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Case report: Delayed radiation pneumonitis induced by chemotherapy
Clinical Radiology (1997) 52, 720-723
Case Report: Delayed Radiation Pneumonitis Induced by Chemotherapy L. T. SOH, W. H. KOO and P. T. ANG Radiation recall is recurrence of the acute toxicity reaction at a previously irradiated site associated with the administration of chemotherapeutic agents. It is thought to be a delayed form of radiosensitization. A 34-year-old woman had mediastinal radiation following debulking surgery for an undifferentiated mediastinal carcinoma. Six weeks later, she had cisplatin/ifosfamide therapy for symptomatic progressive disease. Within 48 h after initiation of chemotherapy, she developed acute breathlessness and cough. Radiological features of a massive pneumonitis in the fields of prior radiation were demonstrated on plain chest X-ray and computed tomography (CT). The rapid resolution of the radiation recall mediastinitis/pneumonitis to steroid therapy was documented on sequential radiological follow-up. Cancer therapy involves surgery, radiation and chemotherapy either alone or in combination. It is not uncommon for previously irradiated patients to receive chemotherapy at some stage in the disease. In patients who have been irradiated previously, it has been reported [1-4] that the administration of chemotherapy can precipitate a reaction in the previously radiated site. This phenomenon is called radiation recall. It is a double-edged sword and can lead to useful potentiation of radiation or unwanted side effects. We report here a case of radiation-recall pneumonitis which is precipitated by cisplatin and ifosfamide combination chemotherapy.
Fig. 1 - CT scan thorax just prior to radiotherapy which showed the mediastinal recurrence.
CASE REPORT The patient was a 34-year-old woman who presented with cough of 4 to 5 months duration. Chest radiograph showed a left pleural effusion. In addition, chest CT showed enlarged lower neck and mediastinal lymph nodes and consolidation of the left lower lobe. Pleural fluid cytology and bronchoscopy did not show evidence of malignancy. She underwent a thoracoscopic exploration of the mediastinal nodes and histology revealed undifferentiated carcinoma. Serum alpha-fetoprotein and human-chorionic gonadotrophin levels were normal. CT of the abdomen and a radionuclide bone scan were normal. She was given four cycles of PEB chemotherapy (IV cisplatin 20 mg/m2 daily for 5 days, IV etoposide 100 mg/m2 daily for 5 days and IV bleomycin 15 u/m 2 on days 1, 8 and 15) with symptomatic improvement. CT scans documented a good partial response and the patient subsequently underwent debulking surgery. Postoperatively, she received mediastinal RT for 5 weeks. The chest CT done just before the radiotherapy showed mediastinal recurrence (Fig. 1). With radiotherapy, the mediastinal lesion regressed completely but she developed new pulmonary lesions (Fig. 2) and bony metastases. Hence, 6 weeks after the completion of radiation, she was given palliative chemotherapy consisting of IV ifusfamide 2 g / m z daily for 5 days and cisplatin 100mg/m2 for 1 day. The CXR (Fig. 3a) done 1 week prior to the chemotherapy appeared normal and the CT scan of the thorax showed pleural thickening (Fig. 4a). On day 3 of the chemotherapy, she developed high fever and complained of breathlessness and chest 'flutter'. The electrocardiogram was normal. The chest radiograph (Fig. 3b) and CT scan of the thorax (Fig. 4b) showed widening of the mediastinum with pulmonary infiltrates in both upper lobes. Interestingly, the CT scan demonstrated the lateral borders of the widened mediastinum to be straight which was consistent with the diagnosis of radiation recall pneumonitis. She was given IV dexamethasone 4 mg 8H and antibiotics. Within 24 h, her symptoms improved and the CXR (Fig. 3c) and CT scan of the thorax Correspondence to: Dr L. T. Soh, Department of Medical Oncology, Singapore General Hospital, Outram Road, Singapore 0316.
Fig. 2 - CT scan thorax post-mediastinal radiotherapy which showed regression of the mediastinal recurrence but development of new pulmonary lesions.
(Fig. 4c) done 3 days later showed complete resolution of the mediastinitis and pneumonitis.
