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Year : 2021  |  Volume : 4  |  Issue : 1  |  Page : 31-39

Radiological imaging and its utility in lung transplantation: Our experience and review of literature

1 Department of Heart and Lung Transplantation, Apollo Hospitals, Chennai, Tamil Nadu, India
2 Department of Respiratory Medicine, Apollo Hospitals, Chennai, Tamil Nadu, India

Date of Submission13-Jun-2021
Date of Acceptance20-Jul-2021
Date of Web Publication22-Sep-2021

Correspondence Address:
Thirugnana Sambandan Sunder
Department of Heart and Lung Transplantation, Apollo Hospitals, 21 Greams Lane, Off Greams Road, Chennai - 600 006, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/japt.japt_27_21

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Lung transplantation (LT) can be considered a definite treatment for end-stage pulmonary disease in appropriate patients. Depending upon various clinical factors, LT can be performed either as a single LT, bilateral LT, or heart LT. Although LT is a well-established procedure now, it is not without its own complications. In post-LT patients, several complications can have overlapping clinical and imaging features; therefore, early and accurate diagnosis can be challenging. Due to this difficulty, an interdisciplinary approach is imperative. Bronchoscopy, bronchoalveolar lavage, and transbronchial biopsy may be required in this approach, in addition to the routine investigations. The treating team should be aware of the possible complications after LT and the associated imaging features that may occur at varying time points following transplantation to provide prompt management. This article describes our experience and reviews the utility of radiological imaging in LT in relation to complications that may occur following LT.

Keywords: Chest X-ray, complications, computed tomography scan, lung transplantation

How to cite this article:
Chinnasamy S, Sunder TS, Thangaraj PR, Kuppuswamy MK, Narasimhan R. Radiological imaging and its utility in lung transplantation: Our experience and review of literature. J Assoc Pulmonologist Tamilnadu 2021;4:31-9

How to cite this URL:
Chinnasamy S, Sunder TS, Thangaraj PR, Kuppuswamy MK, Narasimhan R. Radiological imaging and its utility in lung transplantation: Our experience and review of literature. J Assoc Pulmonologist Tamilnadu [serial online] 2021 [cited 2022 Jan 28];4:31-9. Available from: http://www.japt.com/text.asp?2021/4/1/31/326413

  Introduction Top

Lung transplantation (LT) is now being performed in increasing numbers in India. In appropriate patients, it is now an accepted therapy for end-stage lung disease. Among the various solid organ transplants, in LT, particularly, radiological imaging plays an important and pivotal role in the management of patients after the operation – because lungs have an air-solid interface which lends itself to easier interpretation. This article discusses the use of radiological imaging after LT, common complications encountered and our experience with radiological assessments. Till date, we have performed 57 isolated LTs, of which 50 were double-LT (DLT) and 7 were single-LT. In addition, we have performed 29 combined heart-LTs which also include one patient who underwent combined heart–lung and kidney transplantation. Our 3-year survival following DLT is 76.2%.[1] Most patients requiring LT are patients with end-stage lung disease due to interstitial lung disease (ILD).

  Imaging in Immediate Postoperative Period Top

Immediate postoperative imaging is mandatory to ascertain the correct position of tubing's and vascular lines. A routine chest X-ray performed immediately on arrival to the intensive care unit is shown in [Figure 1].
Figure 1: Immediate postlung transplantation Chest X-ray shows endotracheal tube, nasogastric tube, and intercostal drainage tubes and left internal jugular central venous line

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  Donor-Recipient Size Mismatch Top

The donor and recipient lungs are matched for size preoperatively. Size mismatch between donor and recipient chest cavity may cause mechanical complications. Size matching between donor and recipient is essentially by body height, size differences of 10%–25% between a donor lung, and a recipient thoracic cage have been acceptable.[2] If the donor lung is too large for the recipient chest cavity, especially in patients with ILD, passive atelectasis may manifest on an immediate postoperative chest radiograph. We have encountered atelectasis in 10% of our LT group due to size mismatch, especially in ILD patients with contracted chest [Figure 2].
Figure 2: Chest X-ray showing right lower lobe atelectasis due to size mismatch after double-lung transplantation in patient of idiopathic pulmonary fibrosis with contracted chest

