significant difference in the proportion of preoperative steroid use between patients who had AC (n=734) and those who did not (n=35,304) (OR=1.21, 95% CI: 1.04-1.41, p=0.02). Study populations were homogeneous (I2 = 0%, p=0.88) and fixed effect model was used (Figure 4).

Figure 4: The effect of recipient"s preoperative steroid use on airway complications.
OR: Odds ratio; CI: Confidence interval.

Intraoperative mechanical ventilation: Six studies (sample size=34,875) examined the impact of intraoperative mechanical ventilation on the happening of AC following LTx.[2,6,11,13,19,21] The outcomes of this analysis revealed a significant difference in the proportion of intraoperative mechanical ventilation between patients who had AC (n=613) and those who did not (n=34,262) (OR=1.83, 95% CI: 1.41-2.38, p<0.001). Study populations were homogeneous (I2 =0 %, p=0.82) and fixed effect model was used (Figure 5).

Figure 5: The effect of recipient"s intraoperative mechanical ventilation on airway complications.
OR: Odds ratio; CI: Confidence interval.

Preoperative ECMO: Six studies (sample size=35,404) examined the impact of preoperative ECMO on the happening of AC following LTx.[2,8,9,11,13,24] The outcomes of this analysis revealed a significant difference in the proportion of preoperative ECMO between patients who had AC (n=592) and those who did not (n=34,812) (OR=1.58, 95% CI: 1.1-2.26, p=0.01). Heterogeneity was moderate (I2 =41.47 %, p=0.14) and fixed effect model was used (Figure 6). The forest plot of the all parameters can be seen in Figure 7.

Figure 6: The effect of preoperative ECMO support for recipient on airway complications.
OR: Odds ratio; CI: Confidence interval; ECMO: Extracorporeal membrane oxygenation.

Figure 7: Forest Plot of the 21 studies on the effect of recipient"s risk factors on airway complications.
BMI: Body mass index; COPD: Chronic obstructive pulmonary disease; ECMO: Extracorporeal membrane oxygenation

Discussion

Airway complications have been a major factor limiting the development of LTx throughout history and associated with considerable morbidity and mortality.[2] Among the risk factors of AC, male sex was a significant risk factor in our analysis. The bronchial arteries' origins, number, dimensions, and courses can differ greatly among individuals and between sexes. [27] Men have much more bronchial arteries than women, both in terms of size and number. Men may, therefore, have lower ischemia tolerance.

A similar argument could be possible for the height of the patients. The bronchus is greater in diameter in tall patients, and emphysema patients typically have less peribronchial fatty tissue, which can be used to cover the anastomosis.[20] This is probably due to a recipient-donor size discrepancy, as seen by the recipient's wider bronchial circumference and the donor bronchus' requirement for intussusception.[28] There will, therefore, be a requirement for telescopic anastomosis, which has the potential to result in more AC than end-to-end anastomosis. Similarly, our study supports that the strongest recipient's risk factor is the height.

Mechanical ventilation is an important component in the perioperative management of LTx. Mechanical ventilation poses a risk of bronchial ischemia, as it damages the bronchial mucosa and increases arterial resistance.[29] Ischemia makes the bronchial anastomoses sites more vulnerable to poor healing, infection, and complications with the anastomotic airway. Additionally, perfusion of transplanted airways may be compromised by positive pressure mechanical ventilation, particularly when large inflation pressures are necessary. The pulmonary flow to the main bronchi would be decreased by any allograft parenchymal pathology, such as primary graft disfunction, infection, or rejection, which would impair anastomotic recovery. Anastomotic stress and bronchial wall deterioration can be also caused by positive pressure ventilation. Some studies have found a connection between the likelihood of anastomotic ACs and high airway pressures and longer ventilation periods.[30] Our study showed that intraoperative mechanical ventilation increases the risk of AC after LTx.

Due to the interruption of microcirculation, inflammatory responses that cause endothelial damage, or issues specifically associated with ECMO, it is possible that ECMO would impair the healing of the airways. Due to the fact that ECMO is used to treat AC-related high-risk disorders such as primary graft disfunction, it can also seem to increase the risk.[2] In our study, there was also a slightly higher risk of ECMO.

It is well known that perioperative steroid medication has a negative impact on the repair of bronchial anastomoses; however, recent findings have indicated that this is debatable. High doses of steroids within the first year following surgery increase the chance of AC. Patients receiving high doses of corticosteroids run the risk of having worse early postoperative outcomes, which cannot be ruled out. To optimize the early preoperative course, it is crucial to customize and limit the preoperative steroid dose.[12] In our study, preoperative steroid use moderately increased AC.

