Development Of Reexpansion Pulmonary Edema Research Articles

Risk factors for re-expansion pulmonary edema following chest tube drainage in patients with spontaneous pneumothorax: A systematic review and meta-analysis.

Re-expansion pulmonary edema (RPE) is a rare but potentially life-threatening complication that can occur after rapid lung expansion following the management of lung collapse. This meta-analysis aimed to investigate the risk factors for RPE following chest tube drainage in patients with spontaneous pneumothorax. We conducted a comprehensive systematic literature search in electronic databases of PubMed, ScienceDirect, Cochrane Library, and ProQuest to identify studies that explore the risk factors for RPE following chest tube drainage in spontaneous pneumothorax. Pooled odds ratios (OR) or weighted mean differences (WMD) were calculated to evaluate the risk factors. Statistical analysis was conducted using Review Manager 5.3 software. Five studies involving 1.093 spontaneous pneumothorax patients were included in this meta-analysis. The pooled analysis showed that the following risk factors were significantly associated with increased risk of RPE following chest tube drainage: the presence smoking history (OR=1.94, 95% CI: 1.22-3.10, P=0.005, I2=0%), longer duration of symptoms (WMD=3.76, 95% CI: 2.07-5.45, P<0.0001, I2=30%), and larger size of pneumothorax (WMD=16.76, 95% CI: 8.88-24.64, P<0.0001, I2=78%). Age, sex, and location of pneumothorax had no significant association. In patients with spontaneous pneumothorax, the presence of smoking history, longer duration of symptoms, and larger size of pneumothorax increase the risk of development of RPE following chest tube drainage.

Reexpansion Pulmonary Edema After Intrapleural Fibrinolytic Therapy

We report an empyema treated with antimicrobial therapy that developed reexpansion pulmonary edema after intrapleural fibrinolytic and enzyme therapy. Rapid evacuation of pleural fluid likely contributed to the development of reexpansion pulmonary edema.

Approach to malignant pleural effusions: Role of pleural manometry exemplified by case scenarios.

Issues related to the management of pleural effusion in India are unique. With high incidence of tuberculosis and malignancy, managing patients with pleural effusion may not be the same between patients. Decisions on intercostal chest drain insertion, volume of fluid to be removed during therapeutic thoracentesis, and further diagnostic imaging and investigations are often taken with difficulty in low-resource settings. Pleural manometry can help resolve these issues and help in the management of such patients. Pleural manometry has been advocated as a valuable tool to characterize underlying lung behavior during thoracentesis and has been proposed to be useful in diagnosing unexpandable lung, predicting the success of pleurodesis, and preventing the development of excessively negative pleural pressures which in turn may lead to the development of reexpansion pulmonary edema. There is very little literature on pleural manometry from India and other developing countries. In this article, the utility of pleural manometry in managing patients with malignant pleural effusion is discussed.

Koroner Baypas Sonrası Geç Dönemde Plevral Efüzyon Drenajından Kaynaklanan Reekspansiyon Akciğer Ödemi

Reexpansion pulmonary edema usually follows rapid reinflation of lung parenchyma which collapsed more than three days and can be fatal in up to 21% of cases. A 48-year-old man who had undergone CABG (Coronary Artery Bypass Graft) three weeks ago, admitted to our hospital with a diagnosis of left pleural effusion. He had the clinical findings of pulmonary edema, respiratory insufficiency and shock after tube thoracostomy. He was mechanically ventilated in intensive care unit. During this period, fluid restriction, inotropic agent, diuretic and oxygen support therapy were applied. The patient discharged on 7th day with a full clinical and radiological recovery. The aim of this case report was present to attention the development of re-expansion pulmonary edema which may be fatal, after tube thoracostomy in a patient with pleural effusion following coronary artery bypass surgery.

Reexpansion pulmonary edema following tube thoracostomy for spontaneous pneumothorax in an elderly male

Reexpansion pulmonary edema (RPE) is an important cause of unilateral pulmonary edema that rarely occurs following drainage of pleural effusion or pneumothorax. Most patients develop symptoms within an hour of lung expansion. The presentation is usually rapid and dramatic and may be fatal at times. The duration of lung collapse more than 3 days, large-size pneumothorax, rapidity of lung expansion, and application of negative pleural suction are well-known risk factors for the development of RPE. We present here an elderly male with diabetes mellitus who presented with a large pneumothorax and developed RPE shortly after insertion of a chest tube.

