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An unusual case of acute fatal pulmonary congestion: Oesophageal stenting
International Journal of Cardiology 117 (2007) e64 – e65 www.elsevier.com/locate/ijcard
Letter to the Editor
An unusual case of acute fatal pulmonary congestion: Oesophageal stenting Paolo Sganzerla a , Bruno Passaretti a,⁎, Elena Perlasca a , Alessandro Giovannelli b a
Division of Cardiology, Humanitas Gavazzeni, Bergamo, Italy b General Surgery, Humanitas Gavazzeni, Bergamo, Italy Received 22 September 2006; accepted 12 November 2006 Available online 22 February 2007
Abstract Extrinsic left atrial compression with consequent hemodynamic compromise has been described secondary to aortic aneurysm, huge gastroesophageal distension and neoplastic diseases involving mediastinum. Prompt correction of the primary pathology usually leads to reversal of hemodynamic alterations. We report the case of a lady, who, in order to treat a stenosis of the lower third of the oesophagus, underwent stenting with subsequent hemodynamic deterioration due to compression of the posterior left atrial wall disclosed by echocardiography. The sudden recovery of the oesophageal lumen at the expense of the left atrial volume with the impossibility of prompt removal of the stent led to a progressive and fatal deterioration of the hemodynamic picture. Stenting of the lower part of the oesophagus should be performed only when reciprocal anatomic relationship between heart and oesophagus itself is clearly elucidated and possibly well maintained. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Oesophageal stenting; Left atrial compression
Pulmonary vascular congestion is mainly due to systolic and/or diastolic dysfunction of the left ventricle; the increase in ventricular diastolic pressure is transmitted backward to the left atrium and the venous pulmonary circulation with consequent pulmonary edema. Mechanical obstacles to left atrial emptying, such as mitral valve stenosis, cor triatriatum or myxoma, are a less frequent cause of pulmonary engorgement and edema. Extrinsic compression of the left atrium is probably the most uncommon mechanism of hemodynamic compromise. Among mediastinal structures which have been described to determine left atrial compression [1–3], such as aortic aneurysm, carcinoma, bronchogenic cysts, and lymphoma, the upper gastrointestinal ones (stomach and oesophagus) deserve particular attention because of their strict anatomical contiguity and of their possibility for huge pathologic distension [2]; in this case, endoscopic or surgical treatment of the gastroesophageal
⁎ Corresponding author. E-mail address: [email protected] (B. Passaretti). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.11.132
disease generally allows the resolution of the cardiovascular picture. We report the case of a lady who underwent stenting to palliate an extrinsic oesophageal compression and suddenly developed an irreversible pulmonary edema despite maximal medical treatment. 1. Case report A 70-year-old hypertensive lady had, in august 2005, an intrapericardial, total left pneumonectomy with extensive mediastinal node removal for a spinocellular carcinoma of the lung. By March 2006, she began to complain of dysphagia and barium swallow disclosed a 7-cm-long stenosis of the lower third of the oesophagus due to an extrinsic compression of the lumen with normal overlying mucosa. The patient was cardiologically evaluated due to planned insertion of a stent under general anaesthesia. No signs of heart failure were detectable; the blood pressure, on usual pharmacological treatment, was normal and the echocardiogram showed normal left ventricular wall motion
P. Sganzerla et al. / International Journal of Cardiology 117 (2007) e64–e65
Fig. 1. Echocardiographic subcostal view showing compression of left atrium (LA) by esophageal stent (STENT). LV = left ventricle, Ao = aorta, PE = pericardial effusion.