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On the other hand, an undersized donor lung with large recipient chest cavity can result in mechanical problems related to residual space, such as intractable effusion or residual airspace. Ten percent of our patients suffered residual space problem due to smaller donor lungs in recipients with large chest cavity [Figure 3].
Figure 3: Chest X-ray showing bilateral residual air space due to smaller lungs in a patient with chronic inflammatory lung disease with large chest cavity after double-lung transplantation

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  Primary Graft Dysfunction Top

Primary graft dysfunction (PGD) is defined as a syndrome of acute lung injury that occurs within the first 72 h after LT. PGD is characterized by pulmonary edema with diffuse alveolar damage that clinically manifests itself as progressive hypoxemia and radiographic pulmonary infiltrates without other identifiable causes [Table 1].[3]
Table 1: Listing the grades of primary graft dysfunction based on chest X-ray findings and pressure of arterial oxygen/fraction of inspired oxygen ratio

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PGD is caused by injury inflicted on the donor lung by the transplant process (retrieval, preservation, implantation, and reperfusion) and by other recipient factors such as acid aspiration, pneumonia, and micro-trauma from mechanical ventilation (MV).[4] PGD grades[3] are determined by the presence or absence of pulmonary edema on chest X-ray and ratio of the partial pressure of arterial oxygen (PaO2) and fraction of inspired oxygen (FiO2). This ratio is referred to as P/F ratio.

Patients with PGD less than Grade 3 severity or with Grade 3 severity and normal pulmonary artery pressures improve with conventional supportive treatment, including lung protective ventilation and optimal fluid management. Extracorporeal membrane oxygenation (ECMO) may serve as a life-saving measure for lung transplant recipients with severe forms of PGD (PaO2/FiO2 <100 mmHg), who do not respond to maximal conventional treatment and a trial of inhaled nitric oxide.[5] We have encountered PGD in 30% of our LT patients, of which 20% were of mild-to-moderate grade [Figure 4] and [Figure 5]. These patients responded to supportive management with medications and MV. The remaining 10% of our LT patients had severe PGD [Figure 6] who required ECMO support. Of the patients requiring ECMO post LT for PGD, 80% of patients were weaned off ECMO with good lung function [Figure 7], whereas the remaining 20% of patients succumbed to PGD.
Figure 4: Chest X-ray of heart-lung transplantation patient with mild Primary graft dysfunction with P/F ratio of >300

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Figure 5: Chest X-ray of heart-lung transplantation patient with moderate Primary graft dysfunction P/F ratio of 250

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Figure 6: Bilateral lung opacities involving all zones due to severe Primary graft dysfunction in first postoperative day with P/F ratio of 100 managed with Veno-venous extracorporeal membrane oxygenation, extracorporeal membrane oxygenation cannula and implantable cardioverter-defibrillator in situ

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Figure 7: Chest X-ray just prior to discharge after 3 days of extracorporeal membrane oxygenation in patient with Grade 3 Primary graft dysfunction

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  Acute Rejection Top

Acute rejection (AR) usually occur between 3 weeks and 1 year.[6] There are two types of AR: Acute cellular (ACR) or antibody-mediated rejection (AMR). Around 50% of patients have at least one episode of AR in the 1st year following transplant. Recurrent AR is a risk factor for the development of chronic rejection. AR has computed tomography (CT) appearance of airspace abnormalities such as ground-glass opacities with accompanying septal thickening and pleural effusion may be seen. ACR can be confirmed by histopathology. AMR is sub-categorized into definite, probable, and possible based on the number of diagnostic criteria.[7] Definite AMR include: (I) Exclusion of other causes such as infection, (II) histopathological features, (III) presence of DSA, and (IV) positive C4d staining. Histopathological features of AMR are nonspecific and include neutrophilic capillaritis, neutrophil margination, acute lung injury with or without diffuse alveolar damage, and arteritis.[8] A diagnosis of probable AMR lacks one criteria, a diagnosis of possible AMR lacks two criteria.