DISCUSSION Augmentation of radiation reactions by the concurrent administration of chemotherapy is a well-recognized phenomenon. Radiation reactions can also occur when the administration of a chemotherapeutic agent precipitates radiation tissue reaction within the previously irradiated ports [1-4]. The latter is known as radiation recall which was first described with D-actinomycin in 1959 [1,5,6]. It commonly occurs with drugs such as D-actinomycin or doxorubicin [1,2,5,6]. Other drugs which have been implicated include trimetrexate [7], bleomycin [8], etoposide [8], vinblastine [91, melphalan [10], tamoxifen [11] and taxol [12,13]. In this patient, the recall was precipitated by either of the two drugs, cisplatin or ifosfamide which has not been reported in the literature. The mechanism is unknown. It has been postulated to be © 1997 The Royal College of Radiologists, Clinical Radiology, 52, 715-724.
CASE REPORTS
721
(a)
(c)
(b)
Fig. 3 - (a) Chest radiograph prior to chemotherapy. (b) Chest radiograph on day 3 of the chemotherapy showing widening of the mediastinum with pulmonary infiltrate. (c) Chest radiograph 3 days after discontinuation of the chemotherapy showing complete resolution of the mediastinitis and pneumonitis.
due to the inhibition of the post-radiation cellular recovery. The ability of any tissue to recover from sublethal radiation injury depends on the capacity of the cells to repair the DNA strands breaks caused by the radiation. When given during the post-radiation period, the chemotherapeutic agent impairs the recovery process in the irradiated cells. Recall has also been described in an AIDS (acquired immune deficiency syndrome) patient who had significant immunosuppression and whose CD4 lymphocytes count
was 30 cells//zl [9]. This suggests that the tissue response is not a lymphocyte-mediated event. In Cassady's report [14], the onset of the recall appears to be dose-related. In his patient, the recall did not occur with 39 mg/m 2 of adriamycin but occurred with the 75 mg/m 2 dose. Keith reported increasing risk of recall with higher radiation dose [8]. Recall can occur within hours to days after administration of the cytotoxic drugs. Its relation to the radiation ranges from a few days to many years after the radiotherapy.
© 1997 The Royal College of Radiologists, Clinical Radiology, 52, 715-724.
722
CLINICAL RADIOLOGY
(a)
Burdon [15] described a case which occurred 15 years after the radiation. The commonest site of involvement is the skin manifesting as erythema or painful vesicles [16]. In severe cases, necrosis with persistent painful ulcerations can occur. Severity of the recall reaction is probably related to the dosage of the radiation and the drug. Other factors include individual susceptibility, nutrition and the timing of the administration of the drug relative to the radiation therapy [17-18]. Less frequently, but not uncommonly, pneumonitis secondary to radiation recall can occur [3,19-20], as in this patient. Other sites of involvement which have been reported include the oesophagus [4,14], cardiac [21] and intestine [22]. Steroid appears to be effective both as treatment as well as prophylaxis [3]. In this patient, her symptoms resolved within 24h after instituting the steroid therapy. In McInemey's report [3], the recall did not recur with subsequent administration of the cytotoxic drug under steroid cover. The mechanism is unknown but in animal study, the corticosteroid acts by increasing the lung compliance in rats [23].
REFERENCES
(g)
(c) Fig. 4 - (a) CT scan thorax prior to chemotherapy showing pleural thickening adjacent to the mediastinum. (b) CT scan thorax on day 3 of chemotherapy showing mediastinal widening with pulmonary infiltrates. (c) CT scan ihorax 4 days after discontinuation of chemotherapy showing complete resolution of the mediastinitis and pneumonitis.