and ejection fraction (0.59); the mitral inflow pattern was consistent with hypertension and patient's age; moderate pericardial effusion mainly located at the posterolateral surface of the heart without any hemodynamic influence on the right heart chambers was observed. Chest X-ray demonstrated a normal vascular pattern of the residual lung parenchyma. The endoscopic procedure was carried out uneventfully, but the day after, the patient became hypotensive, diaphoretic, and rapidly complained of increasing dyspnea, orthopnea with a clinical picture of typical pulmonary edema; transient rapid atrial fibrillation was recorded with no acute cardiac ischemic changes at EKG. Cardiac tamponade due to sudden increase in pericardial effusion was the working diagnosis. However, transthoracic echocardiogram showed neither change in pericardial effusion nor cardiac tamponade; confirmed a still normally sized and performing left ventricular cavity and disclosed a significant compression of the posterior left atrial wall exerted by a circular, hyperechoic structure, the oesophageal stent (Fig. 1); the outflow of pulmonary veins was not detectable due to anatomical changes related to previous pneumonectomy. Despite the maximal therapeutic support, the clinical picture rapidly declined and the patient died in cardiogenic shock. 2. Discussion Extrinsic compression of the left atrium is an uncommon clinical–pathological event. Among adjacent anatomical structures potentially involved, the thoracic aorta, stomach and oesophagus, through their sudden pathologic distension, are the ones that most likely can cause an acute encroachment or compression of the left atrial wall [1,2]. As in cardiac tamponade, where the velocity of effusion is physiologically more important than its pure amount, the potentially rapid increase in the volume of the aorta, the stomach and/or the oesophagus is of particular importance in the pathophysiology of atrial compression. Sudden interference with left atrial
e65
inflow determines direct impairment of left ventricular filling with decrease in cardiac output and pulmonary venous congestion causing functional tamponade. The clinical picture observed in our patient was consistent with hemodynamic alteration due to acute interference with atrial function. The concomitance of a pericardial effusion, clearly chronic and therefore not interfering with right heart chambers in baseline conditions, and the alteration of left ventricular diastolic compliance previously recorded, made our patient particularly vulnerable to acute changes in atrial function. Moreover, paroxysmal atrial fibrillation, on an extrinsic mechanical stimulation basis on the atrial wall [3], played a possible, significant adjunctive pathophysiological role. Although several types of complication can occur after oesophageal stenting [4,5], there is no report, to our knowledge, of clinically significant interference with cardiac structures. Anatomical relationship with the heart, limited to a small distal part of the oesophagus, can obviously play a consistent role. In case of stenting of the lower part, instantaneous recover of the normal oesophageal lumen must be accomplished by acute displacement of adjacent anatomical structures. The exact mechanism by which stenting impinged on the left atrium in our patient is not completely elucidated by our echocardiographic pictures. Factors involved could have been changes in anatomical relationship in mediastinum due to the previous surgical procedure, a neoplastic mass surrounding the oesophagus as suggested by the endoscopic report of extrinsic compression and the previous pericardiotomy. A concomitant impingement on the two residual pulmonary veins, although not echocardiographically visualized, cannot be excluded. Since the rapid removal of the deployed stent to outstretch left atrium and/or pulmonary veins was clearly not possible, the return of baseline hemodynamic function was not achieved unlike that in the case of acute gastric distension or achalasia when prompt correction of the primary pathology lead to the resolution of the cardiovascular picture [2]. This case report suggests that, in order to treat stenotic diseases, stenting of the lower part of the oesophagus should be performed only when the reciprocal anatomic relationship between heart and oesophagus itself is clearly elucidated, i.e. by echocardiography, and possibly be well maintained. References [1] Celenk M, Ozeke O, Selcuk MT, Selcuk H, Cagli K. Left atrial compression by thoracic aneurysm mimicking congestive heart failure. Echocardiography 2005;22:677–8. [2] Raza ST, Mukherjee S, Danias P, et al. Hemodynamically significant extrinsic left atrial compression by gastric structures in the mediastinum. Ann Intern Med 1995;123:114–6. [3] Volpi A, Cavalli A, Maggioni AP, Pier-Nerli F. Left atrial compression by a mediastinal bronchogenic cyst presenting with paroxysmal atrial fibrillation. Thorax 1988;43:216–7. [4] Hasan S, Beckly D, Rahamim J. Oesophagorespiratory fistulas as a complication of self-expanding metal oesophageal stents. Endoscopy 2004;36:731–4. [5] Ho HS, Ong HS. A rare life-threatening complication of migrated nitinol self-expanding metallic stent. Surg Endosc 2004;18:347.