Efficacy of intermittent ventilation performed in lungs on operated side for prevention of reexpansion pulmonary edema after pulmonary resection

Objective To evaluate the efficacy of intermittent ventilation performed in lungs on the operated side for prevention of reexpansion pulmonary edema after pulmonary resection. Methods Forty patients of both sexes, aged 16-32 yr, with body mass index of 18-25 kg/m2, of ASA physical status Ⅰ or Ⅱ, scheduled for elective thoracoscope-assisted pulmonary resection, were randomly divided into 2 groups(n=20 each)using a random number table: control group(group C)and intermittent ventilation performed in lungs on the operated side group(group V). After induction of anesthesia, the patients were tracheally intubated and mechanically ventilated.After correct positioning was confirmed by fiberoptic bronchoscopy, one-lung ventilation was performed instead.One-lung ventilation was performed routinely in group C. In group V, the lung on the operated side was ventilated intermittently for 30 s with the tidal volume set at 2 ml/kg and respiration rate at 20 bpm, the bronchial tube was then opened, and the process was repeated at 10 min intervals until the diseased tissues were removed.After resection of diseased tissues, the specimens of normal tissues around the area were obtained for determination of the expression of aquaporin 1(AQP-1)and AQP-5 in lung tissues.The development of pulmonary atelectasis, hyoxemia and reexpansion pulmonary edema was recorded within 24 h after surgery. Results Compared with group C, AQP-1 and AQP-5 expression was significantly up-regulated, the incidence of atelectasis and reexpansion pulmonary edema was decreased within 24 h after surgery, while no significant change was found in the incidence of hyoxemia in group V. Conclusion Intermittent ventilation performed in lungs on the operated side can effectively prevent the development of reexpansion pulmonary edema during one-lung ventilation in the patients undergoing pulmonary resection. Key words: Respiration, artificial; Pulmonary edema; Postoperative complications

Life-threatening Re-expansion Pulmonary Edema

A 45-year-old woman with a high-grade Burkitt lymphoma developed reexpansion pulmonary edema (RPE) after drainage of 900 mL of pleural fluid. Sequential, bilateral therapeutic thoracenteses with pleural manometry were performed 2 weeks after the initial thoracentesis. Pleural manometry showed increased pleural space elastance in both pleural spaces; air-contrast computed tomography of the chest demonstrated visceral pleural thickening, involving both lungs, consistent with the diagnosis of bilateral, unexpandable lung due to the presence of visceral pleural restriction. The pathogenesis of RPE is unknown, but it is believed to involve a microvascular injury from reperfusion. The pathogenetic role of excessively negative pleural pressures in the development of RPE in humans has never been established. This is the first report utilizing pleural manometry to allow safe removal of pleural fluid in a patient who previously developed life-threatening RPE.

Risk factors for the development of reexpansion pulmonary edema in patients with spontaneous pneumothorax

BackgroundReexpansion pulmonary edema (REPE) is known as a rare and fatal complication after tube thoracostomy.ObjectivesWe investigated the risk factors for the development of REPE in patients with spontaneous pneumothorax.MethodsWe selected patients who were diagnosed with spontaneous pneumothorax and were initially treated with tube thoracostomy between August 1, 2003 and December 31, 2011. The patients’ electronic medical records, including operative notes and chest x-ray and computed tomography scans, were reviewed.ResultsREPE developed in 49 of the 306 patients (16.0%). REPE was more common in patients with diabetes (14.3% vs 3.9%, P = 0.004) or tension pneumothorax (46.8% vs 16.2%, P = 0.000). The pneumothorax was larger in patients with REPE than without REPE (57.0 ± 16.0% vs 34.2 ± 17.6%, P = 0.000), and the incidence of REPE increased with the size of pneumothorax. On multivariate analysis, diabetes mellitus [(odds ratio (OR) = 9.93, P = 0.003), and the size of pneumothorax (OR = 1.07, P = 0.000) were independent risk factors of REPE.ConclusionsThe presence of diabetes increases the risk of REPE development in patients with spontaneous pneumothorax. The risk of REPE also increases significantly with the size of pneumothorax.

The Frequency of Reexpansion Pulmonary Edema after Trocar and Hemostat Assisted Thoracostomy in Patients with Spontaneous Pneumothorax

PurposeSeveral risk factors for development of reexpansion pulmonary edema (REPE) after drainage of pneumothoraces have been reported, but the association between the method of thoracostomy and the development of REPE is unknown. The aim of this study was to compare the frequency of REPE after treatment of spontaneous pneumothorax with trocar or hemostat assisted closed thoracostomy.Materials and MethodsWe performed a prospective, observational study including 173 patients with spontaneous pneumothorax who visited the emergency department from January 2007 to December 2008. In 2007, patients were treated with hemostat-assisted drainage, whereas patients in 2008 were treated with trocar-assisted drainage. The main outcome was the development of REPE, determined by computed tomography of the chest 8 hours after closed thoracostomy. Outcomes in both groups were compared using univariate and multivariate analyses.ResultsNinety-two patients were included, 48 (42 males) of which underwent hemostat-assisted drainage and 44 (41 males) underwent trocar-assisted drainage. The groups were similar in mean age (24±10 vs. 26±14 respectively). The frequencies of REPE after hemostat- and trocar-assisted drainage were 63% (30 patients) and 86% (38 patients) respectively (p=0.009). In multivariate analysis, trocar-assisted drainage was the major contributing factor for developing REPE (odds ratio=5.7, 95% confidence interval, 1.5-21). Age, gender, size of pneumothorax, symptom duration and laboratory results were similar between the groups.ConclusionClosed thoracostomy using a trocar is associated with an increased risk of REPE compared with hemostat-assisted drainage in patients with spontaneous pneumothorax.

