DIAGNOSTIC IMAGING IN HEMATOLOGY
AJH Educational Material
A JH
Dysfunctional neobladder causing pulmonary toxicity after combination chemotherapy for lymphoma Ramya Thota,1* Chirayu Shah,2 Travis Richardson,3 and Mark Koury1
Figure 1. A: Axial CT done as a part of the initial diagnostic FDG PET-CT shows small bilateral pleural effusions and relatively normal lung parenchyma. B: Follow-up CT after second episode of hypoxia shows bilateral ground glass opacities, interlobular septal thickening, architectural distortion, and bronchiectasis with associated increased FDG uptake (not shown). C, D: PET-CT fusion and CT images demonstrate retained FDG containing urine in the neobladder despite the presence of a Foley catheter (arrow in D). [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
A 75-year-old man with transitional cell bladder carcinoma status post cystoprostatectomy with neobladder creation from the sigmoid colon was diagnosed with Stage IVA diffuse large B-cell lymphoma involving the kidney in an evaluation for acute-on-chronic renal failure. A [18F] fluorodeoxyglucose positron emission tomography (FDG-PET) and computed tomography (CT) scan at presentation revealed lymphadenopathy above and below the diaphragm. Bone marrow biopsy showed no lymphoma. Worsening renal failure from lymphadenopathy prompted treatment of his lymphoma. Due to Stage IV chronic kidney disease and cardiac ejection fraction of 38%, he received renal-dose adjusted cyclophosphamide, etoposide, vincristine, rituximab, and prednisone (R-CEOP). He received a total of 2 L IV fluid volume with his chemotherapy. His usual chronic in-dwelling Foley catheter was in place before, during, and after chemotherapy. On Day 5 of chemotherapy, he developed gross hemoptysis, hypoxia, and diffuse bilateral rales. Hemoglobin decreased from 10.8 g/dL to 6.3 g/dL with normal platelets and coagulation panel. Infection evaluation was negative. A CT scan demonstrated bilateral ground glass opacities. He was diagnosed with diffuse alveolar hemorrhage 1
Division of Hematology-Oncology, Vanderbilt University School of Medicine, Nashville, Tennessee; 2Department of Radiology, Vanderbilt University Medical Center, Nashville, Tennessee; 3Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee
Conflict of interest: Nothing to report. *Correspondence to: Ramya Thota, Clinical Fellow, Division of Hematology-Oncology, Vanderbilt University School of Medicine, 777 Preston Research Building/2220 Pierce Ave, Nashville, TN 37232-6307. E-mail: [email protected] Received for publication: 12 January 2015; Accepted: 15 January 2015 Am. J. Hematol. 90:468–469, 2015. Published online: 22 January 2015 in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/ajh.23951 C 2015 Wiley Periodicals, Inc. V
468
American Journal of Hematology, Vol. 90, No. 5, May 2015
doi:10.1002/ajh.23951
DIAGNOSTIC IMAGING IN HEMATOLOGY
Chemotherapy-Induced Pulmonary Toxicity
and treated with supportive care. He improved slowly with complete resolution of all symptoms prior to his second cycle of chemotherapy. However, on Day 2 of the second cycle, he developed chest pain with hemoptysis and hypoxia. A FDG PET-CT scan performed to evaluate response to treatment after second cycle showed bilateral ground glass opacities, interlobular septal thickening, architectural distortion, and bronchiectasis with associated increased FDG uptake (Fig. 1B). Given that these lung findings were not apparent on FDG PET-CT done prior to the treatment (Fig. 1A), they were highly suspicious for chemotherapy-induced pulmonary toxicity. Interestingly, despite having a Foley catheter in place, he had abnormal emptying of the neobladder as evidenced by retention of FDG avid urine in the neobladder (Fig. 1C,D). This finding was not evident on the initial FDG PET-CT. This case highlights the importance of closely monitoring patients with neobladders and indwelling Foley catheters prior to,
䊏 References
1. Rosenow EC III, Limper AH. Drug-induced pulmonary disease. Semin Respir Infect 1995;10:86– 95. 2. Ramu K, Perry CS, Ahmed T, et al. Studies on the basis for the toxicity of acrolein mercapturates. Toxicol Appl Pharmacol 1996;140:487–498. 3. Dajczman E, Srolovitz H, Kreisman H, et al. Fatal pulmonary toxicity following oral etoposide therapy. Lung Cancer 1995;12:81–86.