Letter to the Editor
An unusual case of acute fatal pulmonary congestion: Oesophageal stenting Paolo Sganzerla a , Bruno Passaretti a,⁎, Elena Perlasca a , Alessandro Giovannelli b a
Division of Cardiology, Humanitas Gavazzeni, Bergamo, Italy b General Surgery, Humanitas Gavazzeni, Bergamo, Italy Received 22 September 2006; accepted 12 November 2006 Available online 22 February 2007
Abstract Extrinsic left atrial compression with consequent hemodynamic compromise has been described secondary to aortic aneurysm, huge gastroesophageal distension and neoplastic diseases involving mediastinum. Prompt correction of the primary pathology usually leads to reversal of hemodynamic alterations. We report the case of a lady, who, in order to treat a stenosis of the lower third of the oesophagus, underwent stenting with subsequent hemodynamic deterioration due to compression of the posterior left atrial wall disclosed by echocardiography. The sudden recovery of the oesophageal lumen at the expense of the left atrial volume with the impossibility of prompt removal of the stent led to a progressive and fatal deterioration of the hemodynamic picture. Stenting of the lower part of the oesophagus should be performed only when reciprocal anatomic relationship between heart and oesophagus itself is clearly elucidated and possibly well maintained. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Oesophageal stenting; Left atrial compression
Pulmonary vascular congestion is mainly due to systolic and/or diastolic dysfunction of the left ventricle; the increase in ventricular diastolic pressure is transmitted backward to the left atrium and the venous pulmonary circulation with consequent pulmonary edema. Mechanical obstacles to left atrial emptying, such as mitral valve stenosis, cor triatriatum or myxoma, are a less frequent cause of pulmonary engorgement and edema. Extrinsic compression of the left atrium is probably the most uncommon mechanism of hemodynamic compromise. Among mediastinal structures which have been described to determine left atrial compression [1–3], such as aortic aneurysm, carcinoma, bronchogenic cysts, and lymphoma, the upper gastrointestinal ones (stomach and oesophagus) deserve particular attention because of their strict anatomical contiguity and of their possibility for huge pathologic distension [2]; in this case, endoscopic or surgical treatment of the gastroesophageal
⁎ Corresponding author. E-mail address: [email protected] (B. Passaretti). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.11.132
disease generally allows the resolution of the cardiovascular picture. We report the case of a lady who underwent stenting to palliate an extrinsic oesophageal compression and suddenly developed an irreversible pulmonary edema despite maximal medical treatment. 1. Case report A 70-year-old hypertensive lady had, in august 2005, an intrapericardial, total left pneumonectomy with extensive mediastinal node removal for a spinocellular carcinoma of the lung. By March 2006, she began to complain of dysphagia and barium swallow disclosed a 7-cm-long stenosis of the lower third of the oesophagus due to an extrinsic compression of the lumen with normal overlying mucosa. The patient was cardiologically evaluated due to planned insertion of a stent under general anaesthesia. No signs of heart failure were detectable; the blood pressure, on usual pharmacological treatment, was normal and the echocardiogram showed normal left ventricular wall motion
P. Sganzerla et al. / International Journal of Cardiology 117 (2007) e64–e65
Fig. 1. Echocardiographic subcostal view showing compression of left atrium (LA) by esophageal stent (STENT). LV = left ventricle, Ao = aorta, PE = pericardial effusion.
