|Year : 2016 | Volume
| Issue : 1 | Page : 30-32
Reexpansion pulmonary edema following thoracentesis
Ansuman Mukhopadhyay1, Mrinmoy Mitra2, Srabani Chakrabati3
1 Department of Pulmonary Medicine, AMRI Hospital, Salt Lake, West Bengal, India
2 Department of Pulmonary Medicine, Calcutta National Medical College and Hospital, Anandapur, Kolkata, West Bengal, India
3 Department of Pathology, Consultant Pathologist and Laboratory Head, Fortis Hospital, Anandapur, Kolkata, West Bengal, India
|Date of Web Publication||23-Dec-2015|
Tirupati Enclave, BL-B, Flat - 2D, AB - 325, Samar Pally, Barowaritala, Krishnapur, Kolkata - 700 102, West Bengal
Source of Support: None, Conflict of Interest: None
Reexpansion pulmonary edema is an uncommon complication of the treatment of lung atelectasis, pleural effusion or pneumothorax and pathogenesis is unknown. An elderly male patient presented to us with right-sided pleural effusion. 2 h after thoracentesis, he felt chest discomfort and increased breathlessness. His chest examination showed right-sided crackles. Chest radiograph showed right-sided heterogeneous opacity in right lower zone consistent with unilateral pulmonary edema. He was managed conservatively along with bilevel positive airway pressure ventilator support. His condition improved gradually and was discharged successfully after 2 days.
Keywords: Bilevel positive airway pressure, pleural effusion, reexpansion pulmonary edema, thoracentesis
|How to cite this article:|
Mukhopadhyay A, Mitra M, Chakrabati S. Reexpansion pulmonary edema following thoracentesis. J Assoc Chest Physicians 2016;4:30-2
| Introduction|| |
Reexpansion pulmonary edema (REPE) is a rare complication following reexpansion of the lung after rapid emptying of air or liquid from the pleural space by either thoracentesis or chest drainage. The incidence of REPE ranges between 1% and 14%. The exact pathophysiology of REPE is unknown. It is either due to surfactant depletion or due to hypoxic capillary damage that leads to increased capillary permeability. Hypoxemia, hypotension, and even death can occur in REPE. Early recognition and rapid action is the key for a good outcome. Here, we present a case of REPE that occurred after thoracentesis through pigtail drain in a case of pleural effusion.
| Case Report|| |
A 58-year-old gentleman presented with progressive shortness of breath and dry cough for last 15 days. He also had complaint of right-sided pleuritic chest pain and intermittent low-grade fever for the same duration. There were no other complaints. He was a smoker with 14 pack years but nonalcoholic. He had no past history of tuberculosis. His pulse was 76/min, blood pressure 134/82 mm Hg, and respiratory rate 26/min. His body weight was 62 kg and body mass index 23.16 kg/m 2. Chest examination revealed stony dull note on percussion and diminished vesicular breath sound on auscultation on the right side. His chest radiograph postero-anterior view showed right-sided pleural effusion with a slight shift of the mediastinum to left [Figure 1]. The hemogram, liver function tests, renal function tests, and serum electrolytes were within normal limits. The patient underwent diagnostic thoracentesis. Pleural fluid analysis revealed lymphocytic exudate with high adenosine deaminase (58 IU/L). Pleural fluid Ziehl–Neelsen stain was negative for acid fast Bacilli and oncotic cytology was negative. With that background clinical features and pleural fluid analysis, we diagnosed the case as right sided tubercular pleural effusion. Anti-tubercular therapy was started according to body weight with rifampicin 600 mg, isoniazid 300 mg, pyrazinamide 1500 mg, and ethambutol 1000 mg daily. Pigtail catheter of size 8F was inserted inside the right side of the chest for therapeutic thoracentesis. 1.5 L pleural fluid was drained, and the pig-tail catheter was clamped. 2 h later, patient developed severe chest discomfort, cough, and increased shortness of breath. He was tachycardic (heart rate 112/min) and tachypneic (respiratory rate 32/min). His pulse was feeble, and blood pressure was 80/50 mm of Hg. Chest auscultation revealed diffuse inspiratory crackles over the right side of the chest. At that stage, his room air SpO2 was 80%. Oxygen was given via ventury mask at a concentration equivalent to FiO2 0.3. His arterial blood gases report on FiO2 0.3 revealed pH 7.39; PaO2 58.8 mmHg; PaCO2 26.4 mmHg; SaO2 82.4% and HCO3 18.6 mEq/L. At that time, we reached four different differential diagnoses, those were – acute left ventricular failure, acute myocardial infarction, pulmonary embolism, and re-expansion pulmonary edema (REPE). His electrocardiogram was normal, and Troponin C test was negative. His D-dimer value was 150 mcg/L, and NT-proBNP level was 200 ng/ml. An urgent portable chest X-ray anterior-posterior view (AP) showed heterogeneous opacity in the right lower zone with pigtail catheter in situ [Figure 2]. Based on this clinical, radiological, and laboratory findings the diagnosis of REPE was established. The patient was shifted to our intensive care unit. High flow oxygen (10 L/min) was started via nonbreather