Re-expansion pulmonary edema in a boy with spontaneous pneumothorax during an influenza B virus infection

Re-expansion Pulmonary Edema (RPE) is an uncommon complication following rapid re-expansion of the lungs, and the most common disorder associated with RPE is spontaneous pneumothorax. The majority of patients with RPE associated with pneumothorax have been adults; only 4 cases have been reported in children. We present a patient who developed RPE after treatment of spontaneous pneumothorax that occurred during an influenza B virus infection. His condition improved only with oxygen supplementation and intravenous corticosteroids. Infection with influenza B virus leads to increased production of lung epithelial oxidants, which might have contributed to the development of RPE in our patient.

POLYMORPHONUCLEAR LEUKOCYTES ARE ACTIVATED DURING ATELECTASIS BEFORE LUNG REEXPANSION IN RAT

Although reexpansion of a collapsed lung often causes pulmonary edema, the pathogenesis of the condition is not yet fully understood. To determine whether inflammatory changes occur in the pulmonary circulation during atelectasis and study the mechanism underlying the development of reexpansion pulmonary edema, we used a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 1 h. We evaluated the accumulation of polymorphonuclear leukocytes (PMNs) in the lung and the production of reactive oxygen species (ROS) in the pulmonary circulation using a fluorescent imaging technique. We also used confocal laser scanning microscopy and computerized image analysis to evaluate the membrane translocation of p47-phox, one of the nicotinamide adenine dinucleotide phosphate (reduced form) oxidase subunits, in PMNs sequestered in the lung. Polymorphonuclear leukocytes accumulated in the lung during atelectasis, and p47-phox was translocated to the plasma membrane, but no ROS production was observed. Marked PMN ROS production was observed after reexpansion of the collapsed lung with air. Little ROS production was observed when the lung was reexpanded with nitrogen. During atelectasis, PMNs accumulate in the lung, where they are primed for respiratory bursting. After pulmonary reexpansion, oxygen is supplied from the alveoli, and PMN respiratory bursting occurs.

LARGE VOLUME THORACENTESIS AND THE RISK OF RE-EXPANSION PULMONARY EDEMA

PURPOSE: Re-expansion Pulmonary Edema (RPE) is a well described, but rare complication after large volume thoracentesis. The creation of excessive negative pleural pressures (Ppl) has been postulated as a mechanism for the development of RPE. Previous studies in animal models have suggested that RPE is not seen when Ppl is kept greater than -20 cmH20. Similarly, an arbitrary cut-off of 1L has been suggested as a volume limit to minimize the risk of RPE. To date, no large series has examined the safety of large volume thoracentesis and risk of RPE in humans.

Hydrostatic mechanisms may contribute to the pathogenesis of human re-expansion pulmonary edema.

The primary objective was to test the hypothesis that clinical re-expansion pulmonary edema is predominantly due to increased permeability of the alveolar-capillary barrier. A secondary objective was to determine if the alveolar epithelium was functionally intact in patients with re-expansion pulmonary edema by measuring net alveolar epithelial fluid transport in a subset of patients. Retrospective study of mechanically ventilated patients with re-expansion pulmonary edema. Two academic tertiary care hospitals. Seven patients with acute onset of re-expansion pulmonary edema after tube thoracostomy or thoracentesis. Pulmonary edema fluid and plasma were collected at the time of onset of re-expansion edema. Contrary to our hypothesis, the mean initial edema fluid to plasma protein ratio was 0.58+/-0.21, supporting a hydrostatic mechanism of edema formation. Four of the patients had an initial edema fluid to plasma protein ratio of less than 0.65, consistent with pure hydrostatic pulmonary edema, while the others had a slight increase in permeability (edema fluid to plasma ratios of 0.67, 0.71 and 0.77), perhaps due to capillary stress failure from hydrostatic stress. Alveolar fluid clearance (mean 9.8+/-8.0%/h) was intact in the subset of three patients in whom it was measured. This study provides the first direct evidence that hydrostatic forces may contribute to the development of re-expansion pulmonary edema.

Ultrasound-Guided Thoracentesis : Is It a Safer Method?