1 D'Angio GJ, FaDer S, Maddock CL. Potentiation of X-ray effects by actinomycin D. Radiology 1959;73:175. 2 Wang JJ, Cortes E, Sinks LF, Holland JF. Therapeutic effect and toxicity of adriamycin in patients with neoplastic disease. Cancer 1971;28:837-843. 3 McInemey DP. Reactivation of radiation pneumonitis by adriamycin. British Journal of Radiology 1977;50:224-227. 4 Greco FA, Brereton HD, Kent H et al. Adriamycin and enhanced radiation reaction in normal esophagus and skin. Annals of International Medicine 1976;85:294-298. 5 PinkleD'Actin°mycinDinchildh°°dcancer'Pediatrics 1959;23:342347. 6 Tan C, Dargeon HW, Burchenal JH. The effects of actinomycin D on cancer in childhood. Pediatrics 1959;24:544. 7 Weiss RB, James WD, Major WB et aL Skin reaction induced by trimetrexate, an analog of methotrexate. Investigative New Drugs 1986;4:159-163. 8 Stelzer KJ, Griffin TW, Koh WJ. Radiation recall skin toxicity with bleomycin in a patient with Kaposi sarcoma related to acquired immune deficiency syndrome. Cancer 1993;71:1322-1325. 9 Nemechek PM, Corder MC. Radiation recall associated with vinblastine in a patient treated for Kaposi sarcoma related to acquired immune deficiency syndrome. Cancer 1992;70:1605-1606. 10 Kellie SJ, Plowman PN, Malpas JS. Radiation recall and radiosensitisation with alkylating agents. Lancet 1987;1:1149-1150. 11 Parry BR. Radiation recall induced by tamoxifen. Lancet 1992;340:49. 12 Raghavan VT, Bloomer WD, Merkel DE. Taxol and radiation recall dermatitis. Lancet 1993;341:1354. 13 Seilman A, Crown J, Reichman B e t al. Lack of clinical cross resistance of taxol (T) with anthracycline (A) in the treatment of metastatic breast cancer (MBC). Proceedings of the American Society of Clinical Oncology 1993;12:A53. 14 Cassady JR, Richter MP, Pitt AJ, Jaffe N. Radiation-adriamycin interactions: prefiminary clinical observations. Cancer 1975;36:946-949. 15 Burdon J, Bell R, Sullivan J, Henderson M. Adriamycin-induced recall phenomenon 15 years after radiotherapy. Journal of the American Medical Association 1978;239:931. 16 Wang JJ, Cortes E, Sinks LF, Holland JF. Therapeutic effect and toxicity of adriamycin in patients with neoplastic disease. Cancer 1971 ;28:837-843. 17 Philips TL, Fu KK. Quantification of combined radiation therapy and chemotherapy effects on critical normal tissues.-Cancer 1976;37:11861200. 18 Vallejo A, McCormick B, Wittes R et al. Combined therapy effect on normal tissue in the head and neck region. Frontiers of Radiation Therapy and Oncology 1979;13:48-55. 19 Ma LD, Taylor GA, Wharam MD, Wiley JM. Recall pneumonitis: adriamycin potentiation of radiation pneumonitis in two children. Radiology 1993;187:465-467. 20 McInerey DPP, Bullimore J. Reactivation of radiation pneumonitis by adriamycin. British Journal of Radiol 1977;50:224-227. 21 Guaglianone P, Chan K, Hanisch R et al. Phase I clinical trial of © 1997 The Royal College of Radiologists, Clinical Radiology, 52, 715-724.
CaSE P.EPORTS liposomal daunorubicin (Dannoxome) in advanced malignancies. Proceedings of the American Society of Clinical Oncology 1992;11 :A361. 22 Stein RS. Radiation recall enteritis after actinomycin D and adriamycin. Southern Medical Journal 1976;71:960-961.
723
23 Moss WT, Haddy FJ, Sweany SK. Some factors altering the severity of acute radiation pneumonitis; variation with cortisone, heparin and antibiotics. Radiology 1966;75:50-54.
Clinical Radiology (1997) 52, 723-724
Case Report: Demonstration of a Potentially Fatal Complication of Pacing B. M. FOX*, N. J. RING* and A. J. MARSHALL
Department of *Radiology and Cardiology, Derriford Hospital, Plymouth, UK The authors report a rare case of atrial pacing lead retention wire separation, describing an example of the recently
Abnormal hinge
Fracture and perforation
Fracture and lifting
Separation and tenting
publicized problems with the 'Accufix' atrial J pacing lead. A Hazard Notice has recently been issued pertaining to the Telectronics 'Accufix Atrial J Pacemaker Leads' models 330/801 and 329/701. Detection of the relevant complication will usually depend on demonstration of a radiographic abnormality. Essentially the problem is that the 'Atrial J' retention wire fractures and in some cases part of the wire may then migrate through the polyurethane coating (Fig. 1) [1]. In two cases this has resulted in patient death from wire migration through the atrial appendage into the aorta, and in two cases cardiac tamponade has occurred but this has been treated surgically. In five cases fractured wires have been found incidentally at surgery or when the pacing wire was being removed. There are a further four cases with reported positive X-ray findings [2].
<#
Perforation and almost complete separation
Fracture and complete separation
Fig. 1 - Possible appearances of Atrial J wire fracture and perforation of polyurethane coat [1]. Correspondence to: Dr N. J, Ring, Imaging Directorate, Derriford Hospital, Derriford Road, Plymouth PL6 8D4, UK. © 1997 The Royal College of Radiologists, ClinicalRadiology, 52, 715-724.