face mask. But the patient remained tachypneic. Bilevel positive airway pressure (BiPAP) ventilation was applied in spontaneous-trigger mode with inspiratory positive airway pressure of 20 cm of water, expiratory positive airway pressure of 5 cm of water and backup respiratory rate of 20/min. Intravenous Dopamine was started with 7 µg/kg/min. After 24 h of treatment, patient's condition became stable with pulse rate 90/min, respiratory rate 20/min, blood pressure 110/64 mmHg, and SpO2 98% on 1 L/min oxygen through a nasal cannula. His arterial blood gases at that time showed improved oxygenation with pH 7.38; PaO2 80.2 mmHg; PaCO2 36.4 mmHg; SaO2 94.4% and HCO3 23.4. Chest auscultation revealed diminished crackles over the right hemithorax. Dopamine was tapered over the next 12 h. Chest radiograph AP view taken after 1-day revealed marked resolution of right-sided heterogeneous opacity with mild pleural effusion and pigtail catheter in situ [Figure 3]. Pigtail catheter was removed on the next day. His room air arterial blood gases normalized. The patient was discharged with anti-tubercular drugs as advised before.
|Figure 1: Chest radiograph postero-anterior view showed right sided pleural effusion with slight shift of mediastinum to left|
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|Figure 2: Chest X-ray anterior-posterior view showed heterogeneous opacity in right lower zone with pigtail catheter in situ|
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|Figure 3: Chest radiograph anterior-posterior view revealed marked resolution of right-sided heterogeneous opacity with mild pleural effusion and pigtail catheter in situ|
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| Discussion|| |
Reexpansion pulmonary edema is a rare but life-threatening clinical condition due to rapid re-inflation of collapsed lung after treatment of lung atelectasis, pleural effusion or pneumothorax. The mortality of REPE can reach up to 20%. The first reported case of REPE, described in 1958 by Carlson was of a patient who developed REPE after treatment of whole lung collapse secondary to pneumothorax. The risk factors for REPE include younger age, female sex, greater degree and longer duration of lung collapse, a reexpansion of lung in <10 min, use of negative pressure during treatment and evacuation volume more than 2000 ml. REPE can also occur after talc pleurodesis, and it is thought to be secondary to an inflammatory reaction to talc. In our case, though the patient was elderly, male and evacuation volume was 1.5 L, there was the presence of greater degree and longer duration of lung collapse and evacuation time was also short. The pathophysiology of REPE has not been completely understood till date. Several animal models have been studied to elucidate the cause. Chronic lung collapse causes thickening of capillary endothelium by the release of monocyte chemoattractant protein 1, leukotriene B4 and interleukin 8. On reexpansion of the lung, there is sudden stretching of the microvessels that damages the endothelium and causes increased permeability of those microvessels. Alveolar surfactant is also got damaged. There is also decreased perivascular pressure that leads to further endothelial damage and cause REPE. Usually, most of the reported cases of REPE were ipsilateral as in our case, but there were few patients mentioned in other study where edema were contra-lateral or even bilateral. The clinical features vary from asymptomatic radiological findings to respiratory failure with circulatory shock. Patients who develop REPE typically develop severe coughing or chest tightness during or immediately following thoracentesis or chest tube placement. The cough sometimes produces copious amounts of pink frothy sputum. Other symptoms include dyspnea, tachypnea, tachycardia, fever, hypotension, cyanosis, and sometimes nausea, vomiting also. The symptoms generally progress for 24–48 h, and the chest radiograph reveals pulmonary edema throughout the ipsilateral lung. Pulmonary edema may also develop in the contralateral lung in some cases. If the patient does not die within the first 48 h, recovery is usually complete. In our case, we also found that the patient became symptomatic within 2 h of thoracentesis and chest radiograph showed ipsilateral pulmonary edema. The treatment of REPE remains supportive. The cornerstone is positive-pressure mechanical ventilation. The role of positive end-expiratory pressure is to help reexpand collapsed alveoli, increase functional residual capacity, and reduce shunting. Treatment also may include diuresis and vasopressor support. The role of pharmaceutics in treating REPE remains uncertain. In our case, we treated the patient with supportive measures along with vasopressor and BiPAP. In conclusion, we want to publish this case as REPE is a rare but severe complication following thoracentesis. Slow drainage of pleural fluid should be done. Early diagnosis and prompt action is the key to prevent mortality from that life-threatening complication.
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[Figure 1], [Figure 2], [Figure 3]