|Year : 2007 | Volume
| Issue : 2 | Page : 72-74
Reexpansion pulmonary edema- A case report
AK Janmeja, PR Mohapatra, MS Saini, A Khurana
Department of Pulmonary Medicine, Government Medical College and Hospital, Chandigarh., India
A K Janmeja
House no-1117, GMCH Campus, Sector-32, Chandigarh-160030.
Source of Support: None, Conflict of Interest: None
| Abstract|| |
A middle aged male presented to us with right side pneumothorax. Two hours after insertion of intercostals tube he felt discomfort and increased breathlessness. His chest examination showed crepitations. Chest radiograph showed partial expansion of right lung with opacity in right lower zone consistent with unilateral pulmonary edema. He was managed conservatively and improved with complete resolution on chest radiograph. Reexpansion pulmonary edema is an uncommon complication of the treatment of lung atelectasis, pleural effusion or pneumothorax and pathogenesis is unclear.
Keywords: Reexpansion pulmonary edema, Pneumothorax
|How to cite this article:|
Janmeja A K, Mohapatra P R, Saini M S, Khurana A. Reexpansion pulmonary edema- A case report. Lung India 2007;24:72-4
| Introduction|| |
Reexpansion pulmonary edema (REPE) is an uncommon complication following reexpansion of lung as treatment of conditions such as hemopneumothorax, large pleural effusion, pneumothorax, after lobectomy, or even during single-lung ventilation. Among these, majority of REPE cases are encountered with treatment of spontaneous pneumothorax  .The mechanism is unknown and has been related to surfactant depletion or due to hypoxic capillary damage leading to increased capillary permeability  . The onset of REPE can be sudden and dramatic  . Hypoxemia, hypotension, and even death have been observed with the mortality reported as high as 20%  .
| Case Report|| |
Forty eight year old male presented to us with the complaint of progressive breathlessness that was increased with exertion for last 3 months. He also had complaint of cough with mucoid expectoration of the same duration. There were no other complaints. The patient was a known case of type -2 diabetes mellitus that was controlled with oral hypoglycemic agent. He was a chronic smoker with history of 25 pack years and had been consuming alcohol occasionally.
He was obese with body mass index (BMI) of 35.15. Rest of his general physical examination was normal. His pulse was 76/min, blood pressure 136/84 mmHg and respiratory rate 26/minute. Chest examination was suggestive of right side pneumothorax. His chest radiograph revealed complete pneumothorax on right side with slight shift of mediastinum to left [Figure 1]. The hemogram, liver functions and serum electrolytes were within normal limits.
An inter-costal tube (malecot 22 F) was inserted on right side in 5th intercostals space just posterior to mid axillary line and oxygen was given via venturi mask at concentration of FiO 2 0.30. Two hours later he developed chest discomfort, restlessness and increased breathlessness. His pulse was feeble and blood pressure was 80/50 mmHg. He also developed cyanosis. Chest auscultation revealed diffuse coarse crepitations over right hemithorax with few crepitations on the left side. At this stage SpO 2 was 83%. Soon after his arterial blood gases report on FiO 2 0.3 revealed pH 7.38; PaCO 2 34.8 mmHg; PaO 2 64.8 mmHg; SaO 2 89.4% and HCO 3 20.8.
We entertained four main differential diagnoses at that time, those were - reexpansion pulmonary edema, acute left ventricular failure, myocardial infarction and pulmonary embolism. His ECG was normal and Troponin C (Trop T®) test was negative. An urgent portable chest X-ray anteriorposterior (AP) view showed partial expansion of right lung with heterogeneous opacity in right lower zone more towards on lateral side [Figure 2]. Based on the clinical and radiological finding, the diagnosis of reexpansion pulmonary edema was established. Patient was started on intravenous fluids, ionotropic agent (Dopamine; 7 microgram/Kg/min), bronchodilators, nebulization (salbutamol and ipratropium bromide) and oxygen supplementation with FiO 2 0.5. After 24 hour of treatment the condition of the patient was stable with pulse rate 94/minute, blood pressure 130/80 mmHg and SpO 2 98%. His arterial blood gases improved with pH 7.38; PCO2 37 mmHg; PO 2 79.4 mmHg; SaO 2 97% and HCO 3 21.4. The chest auscultation revealed decreased air entry in right infra-clavicular area with no adventitious sounds. Dopamine was tapered off in next 12 hours, however, oxygen supplementation was maintained at FiO 2 0.3. Chest radiograph taken after two days showed marked resolution of pulmonary edema, however about 20% of pneumothorax was still present. Subsequent chest radiograph taken on 11 th day revealed complete expansion of right lung [Figure 3] and the chest tube was removed there after. At this stage his room air arterial blood gases were within normal range (pH 7.39; PCO 2 32.3 mmHg; PO 2 89.8 mmHg; SaO 2 97% and HCO 3 22.4). The spirometry performed subsequently showed obstructive lung disease with no significant post bronchodilator reversibility. He was discharged on regular bronchodilators (salbutamol and ipratropium bromide) in form of dry powder inhalation along with an advice to refrain from smoking strictly.
| Discussion|| |
Unilateral reexpansion pulmonary edema is a rare but life threatening complication of the treatment of lung atelectasis, pleural effusion or pneumothorax  . It is characterized by the development of unilateral pulmonary edema in a lung that has been rapidly re-inflated following a variable period of collapse secondary to a pleural effusion or pneumothorax  . Miller et al  showed that in the experimental animal, REPE occurs only if the lung has been collapsed for more than 3 days and if negative pressure is applied to the pleural space. However reexpansion pulmonary edema in human have been encountered even when no negative pressure used while managing the pleural effusion ,,, .