and ejection fraction (0.59); the mitral inflow pattern was consistent with hypertension and patient's age; moderate pericardial effusion mainly located at the posterolateral surface of the heart without any hemodynamic influence on the right heart chambers was observed. Chest X-ray demonstrated a normal vascular pattern of the residual lung parenchyma. The endoscopic procedure was carried out uneventfully, but the day after, the patient became hypotensive, diaphoretic, and rapidly complained of increasing dyspnea, orthopnea with a clinical picture of typical pulmonary edema; transient rapid atrial fibrillation was recorded with no acute cardiac ischemic changes at EKG. Cardiac tamponade due to sudden increase in pericardial effusion was the working diagnosis. However, transthoracic echocardiogram showed neither change in pericardial effusion nor cardiac tamponade; confirmed a still normally sized and performing left ventricular cavity and disclosed a significant compression of the posterior left atrial wall exerted by a circular, hyperechoic structure, the oesophageal stent (Fig. 1); the outflow of pulmonary veins was not detectable due to anatomical changes related to previous pneumonectomy. Despite the maximal therapeutic support, the clinical picture rapidly declined and the patient died in cardiogenic shock. 2. Discussion Extrinsic compression of the left atrium is an uncommon clinical–pathological event. Among adjacent anatomical structures potentially involved, the thoracic aorta, stomach and oesophagus, through their sudden pathologic distension, are the ones that most likely can cause an acute encroachment or compression of the left atrial wall [1,2]. As in cardiac tamponade, where the velocity of effusion is physiologically more important than its pure amount, the potentially rapid increase in the volume of the aorta, the stomach and/or the oesophagus is of particular importance in the pathophysiology of atrial compression. Sudden interference with left atrial
e65
inflow determines direct impairment of left ventricular filling with decrease in cardiac output and pulmonary venous congestion causing functional tamponade. The clinical picture observed in our patient was consistent with hemodynamic alteration due to acute interference with atrial function. The concomitance of a pericardial effusion, clearly chronic and therefore not interfering with right heart chambers in baseline conditions, and the alteration of left ventricular diastolic compliance previously recorded, made our patient particularly vulnerable to acute changes in atrial function. Moreover, paroxysmal atrial fibrillation, on an extrinsic mechanical stimulation basis on the atrial wall [3], played a possible, significant adjunctive pathophysiological role. Although several types of complication can occur after oesophageal stenting [4,5], there is no report, to our knowledge, of clinically significant interference with cardiac structures. Anatomical relationship with the heart, limited to a small distal part of the oesophagus, can obviously play a consistent role. In case of stenting of the lower part, instantaneous recover of the normal oesophageal lumen must be accomplished by acute displacement of adjacent anatomical structures. The exact mechanism by which stenting impinged on the left atrium in our patient is not completely elucidated by our echocardiographic pictures. Factors involved could have been changes in anatomical relationship in mediastinum due to the previous surgical procedure, a neoplastic mass surrounding the oesophagus as suggested by the endoscopic report of extrinsic compression and the previous pericardiotomy. A concomitant impingement on the two residual pulmonary veins, although not echocardiographically visualized, cannot be excluded. Since the rapid removal of the deployed stent to outstretch left atrium and/or pulmonary veins was clearly not possible, the return of baseline hemodynamic function was not achieved unlike that in the case of acute gastric distension or achalasia when prompt correction of the primary pathology lead to the resolution of the cardiovascular picture [2]. This case report suggests that, in order to treat stenotic diseases, stenting of the lower part of the oesophagus should be performed only when the reciprocal anatomic relationship between heart and oesophagus itself is clearly elucidated, i.e. by echocardiography, and possibly be well maintained. References [1] Celenk M, Ozeke O, Selcuk MT, Selcuk H, Cagli K. Left atrial compression by thoracic aneurysm mimicking congestive heart failure. Echocardiography 2005;22:677–8. [2] Raza ST, Mukherjee S, Danias P, et al. Hemodynamically significant extrinsic left atrial compression by gastric structures in the mediastinum. Ann Intern Med 1995;123:114–6. [3] Volpi A, Cavalli A, Maggioni AP, Pier-Nerli F. Left atrial compression by a mediastinal bronchogenic cyst presenting with paroxysmal atrial fibrillation. Thorax 1988;43:216–7. [4] Hasan S, Beckly D, Rahamim J. Oesophagorespiratory fistulas as a complication of self-expanding metal oesophageal stents. Endoscopy 2004;36:731–4. [5] Ho HS, Ong HS. A rare life-threatening complication of migrated nitinol self-expanding metallic stent. Surg Endosc 2004;18:347.