Contralateral pulmonary edema following surgical repair of a ruptured hemidiaphragm
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《血管的通路杂志》
Department of General Thoracic Surgery and Anesthesiology, Omiya Medical Center, Jichi Medical School, 1-847 Amanuma, Omiya-ku, Saitama, 330-8503 Japan
Abstract
A 24-year-old man underwent surgical correction of a ruptured hemidiaphragm via left thoracotomy and laparotomy. During the procedure, he developed contralateral pulmonary edema that completely resolved after four days of mechanical ventilatory support. Instantaneous unilateral pulmonary edema should be considered in young patients with thoracic compliance abnormalities.
Key Words: Unilateral pulmonary edema; Ruptured hemidiaphragm
1. Introduction
Rapid development of regional pulmonary edema is well known to occur in patients with cardiopulmonary diseases, but it is uncommon for it to occur in those without cardiopulmonary disease. We report a case of contralateral pulmonary edema that developed during an elective surgical repair of a ruptured hemidiaphragm, and we discuss its etiology with reference to previous reviews of this area.
2. Case report
The 24-year-old man was admitted to our institute for elective surgery of the left diaphragmatic herniation. The patient had postprandial dyspnea two years earlier. Chest radiography showed compression of the left lung and mediastinum by abdominal organs (Fig. 1). Chest computed tomography showed migration of abdominal organs into the left pleural cavity: stomach with greater omentum, colon and spleen. Previous history suggested a chronic diaphragmatic herniation due to a blunt chest injury 2 years earlier. Respiratory function was restricted, with vital capacity 70% of the predictive value. Blood examinations including arterial blood gas analysis showed no abnormal findings.
Anesthesia was introduced with propofol followed by the muscle relaxant vecronium. Before inhibition of spontaneous breathing, paradoxical respiratory movement occurred and oxygen saturation dropped to 80% when fitted mask ventilation was impossible due to high airway pressure, even after double lung ventilation via tracheal intubation with 100% oxygen. Emergent chest radiography showed the expansion of the left lung along with the abdominal organs, leading to a mediastinal shift (Fig. 2A); however, blood pressure and heart rate was stabilized. Bronchoscopy showed no airway obstruction. Mechanical ventilation with 100% oxygen was adjusted at 500 ml of a tidal volume, a respiratory rate of 14 beats per minute, and 8 cm H2O of positive end-expiratory pressure. Peak inspiratory airway pressure increased to 30 cm H2O. Left lateral thoracotomy at the right lateral position slightly relieved the high airway mechanical ventilation as well as hypoxia, but selective right lung ventilation provided insufficient oxygenation. Hypoxia, 70 mmHg of arterial oxygen concentration and 50 mmHg of arterial carbon dioxide concentration under bilateral lung ventilation, continued during surgical correction of the abdominal organs into the peritoneal cavity followed by diaphragmatic repairment reinforced with Marlex Mesh. Operation time was 335 min because selective lung ventilation was not available and abdominal organs were severely adhesive to the ruptured diaphragm. Anesthesia time was 455 min. Chest radiography after the operation showed severe pulmonary edema in the right lung (Fig. 2B). Bronchoscopy showed pink frothy secretions exclusively in the right bronchus. The unilateral pulmonary edema resolved after four days of positive airway ventilation without the use of diuretics or bronchodilators. The patient was discharged two weeks after the operation without any further complications.
3. Discussion
Flash unilateral pulmonary edema is an uncommon entity. There are several reports of edema, including a case of an ipsilateral pulmonary edema [1–6], following surgical repair of a ruptured hemidiaphragm [7]. Unilateral pulmonary edema is reported to occur in young patients, who were about twenty years of age, with no cardiopulmonary diseases. Several locoregional factors and/or systemic conditions such as an increase of pro-inflammatory cytokines and neurogenic factors may have roles [8]. The pathophysiology of the lung in young patients, such as thoracic compliance, pulmonary blood flow, and responses of inflammatory cytokines may contribute to the causative mechanisms.