Nonetheless, there are some limitations to this analysis. Although the evaluation or diagnosis of AC was made according to global standards, there was heterogeneity between studies. The follow-up period was also variable between studies, although it was long enough to yield results. Additionally, numerous problems were identified in detail in some research, while others only provided a single definition for them. The primary diseases leading to LTx, for instance, were noticed to be classified differently in each study. Our analysis covered the most frequently studied ones, and we concluded that the primary diagnosis indicative of LTx did not increase the risk of airway problems. Some of the studies also focus on a single variable, treatments or survival. The other limitations could be potential publication bias, heterogeneity, not all variables are comparable, cannot overcome subjectivity, and only deals with main effects.

In conclusion, our analysis show that recipient"s preoperative risk factors such as taller height, preoperative mechanical ventilation, male sex, preoperative extracorporeal membrane oxygenation, and preoperative steroid use can increase the risk of airway complications after lung transplantation based on pooled analyses. Identifying the high-risk recipients or riskless situations can support the personalized approaches such as advancement of selective treatments or prevent the unnecessary avoidances.

Ethics Committee Approval: The study protocol was approved by the Istanbul Medipol University Non-Interventional Clinical Research Ethics Committee (date: 28.07.2023, no: E-10840098-772.02-4639). The study was conducted in accordance with the principles of the Declaration of Helsinki.

Data Sharing Statement: The data that support the findings of this study are available from the corresponding author upon reasonable request.

Author Contributions: All authors contributed equally to the article.

Conflict of Interest: The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

Funding: The authors received no financial support for the research and/or authorship of this article.

References

1) Amesur NB, Orons PD, Iacono AT. Interventional techniques in the management of airway complications following lung transplantation. Semin Intervent Radiol 2004;21:283-95. doi:10.1055/s-2004-861563.

2) Kim HH, Jo KW, Shim TS, Ji W, Ahn JH, Oh DK, et al. Incidence, risk factors, and clinical characteristics of airway complications after lung transplantation. Sci Rep 2023;13:667. doi: 10.1038/s41598-023-27864-1.

3) Shennib H, Massard G. Airway complications in lung transplantation. Ann Thorac Surg 1994;57:506-11. doi:10.1016/0003-4975(94)91038-3.

4) Pasnupneti S, Nicolls MR. Airway hypoxia in lung transplantation. Curr Opin Physiol 2019;7:21-6. doi: 10.1016/j. cophys.2018.12.002.

5) Machuzak M, Santacruz JF, Gildea T, Murthy SC. Airway complications after lung transplantation. Thorac Surg Clin 2015;25:55-75. doi: 10.1016/j.thorsurg.2014.09.008.

6) Atchade E, Ren M, Jean-Baptiste S, Tran Dinh A, Tanaka S, Tashk P, et al. ECMO support as a bridge to lung transplantation is an independent risk factor for bronchial anastomotic dehiscence. BMC Pulm Med 2022;22:482. doi:10.1186/s12890-022-02280-9.

7) Delbove A, Senage T, Gazengel P, Tissot A, Lacoste P, Cellerin L, et al. Incidence and risk factors of anastomotic complications after lung transplantation. Ther Adv Respir Dis 2022;16:17534666221110354. doi:10.1177/17534666221110354.

8) Furukawa M, Chan EG, Morrell MR, Ryan JP, Rivosecchi RM, Iasella CJ, et al. Risk factors of bronchial dehiscence after primary lung transplantation. J Card Surg 2022;37:950-7. doi: 10.1111/jocs.16291.

9) Mendogni P, Pieropan S, Rosso L, Tosi D, Carrinola R, Righi I, et al. Impact of cold ischemic time on airway complications after lung transplantation: A single-center cohort study. Transplant Proc 2019;51:2981-5. doi: 10.1016/j. transproceed.2019.04.092.

10) N?cki M, Pandel A, Urlik M, Anto?czyk R, Latos M, Gaw?da M, et al. The impact of airway complications on survival among lung transplant recipients. Transplant Proc 2020;52:2173-7. doi: 10.1016/j.transproceed.2020.03.051.

11) Malas J, Ranganath NK, Phillips KG, Bittle GJ, Hisamoto K, Smith DE, et al. Early airway dehiscence: Risk factors and outcomes with the rising incidence of extracorporeal membrane oxygenation as a bridge to lung transplantation. J Card Surg 2019;34:933-40. doi: 10.1111/jocs.14157.

12) Kim HE, Paik HC, Kim SY, Park MS, Lee JG. Preoperative corticosteroid use and early postoperative bronchial anastomotic complications after lung transplantation. Korean J Thorac Cardiovasc Surg 2018;51:384-9. doi: 10.5090/ kjtcs.2018.51.6.384.

13) Awori Hayanga JW, Aboagye JK, Shigemura N, Hayanga HK, Murphy E, Khaghani A, et al. Airway complications after lung transplantation: Contemporary survival and outcomes. J Heart Lung Transplant 2016;35:1206-11. doi:10.1016/j.healun.2016.04.019.