Fig. 2 - PA chest film demonstrating Atrial J wire lead in intact form.
Case Report: Delayed Radiation Pneumonitis Induced by Chemotherapy L. T. SOH, W. H. KOO and P. T. ANG Radiation recall is recurrence of the acute toxicity reaction at a previously irradiated site associated with the administration of chemotherapeutic agents. It is thought to be a delayed form of radiosensitization. A 34-year-old woman had mediastinal radiation following debulking surgery for an undifferentiated mediastinal carcinoma. Six weeks later, she had cisplatin/ifosfamide therapy for symptomatic progressive disease. Within 48 h after initiation of chemotherapy, she developed acute breathlessness and cough. Radiological features of a massive pneumonitis in the fields of prior radiation were demonstrated on plain chest X-ray and computed tomography (CT). The rapid resolution of the radiation recall mediastinitis/pneumonitis to steroid therapy was documented on sequential radiological follow-up. Cancer therapy involves surgery, radiation and chemotherapy either alone or in combination. It is not uncommon for previously irradiated patients to receive chemotherapy at some stage in the disease. In patients who have been irradiated previously, it has been reported [1-4] that the administration of chemotherapy can precipitate a reaction in the previously radiated site. This phenomenon is called radiation recall. It is a double-edged sword and can lead to useful potentiation of radiation or unwanted side effects. We report here a case of radiation-recall pneumonitis which is precipitated by cisplatin and ifosfamide combination chemotherapy.
Fig. 1 - CT scan thorax just prior to radiotherapy which showed the mediastinal recurrence.
CASE REPORT The patient was a 34-year-old woman who presented with cough of 4 to 5 months duration. Chest radiograph showed a left pleural effusion. In addition, chest CT showed enlarged lower neck and mediastinal lymph nodes and consolidation of the left lower lobe. Pleural fluid cytology and bronchoscopy did not show evidence of malignancy. She underwent a thoracoscopic exploration of the mediastinal nodes and histology revealed undifferentiated carcinoma. Serum alpha-fetoprotein and human-chorionic gonadotrophin levels were normal. CT of the abdomen and a radionuclide bone scan were normal. She was given four cycles of PEB chemotherapy (IV cisplatin 20 mg/m2 daily for 5 days, IV etoposide 100 mg/m2 daily for 5 days and IV bleomycin 15 u/m 2 on days 1, 8 and 15) with symptomatic improvement. CT scans documented a good partial response and the patient subsequently underwent debulking surgery. Postoperatively, she received mediastinal RT for 5 weeks. The chest CT done just before the radiotherapy showed mediastinal recurrence (Fig. 1). With radiotherapy, the mediastinal lesion regressed completely but she developed new pulmonary lesions (Fig. 2) and bony metastases. Hence, 6 weeks after the completion of radiation, she was given palliative chemotherapy consisting of IV ifusfamide 2 g / m z daily for 5 days and cisplatin 100mg/m2 for 1 day. The CXR (Fig. 3a) done 1 week prior to the chemotherapy appeared normal and the CT scan of the thorax showed pleural thickening (Fig. 4a). On day 3 of the chemotherapy, she developed high fever and complained of breathlessness and chest 'flutter'. The electrocardiogram was normal. The chest radiograph (Fig. 3b) and CT scan of the thorax (Fig. 4b) showed widening of the mediastinum with pulmonary infiltrates in both upper lobes. Interestingly, the CT scan demonstrated the lateral borders of the widened mediastinum to be straight which was consistent with the diagnosis of radiation recall pneumonitis. She was given IV dexamethasone 4 mg 8H and antibiotics. Within 24 h, her symptoms improved and the CXR (Fig. 3c) and CT scan of the thorax Correspondence to: Dr L. T. Soh, Department of Medical Oncology, Singapore General Hospital, Outram Road, Singapore 0316.
Fig. 2 - CT scan thorax post-mediastinal radiotherapy which showed regression of the mediastinal recurrence but development of new pulmonary lesions.
(Fig. 4c) done 3 days later showed complete resolution of the mediastinitis and pneumonitis.