Previous reviews have discussed various etiologies, including the rapid re-expansion of a collapsed lung (re-expansion pulmonary edema), down lung syndrome (gravitational edema), systemic-to-pulmonary arterial shunts, heart failure, compression or occlusion of pulmonary vasculatures, obstruction of a bronchus (negative pressure pulmonary edema), barotrauma edema, and an acute manifestation of neuropulmonary reaction (neurogenic pulmonary edema) [1–7]. Negative-pressure pulmonary edema may easily develop if subatmospheric pressure is generated at the alveolar level when markedly negative intrathoracic pressure is caused by forced inspiration against a closed airway and the subsequent increase in pulmonary vascular volume. This can occur at the introduction of anesthesia as previously reported [9,10]. Re-expansion pulmonary edema occurs when a chronically collapsed lung is rapidly re-expanded after thoracocentesis and pneumothorax. The edema is usually on the ipsilateral side, but can be contralateral or bilateral [2,3]. There are reports associated with re-expansion pulmonary edema after selective unilateral ventilation, in which there is no chronically collapsed lung; thought to be caused by the disruption of the capillary-alveolar membrane, though an inflammatory response is also thought to have a role in the development of this edema. An experimental study suggested that pro-inflammatory cytokines are up-regulated upon re-expansion and ventilation after a short period of lung collapse [8].
The causative mechanisms of the unilateral pulmonary edema were as follows. First, negative-pressure pulmonary edema was induced when paradoxical respiratory movement with hypoxia occurred at the introduction of anesthesia. Second, reperfusion injury after sudden release of the mediastinal shift causing the kinking of the right pulmonary artery was associated. Third, compression of the right lung by the overexpansion of the left pleural cavity and right decubitus position induced the collapsed right lung that then resulted in the re-expansion pulmonary edema when the patient was changed from the supine position.
Thoracic surgeons and anesthesiologists need to consider instantaneous unilateral pulmonary edema during surgical procedures for diaphragmatic herniation, especially in young patients. Positive airway ventilatory support is necessary if it occurs.
References
Tsai YS, Wang SJ, Shih HC, Huang YC, Chi KP, Tseng CS, Ho WM. Unilateral pulmonary edema during general anesthesia – report of two cases. Acta Anaesthesiol Sin 1997; 35:175–180.
Cohen JD, Loewinger J, Zelikovski A, Gassner S. Unilateral pulmonary oedema of the contralateral lung following transaxillary sympathectomy. Anaesthesia 1991; 46:651–653.
Gordon AH, Grant GP, Kaul SK. Reexpansion pulmonary edema after resolution of tension pneumothorax in the contralateral lung of a previously lung injured patient. J Clin Anesth 2004; 16:289–292.
Perrin C, Jullien V, Venissac N, Lonjon M, Blaive B. Unilateral neurogenic pulmonary edema. A case report. Rev Pneumol Clin 2004; 60:43–45.
Fujino S, Tezuka N, Inoue S, Ichinose M, Hanaoka J, Sawai S, Kontani K. Reexpansion pulmonary edema due to high-frequency jet ventilation: report of a case. Surg Today 2000; 30:1110–1111.
Baraka A, Moghrabi R, Yazigi A. Unilateral pulmonary oedema/atelectasis in the lateral decubitus position. Anaesthesia 1987; 42:171–174.
Khoo ST, Chen FG. Acute localised pulmonary oedema. Re-expansion pulmonary oedema following the surgical repair of a ruptured hemidiaphragm. Anaesthesia 1988; 43:486–489.
Funakoshi T, Ishibe Y, Okazaki N, Miura K, Liu R, Nagai S, Minami Y. Effect of re-expansion after short-period lung collapse on pulmonary capillary permeability and pro-inflammatory cytokine gene expression in isolated rabbit lungs. Br J Anaesth 2004; 92:558–563.
Oswalt CE, Gates GA, Holmstrom MG. Pulmonary edema as a complication of acute airway obstruction. J Am Med Assoc 1977; 238:1833–1835.