14) Yserbyt J, Dooms C, Vos R, Dupont LJ, Van Raemdonck DE, Verleden GM. Anastomotic airway complications after lung transplantation: Risk factors, treatment modalities and outcome-a single-centre experience. Eur J Cardiothorac Surg 2016;49:e1-8. doi: 10.1093/ejcts/ezv363.

15) Cho EN, Haam SJ, Kim SY, Chang YS, Paik HC. Anastomotic airway complications after lung transplantation. Yonsei Med J 2015;56:1372-8. doi: 10.3349/ymj.2015.56.5.1372.

16) FitzSullivan E, Gries CJ, Phelan P, Farjah F, Gilbert E, Keech JC, et al. Reduction in airway complications after lung transplantation with novel anastomotic technique. Ann Thorac Surg 2011;92:309-15. doi: 10.1016/j.athoracsur.2011.01.077.

17) Fernández-Bussy S, Majid A, Caviedes I, Akindipe O, Baz M, Jantz M. Treatment of airway complications following lung transplantation. Arch Bronconeumol 2011;47:128-33. Spanish. doi: 10.1016/j.arbres.2010.10.011.

18) Weder W, Inci I, Korom S, Kestenholz PB, Hillinger S, Eich C, et al. Airway complications after lung transplantation: Risk factors, prevention and outcome. Eur J Cardiothorac Surg 2009;35:293-8. doi: 10.1016/j.ejcts.2008.09.035.

19) Moreno P, Alvarez A, Algar FJ, Cano JR, Espinosa D, Cerezo F, et al. Incidence, management and clinical outcomes of patients with airway complications following lung transplantation. Eur J Cardiothorac Surg 2008;34:1198-205. doi: 10.1016/j.ejcts.2008.08.006.

20) Van De Wauwer C, Van Raemdonck D, Verleden GM, Dupont L, De Leyn P, Coosemans W, et al. Risk factors for airway complications within the first year after lung transplantation. Eur J Cardiothorac Surg 2007;31:703-10. doi:10.1016/j.ejcts.2007.01.025.

21) Alvarez A, Algar J, Santos F, Lama R, Aranda JL, Baamonde C, et al. Airway complications after lung transplantation: A review of 151 anastomoses. Eur J Cardiothorac Surg 2001;19:381-7. doi: 10.1016/s1010-7940(01)00619-4.

22) Herrera JM, McNeil KD, Higgins RS, Coulden RA, Flower CD, Nashef SA, et al. Airway complications after lung transplantation: Treatment and long-term outcome. Ann Thorac Surg 2001;71:989-93. doi: 10.1016/s0003- 4975(00)02127-5.

23) Date H, Trulock EP, Arcidi JM, Sundaresan S, Cooper JD, Patterson GA. Improved airway healing after lung transplantation. An analysis of 348 bronchial anastomoses. J Thorac Cardiovasc Surg 1995;110:1424-32. doi: 10.1016/ S0022-5223(95)70065-X.

24) Golovinskiy SV, Nechaev NB, Poptsov VN, Rusakov MA. Treatment of distal bronchial stenosis after bilateral lung transplantation. Vestnik Transplantologii i Iskusstvennykh Organov 2017;19:41-7.

25) Ruttmann E, Ulmer H, Marchese M, Dunst K, Geltner C, Margreiter R, et al. Evaluation of factors damaging the bronchial wall in lung transplantation. J Heart Lung Transplant 2005;24:275-81. doi: 10.1016/j.healun.2004.01.008.

26) Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. The PRISMA 2020 statement: An updated guideline for reporting systematic reviews. Syst Rev 2021;10:89. doi: 10.1186/s13643-021-01626-4.

27) Yener Ö, Türkvatan A, Yüce G, Yener AÜ. The normal anatomy and variations of the bronchial arteries: Evaluation with multidetector computed tomography. Can Assoc Radiol J 2015;66:44-52. doi: 10.1016/j.carj.2014.07.001.

28) Frye L, Machuzak M. Airway complications after lung transplantation. Clin Chest Med 2017;38:693-706. doi:10.1016/j.ccm.2017.07.010.

29) Murthy SC, Blackstone EH, Gildea TR, Gonzalez-Stawinski GV, Feng J, Budev M, et al. Impact of anastomotic airway complications after lung transplantation. Ann Thorac Surg 2007;84:401-9, 409.e1-4. doi: 10.1016/j. athoracsur.2007.05.018.

30) Barnes L, Reed RM, Parekh KR, Bhama JK, Pena T, Rajagopal S, et al. Mechanical ventilation for the lung transplant recipient. Curr Pulmonol Rep 2015;4:88-96. doi:10.1007/s13665-015-0114-8.