In our group of LT patients, 20% experienced AR in the 1st year. The diagnosis of AR in our hospital is done by clinical assessment, radiological, and histopathological features. Assessment of donor-specific antibodies contributes to the diagnosis of possible AMR [Figure 8],[Figure 9],[Figure 10],[Figure 11].
Figure 8: Chest X-ray showing bilateral nonhomogeneous opacity with CP angle blunting in a patient of postheart lung transplantation with acute rejection

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Figure 9: Computed tomography of the chest showing bilateral GGO, septal thickening, and minimal pleural effusion in a patient with acute rejection

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Figure 10: Histopathology showing lymphocytic infiltration in a perivascular distribution suggestive of acute cellular rejection in the same patient

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Figure 11: Chest X-ray showing clearance of opacity after adequate management of acute rejection in a patient after heart-lung transplantation

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  Pleural Complications Top

Pleural complications, including pleural effusion, pneumothorax, hemothorax, empyema, and air leaks, occur in 22%–34% of patients following LT.[9]

Pleural effusion

The development of early pleural effusion is thought to be due to ischemia, denervation, and subsequent reperfusion of the allograft or by disruption of the pulmonary lymphatics. Pleural effusions are usually self-limiting and resolve within 2 weeks [Figure 12]. Persistent or delayed effusions suggest complicated effusions such as empyema, organized hematoma, rejection, and posttransplantation lymph proliferative disorder.[9] Empyema should be excluded in the presence of a new or enlarging pleural effusion [Figure 13].
Figure 12: Chest X-ray showing bilateral lower zone homogeneous opacities with CP angle blunting suggestive of effusion in postdouble-lung transplantation patient

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Figure 13: Computed tomography of the chest showing right-sided pleural effusion which required ultrasonography-guided aspiration

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In our experience, the most common pleural complication was pleural effusion which occurred in 25% of our patients.

Pneumothorax/residual air apace

Minor degrees of pneumothorax do occur in the immediate postoperative period and are often due to minor alveolar leaks which heal spontaneously. Sometimes, pneumothorax occurs which delay the removal of implantable cardioverter-defibrillator (ICDs) may placed during LT operation. As long as the gas exchange is adequate with no respiratory distress, the patient can be watched, leaving the ICDs until the air leak settles and pneumothorax resolves. The appearance of new pneumothorax usually requires and resolves with the insertion of an ICD – should the cause be minor alveolar leaks which heal spontaneously. If there is a persistent or enlarging pneumothorax with significant air leak, a bronchoscopic examination is required to assess the bronchial anastomoses – mainly to exclude bronchial dehiscence.

Ten percent of our LT patients had pneumothorax with alveolar air leak. These patients responded to conservative management with intercostal drains which were kept in place for prolonged period ranging from 6 to 12 days [Figure 14] and [Figure 15].
Figure 14: Chest X-ray showing right-sided pneumothorax after 10 days of lung transplantation required additional implantable cardioverter-defibrillator insertion

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Figure 15: Chest X-ray showing lung re-expansion after additional implantable cardioverter-defibrillator insertion in lung transplantation patient with pneumothorax

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  Pulmonary Infections Top

Pulmonary infection after LT remains an important complication that is associated with high morbidity and mortality. The incidence of infection is more frequent in the LT recipients than any other organ transplant recipients. This is due to the higher level of immunosuppressants, direct exposure of the graft to the environment, and loss of local pulmonary host defences characterized by the reduction in lymphatic drainage and reduced mucociliary clearance.