Nawa Y, Masuda Y, Imaizumi H, Susa Y, Tokuda C, Namiki A. Two cases of negative pressure pulmonary edema after induction of anesthesia and extubation. Masui 2004; 53:672–674.(Shunsuke Endo, Hiroyoshi )
Abstract
A 24-year-old man underwent surgical correction of a ruptured hemidiaphragm via left thoracotomy and laparotomy. During the procedure, he developed contralateral pulmonary edema that completely resolved after four days of mechanical ventilatory support. Instantaneous unilateral pulmonary edema should be considered in young patients with thoracic compliance abnormalities.
Key Words: Unilateral pulmonary edema; Ruptured hemidiaphragm
1. Introduction
Rapid development of regional pulmonary edema is well known to occur in patients with cardiopulmonary diseases, but it is uncommon for it to occur in those without cardiopulmonary disease. We report a case of contralateral pulmonary edema that developed during an elective surgical repair of a ruptured hemidiaphragm, and we discuss its etiology with reference to previous reviews of this area.
2. Case report
The 24-year-old man was admitted to our institute for elective surgery of the left diaphragmatic herniation. The patient had postprandial dyspnea two years earlier. Chest radiography showed compression of the left lung and mediastinum by abdominal organs (Fig. 1). Chest computed tomography showed migration of abdominal organs into the left pleural cavity: stomach with greater omentum, colon and spleen. Previous history suggested a chronic diaphragmatic herniation due to a blunt chest injury 2 years earlier. Respiratory function was restricted, with vital capacity 70% of the predictive value. Blood examinations including arterial blood gas analysis showed no abnormal findings.
Anesthesia was introduced with propofol followed by the muscle relaxant vecronium. Before inhibition of spontaneous breathing, paradoxical respiratory movement occurred and oxygen saturation dropped to 80% when fitted mask ventilation was impossible due to high airway pressure, even after double lung ventilation via tracheal intubation with 100% oxygen. Emergent chest radiography showed the expansion of the left lung along with the abdominal organs, leading to a mediastinal shift (Fig. 2A); however, blood pressure and heart rate was stabilized. Bronchoscopy showed no airway obstruction. Mechanical ventilation with 100% oxygen was adjusted at 500 ml of a tidal volume, a respiratory rate of 14 beats per minute, and 8 cm H2O of positive end-expiratory pressure. Peak inspiratory airway pressure increased to 30 cm H2O. Left lateral thoracotomy at the right lateral position slightly relieved the high airway mechanical ventilation as well as hypoxia, but selective right lung ventilation provided insufficient oxygenation. Hypoxia, 70 mmHg of arterial oxygen concentration and 50 mmHg of arterial carbon dioxide concentration under bilateral lung ventilation, continued during surgical correction of the abdominal organs into the peritoneal cavity followed by diaphragmatic repairment reinforced with Marlex Mesh. Operation time was 335 min because selective lung ventilation was not available and abdominal organs were severely adhesive to the ruptured diaphragm. Anesthesia time was 455 min. Chest radiography after the operation showed severe pulmonary edema in the right lung (Fig. 2B). Bronchoscopy showed pink frothy secretions exclusively in the right bronchus. The unilateral pulmonary edema resolved after four days of positive airway ventilation without the use of diuretics or bronchodilators. The patient was discharged two weeks after the operation without any further complications.
3. Discussion
Flash unilateral pulmonary edema is an uncommon entity. There are several reports of edema, including a case of an ipsilateral pulmonary edema [1–6], following surgical repair of a ruptured hemidiaphragm [7]. Unilateral pulmonary edema is reported to occur in young patients, who were about twenty years of age, with no cardiopulmonary diseases. Several locoregional factors and/or systemic conditions such as an increase of pro-inflammatory cytokines and neurogenic factors may have roles [8]. The pathophysiology of the lung in young patients, such as thoracic compliance, pulmonary blood flow, and responses of inflammatory cytokines may contribute to the causative mechanisms.