DISCUSSION Augmentation of radiation reactions by the concurrent administration of chemotherapy is a well-recognized phenomenon. Radiation reactions can also occur when the administration of a chemotherapeutic agent precipitates radiation tissue reaction within the previously irradiated ports [1-4]. The latter is known as radiation recall which was first described with D-actinomycin in 1959 [1,5,6]. It commonly occurs with drugs such as D-actinomycin or doxorubicin [1,2,5,6]. Other drugs which have been implicated include trimetrexate [7], bleomycin [8], etoposide [8], vinblastine [91, melphalan [10], tamoxifen [11] and taxol [12,13]. In this patient, the recall was precipitated by either of the two drugs, cisplatin or ifosfamide which has not been reported in the literature. The mechanism is unknown. It has been postulated to be © 1997 The Royal College of Radiologists, Clinical Radiology, 52, 715-724.
CASE REPORTS
721
(a)
(c)
(b)
Fig. 3 - (a) Chest radiograph prior to chemotherapy. (b) Chest radiograph on day 3 of the chemotherapy showing widening of the mediastinum with pulmonary infiltrate. (c) Chest radiograph 3 days after discontinuation of the chemotherapy showing complete resolution of the mediastinitis and pneumonitis.
due to the inhibition of the post-radiation cellular recovery. The ability of any tissue to recover from sublethal radiation injury depends on the capacity of the cells to repair the DNA strands breaks caused by the radiation. When given during the post-radiation period, the chemotherapeutic agent impairs the recovery process in the irradiated cells. Recall has also been described in an AIDS (acquired immune deficiency syndrome) patient who had significant immunosuppression and whose CD4 lymphocytes count
was 30 cells//zl [9]. This suggests that the tissue response is not a lymphocyte-mediated event. In Cassady's report [14], the onset of the recall appears to be dose-related. In his patient, the recall did not occur with 39 mg/m 2 of adriamycin but occurred with the 75 mg/m 2 dose. Keith reported increasing risk of recall with higher radiation dose [8]. Recall can occur within hours to days after administration of the cytotoxic drugs. Its relation to the radiation ranges from a few days to many years after the radiotherapy.
© 1997 The Royal College of Radiologists, Clinical Radiology, 52, 715-724.
722
CLINICAL RADIOLOGY
(a)
Burdon [15] described a case which occurred 15 years after the radiation. The commonest site of involvement is the skin manifesting as erythema or painful vesicles [16]. In severe cases, necrosis with persistent painful ulcerations can occur. Severity of the recall reaction is probably related to the dosage of the radiation and the drug. Other factors include individual susceptibility, nutrition and the timing of the administration of the drug relative to the radiation therapy [17-18]. Less frequently, but not uncommonly, pneumonitis secondary to radiation recall can occur [3,19-20], as in this patient. Other sites of involvement which have been reported include the oesophagus [4,14], cardiac [21] and intestine [22]. Steroid appears to be effective both as treatment as well as prophylaxis [3]. In this patient, her symptoms resolved within 24h after instituting the steroid therapy. In McInemey's report [3], the recall did not recur with subsequent administration of the cytotoxic drug under steroid cover. The mechanism is unknown but in animal study, the corticosteroid acts by increasing the lung compliance in rats [23].
REFERENCES
(g)
(c) Fig. 4 - (a) CT scan thorax prior to chemotherapy showing pleural thickening adjacent to the mediastinum. (b) CT scan thorax on day 3 of chemotherapy showing mediastinal widening with pulmonary infiltrates. (c) CT scan ihorax 4 days after discontinuation of chemotherapy showing complete resolution of the mediastinitis and pneumonitis.