Bacterial infections

Bacterial infections are the most frequent in the 1st month after LT. Gram-negative bacteria such as Pseudomonas and Klebsiella species are common. Radiographic manifestation of bacterial pneumonia may be nonspecific.[10]

It may present as patchy or confluent consolidation, ground-glass opacity, septal thickening, and pleural effusions. The presence of tree-in-bud opacity along with the above nonspecific features makes bacterial pneumonia more likely.[10] In our group, 20% of patients developed bacterial pneumonia within the 1st month [Figure 16] and [Figure 17].
Figure 16: Computed tomography chest showing postlung transplantation patient on the 7th POD showed bilateral dense lower and middle lobe consolidation due to multi-drug-resistant Klebsiella pneumoniae

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Figure 17: Computed tomography chest of postlung transplant patient showing right lower lobe consolidation due to pseudomonas on the 10th POD

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Fungal infections

Fungal infections, most commonly occur due to Candida and Aspergillus species. It usually occurs between 10 and 60 days after LT. Aspergillosis is more common in LT patients than in other immunocompromised patients. Aspergillus organisms can cause indolent pneumonia or fulminant angio-invasive infection with systemic dissemination. Symptoms of Aspergillus infection are nonspecific and include fever, cough, pleuritic chest pain, and hemoptysis. CT of the chest commonly reveals a combination of ill-defined nodules, cavitary opacities, consolidation, and ground-glass opacity.[11] Aspergillus infection around the anastomosis and airway are seen in about 5% of the patients; it occurs mostly in the first 6 months. They are usually asymptomatic and are often detected on surveillance bronchoscopy. Such an infection may cause ulcerative tracheobronchitis that is usually radiologically occult and can lead to bronchial dehiscence, stenosis, or bronchomalacia. In our LT patients, 5% patients developed fungal pneumonia due to Candida and Aspergillus species. The risk factors found for fungal pneumonia in our patients were prolonged preoperative hospitalization and preoperative high dose of steroids due to disease progression and acute exacerbation [Figure 18].
Figure 18: Computed tomography chest showing ill-defined nodules with patchy consolidation in a patient 5 months after heart-lung transplantation in whom galactomannon was positive in BAL and the culture grew Aspergillus fumigatus

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Viral infections

Cytomegalovirus (CMV) is the second most common cause of pneumonia in LT patients and is the most common opportunistic infection. CMV pneumonia most commonly occurs between 1 and 12 months, with a peak incidence at 1–4 months. Chest radiographs may be normal or may show diffuse parenchymal haziness or reticulonodular interstitial opacities. CT findings include areas of ground-glass attenuation, micronodules, consolidation, reticulation, and small pleural effusions.[12],[13] In our group of LT patients, we encountered CMV infection in only 2% of outpatients [Figure 19].
Figure 19: Computed tomography chest of the patient with double-lung transplant showing GGO, micronodules, and consolidation with pleural effusion. A high viral load in BAL and blood samples confirmed the diagnosis of Cytomegalovirus pneumonia

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  Airway Complications Top

Airway stenosis

The reported prevalence of airway stenosis following LT is approximately 15%–20%.[14] In our experience, 20% of our patients had narrowing at the anastomotic site. While most of the patients did not require intervention, balloon bronchoplasty was required in 10% of our patients. Most patients settle with 2–3 sittings of bronchoscopic dilatations.

Rarely, patients require additional procedures such as mitomycin injections with or without cryo-ablation of excessive granulation at the anastomotic site.

In our series, 1% of patients required additional bronchoscopic intervention [Figure 20], [Figure 21], [Figure 22].
Figure 20: Computed tomography of the chest showing right bronchial stenosis after 2 months postlung transplant

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Figure 21: Reconstructed image showing right bronchial stenosis 3 months after lung transplantation which was managed with balloon bronchoplasty

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Figure 22: Bronchoscopic image showing partial anastomotic dehiscence in a lung transplantation patient after 30 days of positive pressure ventilation

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Airway dehiscence

Dehiscence is a rare airway complication of transplantation. Dehiscence may be of two types: partial and complete dehiscence. Partial dehiscence involving less than one-third of the circumference can usually be manage conservatively – providing there is no pneumothorax, breathlessness, or clinical deterioration. In our group of LT patients, 5% developed dehiscence. Among those patients, only 2% of LT patients required intervention like self-expanding metallic stent insertion others were improved with conservative management [Figure 23] and [Figure 24]. Dehiscence and infection are seen earlier in the postoperative period (1 week-2 months), whereas stenosis and bronchomalacia are seen later at 2–4 months postprocedure. The key factors predisposing to airway-related complications include donor bronchus ischemia caused by disruption of native bronchial circulation, followed by recurrent rejection and infection.
Figure 23: Chest X-ray showing the presence of bilateral self-expanding metallic stent for bronchial dehiscence following lung transplantation