Previous reviews have discussed various etiologies, including the rapid re-expansion of a collapsed lung (re-expansion pulmonary edema), down lung syndrome (gravitational edema), systemic-to-pulmonary arterial shunts, heart failure, compression or occlusion of pulmonary vasculatures, obstruction of a bronchus (negative pressure pulmonary edema), barotrauma edema, and an acute manifestation of neuropulmonary reaction (neurogenic pulmonary edema) [1–7]. Negative-pressure pulmonary edema may easily develop if subatmospheric pressure is generated at the alveolar level when markedly negative intrathoracic pressure is caused by forced inspiration against a closed airway and the subsequent increase in pulmonary vascular volume. This can occur at the introduction of anesthesia as previously reported [9,10]. Re-expansion pulmonary edema occurs when a chronically collapsed lung is rapidly re-expanded after thoracocentesis and pneumothorax. The edema is usually on the ipsilateral side, but can be contralateral or bilateral [2,3]. There are reports associated with re-expansion pulmonary edema after selective unilateral ventilation, in which there is no chronically collapsed lung; thought to be caused by the disruption of the capillary-alveolar membrane, though an inflammatory response is also thought to have a role in the development of this edema. An experimental study suggested that pro-inflammatory cytokines are up-regulated upon re-expansion and ventilation after a short period of lung collapse [8].
The causative mechanisms of the unilateral pulmonary edema were as follows. First, negative-pressure pulmonary edema was induced when paradoxical respiratory movement with hypoxia occurred at the introduction of anesthesia. Second, reperfusion injury after sudden release of the mediastinal shift causing the kinking of the right pulmonary artery was associated. Third, compression of the right lung by the overexpansion of the left pleural cavity and right decubitus position induced the collapsed right lung that then resulted in the re-expansion pulmonary edema when the patient was changed from the supine position.
Thoracic surgeons and anesthesiologists need to consider instantaneous unilateral pulmonary edema during surgical procedures for diaphragmatic herniation, especially in young patients. Positive airway ventilatory support is necessary if it occurs.
References
Tsai YS, Wang SJ, Shih HC, Huang YC, Chi KP, Tseng CS, Ho WM. Unilateral pulmonary edema during general anesthesia – report of two cases. Acta Anaesthesiol Sin 1997; 35:175–180.
Cohen JD, Loewinger J, Zelikovski A, Gassner S. Unilateral pulmonary oedema of the contralateral lung following transaxillary sympathectomy. Anaesthesia 1991; 46:651–653.
Gordon AH, Grant GP, Kaul SK. Reexpansion pulmonary edema after resolution of tension pneumothorax in the contralateral lung of a previously lung injured patient. J Clin Anesth 2004; 16:289–292.
Perrin C, Jullien V, Venissac N, Lonjon M, Blaive B. Unilateral neurogenic pulmonary edema. A case report. Rev Pneumol Clin 2004; 60:43–45.
Fujino S, Tezuka N, Inoue S, Ichinose M, Hanaoka J, Sawai S, Kontani K. Reexpansion pulmonary edema due to high-frequency jet ventilation: report of a case. Surg Today 2000; 30:1110–1111.
Baraka A, Moghrabi R, Yazigi A. Unilateral pulmonary oedema/atelectasis in the lateral decubitus position. Anaesthesia 1987; 42:171–174.
Khoo ST, Chen FG. Acute localised pulmonary oedema. Re-expansion pulmonary oedema following the surgical repair of a ruptured hemidiaphragm. Anaesthesia 1988; 43:486–489.
Funakoshi T, Ishibe Y, Okazaki N, Miura K, Liu R, Nagai S, Minami Y. Effect of re-expansion after short-period lung collapse on pulmonary capillary permeability and pro-inflammatory cytokine gene expression in isolated rabbit lungs. Br J Anaesth 2004; 92:558–563.
Oswalt CE, Gates GA, Holmstrom MG. Pulmonary edema as a complication of acute airway obstruction. J Am Med Assoc 1977; 238:1833–1835.
Nawa Y, Masuda Y, Imaizumi H, Susa Y, Tokuda C, Namiki A. Two cases of negative pressure pulmonary edema after induction of anesthesia and extubation. Masui 2004; 53:672–674.(Shunsuke Endo, Hiroyoshi )