1 D'Angio GJ, FaDer S, Maddock CL. Potentiation of X-ray effects by actinomycin D. Radiology 1959;73:175. 2 Wang JJ, Cortes E, Sinks LF, Holland JF. Therapeutic effect and toxicity of adriamycin in patients with neoplastic disease. Cancer 1971;28:837-843. 3 McInemey DP. Reactivation of radiation pneumonitis by adriamycin. British Journal of Radiology 1977;50:224-227. 4 Greco FA, Brereton HD, Kent H et al. Adriamycin and enhanced radiation reaction in normal esophagus and skin. Annals of International Medicine 1976;85:294-298. 5 PinkleD'Actin°mycinDinchildh°°dcancer'Pediatrics 1959;23:342347. 6 Tan C, Dargeon HW, Burchenal JH. The effects of actinomycin D on cancer in childhood. Pediatrics 1959;24:544. 7 Weiss RB, James WD, Major WB et aL Skin reaction induced by trimetrexate, an analog of methotrexate. Investigative New Drugs 1986;4:159-163. 8 Stelzer KJ, Griffin TW, Koh WJ. Radiation recall skin toxicity with bleomycin in a patient with Kaposi sarcoma related to acquired immune deficiency syndrome. Cancer 1993;71:1322-1325. 9 Nemechek PM, Corder MC. Radiation recall associated with vinblastine in a patient treated for Kaposi sarcoma related to acquired immune deficiency syndrome. Cancer 1992;70:1605-1606. 10 Kellie SJ, Plowman PN, Malpas JS. Radiation recall and radiosensitisation with alkylating agents. Lancet 1987;1:1149-1150. 11 Parry BR. Radiation recall induced by tamoxifen. Lancet 1992;340:49. 12 Raghavan VT, Bloomer WD, Merkel DE. Taxol and radiation recall dermatitis. Lancet 1993;341:1354. 13 Seilman A, Crown J, Reichman B e t al. Lack of clinical cross resistance of taxol (T) with anthracycline (A) in the treatment of metastatic breast cancer (MBC). Proceedings of the American Society of Clinical Oncology 1993;12:A53. 14 Cassady JR, Richter MP, Pitt AJ, Jaffe N. Radiation-adriamycin interactions: prefiminary clinical observations. Cancer 1975;36:946-949. 15 Burdon J, Bell R, Sullivan J, Henderson M. Adriamycin-induced recall phenomenon 15 years after radiotherapy. Journal of the American Medical Association 1978;239:931. 16 Wang JJ, Cortes E, Sinks LF, Holland JF. Therapeutic effect and toxicity of adriamycin in patients with neoplastic disease. Cancer 1971 ;28:837-843. 17 Philips TL, Fu KK. Quantification of combined radiation therapy and chemotherapy effects on critical normal tissues.-Cancer 1976;37:11861200. 18 Vallejo A, McCormick B, Wittes R et al. Combined therapy effect on normal tissue in the head and neck region. Frontiers of Radiation Therapy and Oncology 1979;13:48-55. 19 Ma LD, Taylor GA, Wharam MD, Wiley JM. Recall pneumonitis: adriamycin potentiation of radiation pneumonitis in two children. Radiology 1993;187:465-467. 20 McInerey DPP, Bullimore J. Reactivation of radiation pneumonitis by adriamycin. British Journal of Radiol 1977;50:224-227. 21 Guaglianone P, Chan K, Hanisch R et al. Phase I clinical trial of © 1997 The Royal College of Radiologists, Clinical Radiology, 52, 715-724.
CaSE P.EPORTS liposomal daunorubicin (Dannoxome) in advanced malignancies. Proceedings of the American Society of Clinical Oncology 1992;11 :A361. 22 Stein RS. Radiation recall enteritis after actinomycin D and adriamycin. Southern Medical Journal 1976;71:960-961.
723
23 Moss WT, Haddy FJ, Sweany SK. Some factors altering the severity of acute radiation pneumonitis; variation with cortisone, heparin and antibiotics. Radiology 1966;75:50-54.
Clinical Radiology (1997) 52, 723-724
Case Report: Demonstration of a Potentially Fatal Complication of Pacing B. M. FOX*, N. J. RING* and A. J. MARSHALL
Department of *Radiology and Cardiology, Derriford Hospital, Plymouth, UK The authors report a rare case of atrial pacing lead retention wire separation, describing an example of the recently
Abnormal hinge
Fracture and perforation
Fracture and lifting
Separation and tenting
publicized problems with the 'Accufix' atrial J pacing lead. A Hazard Notice has recently been issued pertaining to the Telectronics 'Accufix Atrial J Pacemaker Leads' models 330/801 and 329/701. Detection of the relevant complication will usually depend on demonstration of a radiographic abnormality. Essentially the problem is that the 'Atrial J' retention wire fractures and in some cases part of the wire may then migrate through the polyurethane coating (Fig. 1) [1]. In two cases this has resulted in patient death from wire migration through the atrial appendage into the aorta, and in two cases cardiac tamponade has occurred but this has been treated surgically. In five cases fractured wires have been found incidentally at surgery or when the pacing wire was being removed. There are a further four cases with reported positive X-ray findings [2].
<#
Perforation and almost complete separation
Fracture and complete separation
Fig. 1 - Possible appearances of Atrial J wire fracture and perforation of polyurethane coat [1]. Correspondence to: Dr N. J, Ring, Imaging Directorate, Derriford Hospital, Derriford Road, Plymouth PL6 8D4, UK. © 1997 The Royal College of Radiologists, ClinicalRadiology, 52, 715-724.
Fig. 2 - PA chest film demonstrating Atrial J wire lead in intact form.