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Figure 24: Reconstructed image showing left bronchial stenosis 8 months after lung transplantation which was managed with balloon bronchoplasty

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  Chronic Rejection Top

Chronic rejection is the main factor limiting long-term survival after LT. It affects about 45% of patients who survive 5 years or more and is responsible for around 57% of the deaths occurring after the 1st year of LT. Chronic rejection usually begins 6 months after LT. There are two types of chronic allograft dysfunction (CLAD). Bronchiolitis obliterans syndrome (BOS) accounts for approximately 74% of all cases of CLAD; around 48% of lung transplant patients have this disorder within 5 years of transplant.[15] BOS is characterized by irreversible small airway obstruction secondary to fibrosis that results in an obstructive physiologic profile. PGD, AR, human leukocyte antigen mismatching, CMV pneumonitis, aspiration, bacterial pneumonia, and noncompliance to medication are the common risk factors involved in the pathogenesis of BOS.[16] Posttransplant spirometry shows an obstructive pattern. Progressive decline in forced expiratory volume in 1 s corresponds to severe stages of BOS and correlates with prognosis.[17] The utility of high-resolution CT (HRCT) for diagnosing BOS without clinical manifestations is limited; in HRCT, mosaic perfusion, bronchiectasis, and bronchial wall thickening are used to diagnose BOS in the absence of spirometric findings. In our LT group, 30% of patients had BOS [Figure 25]. Restrictive allograft syndrome (RAS) is the second most common form of irreversible CLAD. The prognosis compared with that of BOS is grim; HRCT features include volume loss resulting in hilar retraction and traction bronchiectasis and bronchiolectasis.[18] In our experience, 10% of our LT group developed RAS in 3–5 years of transplant [Figure 26] and [Figure 27].
Figure 25: High-resolution computed tomography showing features bronchiectasis and bronchial wall thickening in heart-lung transplantation patient. Spirometry was suggestive of Bronchioloitis obliterans syndrome

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Figure 26: Chest X-ray showing features of chronic rejection – restrictive allograft syndrome in a patient 4 years after heart-lung transplantation. There is with evidence of right lung volume loss with tracheal shift and hilar retraction

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Figure 27: Computed tomography chest showing right lung volume loss with fibrosis and bronchiectasis and fibrotic bands in the left upper lobe

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  Vascular Complications Top

Vascular anastomotic complications are uncommon and include pulmonary artery and vein stenosis, pulmonary embolism, and pulmonary infarction. The risk of infarction could be due to the insufficient bronchial arterial supply in the early postoperative period and because of fewer available types of collateral. In our LT group, we found pulmonary embolism in 5% of patients [Figure 28].
Figure 28: Computed tomography chest of postlung transplant patient showing right segmental pulmonary embolism