The etiology of REPE remains incompletely defined and is multi factorial in nature  . It appears to be due to increased permeability of the pulmonary vasculature. High protein content found in edema fluid  indicates that it is leakiness of the capillaries rather than an increased hydrostatic pressure difference that leads to the edema. It has also been suggested that the lung injury could be due to reperfusion and oxygen free radical formation in the collapsed lung  . This hypothesis is supported by the observation that inhalation of oxygen at FiO 2 0.4 prevents pulmonary edema when lungs are reexpanded  .
The clinical picture varies considerably from asymptomatic radiological findings to dramatic respiratory failure with circulatory shock. The commonest presentation is pernicious cough or chest tightness during or immediately following thoracentesis or chest tube placement. The cough can be productive with copious amounts of frothy pink sputum. Other signs and symptoms include dyspnea, tachypnea, tachycardia, fever, hypotension, nausea, vomiting, and cyanosis. The symptoms progress for 24 to 48 hours and chest radiograph reveals pulmonary edema in the ipsilateral lung. Rarely pulmonary edema can be bilateral or in contra-lateral lung. If the patient does not die within the first 48 hours, recovery is usually complete  . There were 11 deaths (20%) in a review of 53 reported cases by Mahfood et al  .
The duration of collapse seems to be a risk factor for reexpansion pulmonary edema in patients with effusions or pneumothoraces who are undergoing tube thoracostomy or thoracentesis  . In such cases underwater-seal drainage should be preferred rather than to a negative pressure apparatus and the amount of pleural fluid withdrawn during thoracentesis should not exceed to 1000 ml unless pleural pressures are monitored  . Matsura et al revealed young age and extent of lung collapse as independent risk factors for reexpansion pulmonary edema  .
The management of reexpansion pulmonary edema differs distinctly from that of cardiogenic pulmonary edema  . The best treatment of reexpansion pulmonary edema remains supportive with intravenous fluids, oxygen, and morphine. Diuresis is detrimental due to hypovolemic status and should be avoided  . In severe conditions mechanical ventilation is required; however there are a few literature case reports of the treatment of reexpansion pulmonary edema with non-invasive continuous positive airway pressure  .
| References|| |
|1.||Murat A, Arslan A, Balci AE. Re-expansion pulmonary edema. Acta Radiol. 2004 ;45:431-3. |
|2.||Miller WC, Toon R, Palat H, et al. Experimental pulmonary edema following re-expansion of pneumothorax. Am Rev Respir Dis1973;8:664-6. |
|3.||Trachiotis GD, Vricella LA, Aaron BL, Hix WR. Reexpansion pulmonary edema. Updated in 1997. Ann Thorac Surg 1997;63:1207. |
|4.||Mahfood S, Hix WR, Aaron BI, et al. Re-expansion pulmonary edema. Ann Thorac Surg 1988;45:340-345. |
|5.||Volpicelli G, Fogliati C, Radeschi G, Frascisco M. A case of unilateral re-expansion pulmonary oedema successfully treated with non-invasive continuous positive airway pressusure. Eur J Emerg Med. 2004;11:291-4. |
|6.||Tarver RD, Broderick LS, Conces DJ Jr. Reexpansion pulmonary edema. J Thorac Imaging 1996;11:198-202. [PUBMED] |
|7.||Olcott EW. Fatal Reexpansion pulmonary edema following pleural catheter placement. J Vasc Interv Radiol 1994;5:176-178. [PUBMED] |
|8.||Waqaruddin M, Bernstein A. Re-expansion pulmpnary edema. Thorax 1975;30:54-60. [PUBMED] [FULLTEXT]|
|9.||Pavlin DJ. Lung re-expansion: for better or worse. Chest 1986; 89:2-3. [PUBMED] [FULLTEXT]|
|10.||Pavlin DI, Nessly ML, Cheney FW. Hemodynamic effects of rapidly evacuating prolonged pneumothorax in rabbits. J Appl Physiol 1987;62:477-484. |
|11.||Light RW. Thoracentesis and pleural biopsy. In Light RW, editor Pleural Disease. 4th ed. Baltimore:WrDiams & Wrlkins, 2003; 358-377. |
|12.||MatsuraY, Nomimura T, Murakami H, Matsushima T, Kakehashi M, Kajihara H. Clinical analysis of reexpansion pulmonary edema.Chest 1991,100 . 1562-1566. |
|13.||Beng ST, Mahadevan M. An uncommon life-threatening complication after chest tube drainage of pneumothorax in the ED. Am J Emerg Med. 2004;22:615-619. |
[Figure 1], [Figure 2], [Figure 3]