doi:10.1002/ajh.23951
during, and after the administration of chemotherapy. Cyclophosphamide and etoposide are commonly used to treat hematological malignancies. Acute lung injury related to these agents is rare [1]. The active metabolites of cyclophosphamide, such as acrolein, were reported to induce pulmonary toxicity [2]. The pathogenesis of cyclophosphamide- or etoposide-induced lung injury is unclear, but a few case reports suggest favorable responses to corticosteroids [3–7]. However, this patient received prednisone as part of the chemotherapy. Delayed clearance due to absorption of drugs or their metabolites from the urine via a dysfunctional neobladder may lead to serious toxicity. Additionally, in patients with improper emptying of the neobladder, continuous irrigation during chemotherapy administration has been recommended to prevent toxicity [8]. In the appropriate clinical setting, patients should be screened for proper neobladder drainage prior to the initiation of chemotherapy.
4. Hamada K, Nagai S, Kitaichi M, et al. Cyclophosphamide-induced late-onset lung disease. Intern Med 2003;42:82–87. 5. Hatakeyama S, Tachibana A, Morita M, et al. Etoposide-induced pneumonitis. Nihon Kyobu Shikkan Gakkai Zasshi 1997;35:210–214. 6. Patel JM. Metabolism and pulmonary toxicity of cyclophosphamide. Pharmacol Ther 1990;47:137– 146. 7. Araki N, Matsumoto K, Ikuta N, et al. A case of drug induced pneumonitis caused by oral etopo-
side. Nihon Kyobu Shikkan Gakkai Zasshi 1993; 31:903–907. 8. Broderick GA, Stone AR, deVere White R. Neobladders: Clinical management and considerations for patients receiving chemotherapy. Semin Oncol 1990;17:598–605.
American Journal of Hematology, Vol. 90, No. 5, May 2015
469
AJH Educational Material
A JH
Dysfunctional neobladder causing pulmonary toxicity after combination chemotherapy for lymphoma Ramya Thota,1* Chirayu Shah,2 Travis Richardson,3 and Mark Koury1
Figure 1. A: Axial CT done as a part of the initial diagnostic FDG PET-CT shows small bilateral pleural effusions and relatively normal lung parenchyma. B: Follow-up CT after second episode of hypoxia shows bilateral ground glass opacities, interlobular septal thickening, architectural distortion, and bronchiectasis with associated increased FDG uptake (not shown). C, D: PET-CT fusion and CT images demonstrate retained FDG containing urine in the neobladder despite the presence of a Foley catheter (arrow in D). [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
A 75-year-old man with transitional cell bladder carcinoma status post cystoprostatectomy with neobladder creation from the sigmoid colon was diagnosed with Stage IVA diffuse large B-cell lymphoma involving the kidney in an evaluation for acute-on-chronic renal failure. A [18F] fluorodeoxyglucose positron emission tomography (FDG-PET) and computed tomography (CT) scan at presentation revealed lymphadenopathy above and below the diaphragm. Bone marrow biopsy showed no lymphoma. Worsening renal failure from lymphadenopathy prompted treatment of his lymphoma. Due to Stage IV chronic kidney disease and cardiac ejection fraction of 38%, he received renal-dose adjusted cyclophosphamide, etoposide, vincristine, rituximab, and prednisone (R-CEOP). He received a total of 2 L IV fluid volume with his chemotherapy. His usual chronic in-dwelling Foley catheter was in place before, during, and after chemotherapy. On Day 5 of chemotherapy, he developed gross hemoptysis, hypoxia, and diffuse bilateral rales. Hemoglobin decreased from 10.8 g/dL to 6.3 g/dL with normal platelets and coagulation panel. Infection evaluation was negative. A CT scan demonstrated bilateral ground glass opacities. He was diagnosed with diffuse alveolar hemorrhage 1
Division of Hematology-Oncology, Vanderbilt University School of Medicine, Nashville, Tennessee; 2Department of Radiology, Vanderbilt University Medical Center, Nashville, Tennessee; 3Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee
Conflict of interest: Nothing to report. *Correspondence to: Ramya Thota, Clinical Fellow, Division of Hematology-Oncology, Vanderbilt University School of Medicine, 777 Preston Research Building/2220 Pierce Ave, Nashville, TN 37232-6307. E-mail: [email protected] Received for publication: 12 January 2015; Accepted: 15 January 2015 Am. J. Hematol. 90:468–469, 2015. Published online: 22 January 2015 in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/ajh.23951 C 2015 Wiley Periodicals, Inc. V
468
American Journal of Hematology, Vol. 90, No. 5, May 2015
doi:10.1002/ajh.23951
DIAGNOSTIC IMAGING IN HEMATOLOGY
Chemotherapy-Induced Pulmonary Toxicity
and treated with supportive care. He improved slowly with complete resolution of all symptoms prior to his second cycle of chemotherapy. However, on Day 2 of the second cycle, he developed chest pain with hemoptysis and hypoxia. A FDG PET-CT scan performed to evaluate response to treatment after second cycle showed bilateral ground glass opacities, interlobular septal thickening, architectural distortion, and bronchiectasis with associated increased FDG uptake (Fig. 1B). Given that these lung findings were not apparent on FDG PET-CT done prior to the treatment (Fig. 1A), they were highly suspicious for chemotherapy-induced pulmonary toxicity. Interestingly, despite having a Foley catheter in place, he had abnormal emptying of the neobladder as evidenced by retention of FDG avid urine in the neobladder (Fig. 1C,D). This finding was not evident on the initial FDG PET-CT. This case highlights the importance of closely monitoring patients with neobladders and indwelling Foley catheters prior to,
䊏 References
1. Rosenow EC III, Limper AH. Drug-induced pulmonary disease. Semin Respir Infect 1995;10:86– 95. 2. Ramu K, Perry CS, Ahmed T, et al. Studies on the basis for the toxicity of acrolein mercapturates. Toxicol Appl Pharmacol 1996;140:487–498. 3. Dajczman E, Srolovitz H, Kreisman H, et al. Fatal pulmonary toxicity following oral etoposide therapy. Lung Cancer 1995;12:81–86.
doi:10.1002/ajh.23951
during, and after the administration of chemotherapy. Cyclophosphamide and etoposide are commonly used to treat hematological malignancies. Acute lung injury related to these agents is rare [1]. The active metabolites of cyclophosphamide, such as acrolein, were reported to induce pulmonary toxicity [2]. The pathogenesis of cyclophosphamide- or etoposide-induced lung injury is unclear, but a few case reports suggest favorable responses to corticosteroids [3–7]. However, this patient received prednisone as part of the chemotherapy. Delayed clearance due to absorption of drugs or their metabolites from the urine via a dysfunctional neobladder may lead to serious toxicity. Additionally, in patients with improper emptying of the neobladder, continuous irrigation during chemotherapy administration has been recommended to prevent toxicity [8]. In the appropriate clinical setting, patients should be screened for proper neobladder drainage prior to the initiation of chemotherapy.
4. Hamada K, Nagai S, Kitaichi M, et al. Cyclophosphamide-induced late-onset lung disease. Intern Med 2003;42:82–87. 5. Hatakeyama S, Tachibana A, Morita M, et al. Etoposide-induced pneumonitis. Nihon Kyobu Shikkan Gakkai Zasshi 1997;35:210–214. 6. Patel JM. Metabolism and pulmonary toxicity of cyclophosphamide. Pharmacol Ther 1990;47:137– 146. 7. Araki N, Matsumoto K, Ikuta N, et al. A case of drug induced pneumonitis caused by oral etopo-
side. Nihon Kyobu Shikkan Gakkai Zasshi 1993; 31:903–907. 8. Broderick GA, Stone AR, deVere White R. Neobladders: Clinical management and considerations for patients receiving chemotherapy. Semin Oncol 1990;17:598–605.
American Journal of Hematology, Vol. 90, No. 5, May 2015
469