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  Conclusion Top

Radiological imaging plays a crucial role in the diagnosis and management of complications following LT. Familiarity with radiological appearances helps in the management of the transplant patient. Correlation of the clinical and radiological features in relation to time course since transplantation immensely helps in narrowing the differential diagnosis.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Sunder T, Ramesh PT, Kuppuswamy MK, Chaudhary SK, Hote MP, Devagourou V, et al. Lung Transplantation: The Indian experience and suggested guidelines Part II A: The technique of lung transplantation. J Pract Cardiovasc Sci 2020;6:278-91.  Back to cited text no. 1
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Mason DP, Batizy LH, Wu J, Nowicki ER, Murthy SC, McNeill AM, et al. Matching donor to recipient in lung transplantation: How much does size matter? J Thorac Cardiovasc Surg 2009;137:1234-40.  Back to cited text no. 2
Snell GI, Yusen RD, Weill D, Strueber M, Garrity E, Reed A, et al. Report of the ISHLT Working Group on Primary Lung Graft Dysfunction, part I: Definition and grading – A 2016 consensus group statement of the international society for heart and lung transplantation. J Hear Lung Transplant 2017;36:1097-103.  Back to cited text no. 3
de Perrot M, Liu M, Waddell TK, Keshavjee S. Ischemia-reperfusion-induced lung injury. Am J Respir Crit Care Med 2003;167:490-511.  Back to cited text no. 4
Fischer S, Bohn D, Rycus P, Pierre AF, de Perrot M, Waddell TK, et al. Extracorporeal membrane oxygenation for primary graft dysfunction after lung transplantation: Analysis of the Extracorporeal Life Support Organization (ELSO) registry. J Hear Lung Transplant 2007;26:472-7.  Back to cited text no. 5
Martinu T, Chen DF, Palmer SM. Acute rejection and humoral sensitization in lung transplant recipients. Proc Am Thorac Soc 2009;6:54-65.  Back to cited text no. 6
Levine DJ, Glanville AR, Aboyoun C, Belperio J, Benden C, Berry GJ, et al. Antibody-mediated rejection of the lung: A consensus report of the International Society for Heart and Lung Transplantation. J Hear Lung Transplant 2016;35:397-406.  Back to cited text no. 7
Berry G, Burke M, Andersen C, Angelini A, Bruneval P, Calabrese F, et al. Pathology of pulmonary antibody-mediated rejection: 2012 update from the Pathology Council of the ISHLT. J Hear Lung Transplant 2013;32:14-21.  Back to cited text no. 8
Ferrer J, Roldan J, Roman A, Bravo C, Monforte V, Pallissa E, et al. Acute and chronic pleural complications in lung transplantation. J Heart Lung Transplant 2003;22:1217-25.  Back to cited text no. 9
Diez Martinez P, Pakkal M, Prenovault J, Chevriera M, Chalaouia J, Gorgosa A, et al. Pictorial essay Postoperative imaging after lung transplantation ☆. J Clin Imaging 2013;37:617-23.  Back to cited text no. 10
Collins J, Muller NL, Kazerooni EA, Paciocco G. CT findings of pneumonia after lung transplantation. Am J Roentgenol 2000;175:811-8.  Back to cited text no. 11
Krishnam MS, Suh RD, Tomasian A, Goldin JG, Lai C, Brown K, et al. Postoperative complications of lung transplantation: RadioLogic findings along a time continuum. Radiographics 2007;27:957-74.  Back to cited text no. 12
Ng YL, Paul N, Patsios D, Walsham A, Chung TB, Keshavjee S, et al. Imaging of lung transplantation: Review. Am J Roentgenol 2009;192 Suppl 3:S1-13.  Back to cited text no. 13
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.  Back to cited text no. 14
Bando K, Paradis IL, Similo S, Konishi H, Komatsu K, Zullo TG, et al. Obliterative bronchiolitis after lung and heart-lung transplantation. An analysis of risk factors and management. J Thorac Cardiovasc Surg 1995;110:4-14.  Back to cited text no. 15
Husain AN, Siddiqui MT, Holmes EW, Chandrasekhar AJ, McCabe M, Radvany R, et al. Analysis of risk factors for the development of bronchiolitis obliterans syndrome. Am J Respir Crit Care Med 1999;159:829-33.  Back to cited text no. 16
Girgis RE, Tu I, Berry GJ, Reichenspurner H, Valentine VG, Conte JV, et al. Risk factors for the development of obliterative bronchiolitis after lung transplantation. J Heart Lung Transplant 1996;15:1200-8.  Back to cited text no. 17
Heng D, Sharples LD, McNeil K, Stewart S, Wreghitt T, Wallwork J. Bronchiolitis obliterans syndrome: Incidence, natural history, prognosis, and risk factors. J Heart Lung Transplant 1998;17:1255-63.  Back to cited text no. 18


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18], [Figure 19], [Figure 20], [Figure 21], [Figure 22], [Figure 23], [Figure 24], [Figure 25], [Figure 26], [Figure 27], [Figure 28]

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Primary Graft Dy...
Acute Rejection
Pleural Compl...
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Chronic Rejection
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