The objectives of this study are as follows: (1) to determine the incidence of complications from thoracentesis performed under ultrasound guidance by interventional radiologists in a tertiary referral teaching hospital; (2) to evaluate the incidence of vasovagal events without the use of atropine prior to thoracentesis; and (3) to evaluate patient or radiographic factors that may contribute to, or be predictive of, the development of re-expansion pulmonary edema after ultrasound-guided thoracentesis. Prospective descriptive study. Saint Thomas Hospital, a tertiary referral teaching hospital in Nashville, TN. All patients referred to interventional radiology for diagnostic and/or therapeutic ultrasound-guided thoracentesis between August 1997 and September 2000. A total of 941 thoracenteses in 605 patients were performed during the study period. The following complications were recorded: pain (n = 25; 2.7%), pneumothorax (n = 24; 2.5%), shortness of breath (n = 9; 1.0%), cough (n = 8; 0.8%), vasovagal reaction (n = 6; 0.6%), bleeding (n = 2; 0.2%), hematoma (n = 2; 0.2%), and re-expansion pulmonary edema (n = 2; 0.2%). Eight patients with pneumothorax received tube thoracostomies (0.8%). When > 1,100 mL of fluid were removed, the incidence of pneumothorax requiring tube thoracostomy and pain was increased (p < 0.05). Fifty-seven percent of patients with shortness of breath during the procedure were noted to have pneumothorax on postprocedure radiographs, while 16% of patients with pain were noted to have pneumothorax on postprocedure radiographs. Vasovagal reactions occurred in 0.6% despite no administration of prophylactic atropine. Re-expansion pulmonary edema complicated 2 of 373 thoracenteses (0.5%) in which > 1,000 mL of pleural fluid were removed. The complication rate with thoracentesis performed by interventional radiologists under ultrasound guidance is lower than that reported for non-image-guided thoracentesis. Premedication with atropine is unnecessary given the low incidence of vasovagal reactions. Re-expansion pulmonary edema is uncommon even when > 1,000 mL of pleural fluid are removed, as long as the procedure is stopped when symptoms develop.

Association of IL-8 and MCP-1 with the development of reexpansion pulmonary edema in rabbits

Background. The aim of this study is to determine the relationships between the cytokines and the inflammatory response in reexpansion pulmonary edema (RPE).Methods. We examined the cell population, epithelial permeability measured by Evans blue dye (EB), βglucuronidase and cytokine concentrations in bronchoalveolar lavage fluid (BALF) and/or blood using a rabbit RPE model.Results. We confirmed that RPE is characterized by recruitment of polymorphonuclear leukocytes (PMNs), the release of PMN granular contents into the air spaces, and increased vascular permeability. These findings were highly correlated with increased interleukin-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) concentrations in the BALF. Growth related oncogene (GRO) was detected in the BALF from only 2 of the 7 reexpanded lungs while TNFα was not detected in any rabbits. A similar but less severe inflammatory response to the reexpanded lung was found in the contralateral lung.Conclusions. IL-8 and MCP-1 may play important roles in the development of RPE; the inflammatory response is independent of TNFα and unilateral reexpansion of the lung induces an inflammatory response not only in the reexpanded lung but also in the contralateral lung.

Neutrophils in reexpansion pulmonary edema.

This study investigated the possible contribution of neutrophils to development of reexpansion pulmonary edema (RPE) in rabbits. Rabbits' right lungs were collapsed for 7 days and then reexpanded with negative intrathoracic pressure for 2 h before study, a model that creates unilateral edema in the reexpanded lungs but not in contralateral left lungs. Two hours after lung reexpansion, significant increases in lavage albumin concentration (17-fold), percent neutrophils (14-fold), and total number of neutrophils (7-fold) recovered occurred in the reexpanded lung but not in the left. After 2 h of reexpansion increased leukotriene B4 was detected in lavage supernatant from right lungs (335 +/- 33 pg/ml) compared with the left (110 +/- 12 pg/mg, P less than 0.01), and right lung lavage acid phosphatase activity similarly increased (6.67 +/- 0.35 U/l) compared with left (4.73 +/- 0.60 U/l, P less than 0.05). Neutropenia induced by nitrogen mustard (17 +/- 14 greater than neutrophils/microliters) did not prevent RPE, because reexpanded lungs from six neutropenic rabbits were edematous (wet-to-dry lung weight ratio 6.34 +/- 0.43) compared with their contralateral lungs (4.97 +/- 0.04, P less than 0.01). An elevated albumin concentration in reexpanded lung lavage from neutropenic rabbits (8-fold) confirmed an increase in permeability. Neutrophil depletion before reexpansion did not prevent unilateral edema, although neutrophils were absent from lung sections and alveolar lavage fluid from neutropenic rabbits.