Severe re-expansion pulmonary edema after chest tube insertion for the treatment of spontaneous pneumothorax: A case report

Rationale:Re-expansion pulmonary edema (REPE) is a rare complication after chest tube insertion for the treatment of spontaneous pneumothorax. However, this complication can be life threatening when it occurs. Therefore, it is necessary to recognize REPE early and treat it appropriately. In the present study, we report a severe REPE case occurring after chest tube insertion in a patient with spontaneous pneumothorax.Patient concerns:A 27-year-old male patient visited out hospital with chest pain on the left, which had started a week ago. After diagnosed with pneumothorax and having chest tube insertion, the patient complained of sudden shortness of breath, persistent cough, foamy sputum, and vomiting.Diagnosis:Based on the symptoms and imaging findings, the patient was diagnosed as REPE.Interventions:After the condition of the patient deteriorated rapidly, he was transferred to intensive care unit and then mechanical ventilation and conservative treatment were performed after endotracheal intubation.Outcomes:After mechanical ventilation and conservative treatment in the intensive care unit, the symptoms and radiological findings improved, and then mechanical ventilation was weaned and the chest tube was removed from the patient. However, due to recurrent pneumothorax after removal of the chest tube, video assisted thoracoscopic surgery (VATS) wedge resection was performed. At 6 months post-operative follow up, he was well with normal radiological findings.Lessons:REPE occurs rarely, but once it does, it causes a serious condition that can be life-threatening. Therefore, patients with the risk factors related to it should receive a closed observation after chest tube insertion. Moreover, if REPE occurs, appropriate treatments should be carried out by recognizing it early.     

An analysis of and new risk factors for reexpansion pulmonary edema following spontaneous pneumothorax

Background

The major risk factor for reexpansion pulmonary edema (RPE) following the treatment of spontaneous pneumothorax is thought to be chronic lung collapse. However, a long-term collapsed lung does not always cause RPE. The purpose of this study was to define other risk factors for RPE among patients undergoing drainage for the treatment of spontaneous pneumothorax.

Methods

We retrospectively reviewed all the patients with spontaneous pneumothorax who had been treated at our hospital during a 5-year period. The duration of symptoms, location and size of the pneumothorax, size of the chest tube, and pleural effusion, which can occur coincidentally with pneumothorax, were compared in patients who did and did not experience RPE.

Results

Forty patients were underwent drainage for the treatment of a spontaneous pneumothorax between January 2007 and December 2012. RPE developed in 13 of the 40 (32.5%) patients. In the multivariate analysis, the presence of pleural effusion coincident with pneumothorax contributed to the risk for RPE [odds ratios (OR), 1.557; 95% confidence intervals (CI), 1.290-1.880]. The duration of symptoms, location and size of the pneumothorax and size of the chest tube were similar between the groups. Symptomatic RPE was associated with a larger pneumothorax size.

Conclusions

The rate of RPE following spontaneous pneumothorax is higher than was previously reported. Our findings suggest the presence of pleural effusion coincidentally with pneumothorax may therefore be a new risk factor for RPE.     

Re-expansion pulmonary oedema: revisited

A case of re-expansion pulmonary oedema (RPO) following chest tube insertion for left spontaneous pneumothorax is reported. There were no severe symptoms and routine chest radiograph done four hours after tube thoracostomy showed features of pulmonary oedema in the re-expanded left lung. RPO is an uncommon complication of rapid pleural drainage of air or fluid with potentially serious cardiopulmonary manifestations but appears to run a benign course if there is no prior systemic hypoxaemia and if pneumothorax is drained without suction. Chest radiograph should be done routinely within four hours after chest tube insertion for early detection of RPO.     

Spontaneous pneumothorax as a complication of septic pulmonary embolism in an intravenous drug user: a case report

Infective endocarditis has been the major cause of morbidity and mortality among intravenous drug users (IDUs) with infections, mostly involving the tricuspid valve and presenting multiple septic pulmonary embolisms. Numerous pulmonary complications of septic pulmonary embolism have been described, but only a few have reported spontaneous pneumothorax. Our patient, a 23-year-old heroin addict, was hospitalized for tricuspid endocarditis and septic pulmonary embolism. Acute onset of respiratory distress occurred on his seventh hospital day and rapidly resulted in hypoxemia. Immediate bedside chest radiograph demonstrated left pneumothorax. It was thought to be a spontaneous pneumothorax, because he had not undergone any invasive procedure before the occurrence of pneumothorax. His clinical condition improved after the insertion of an intercostal chest tube. He later underwent surgery to replace the tricuspid valve as a result of the large size of the vegetation and poor control of infection. He ultimately survived. Pneumothorax is a possible lethal complication of septic pulmonary embolism in IDUs with right-sided endocarditis and should be considered in such patients when respiratory distress occurs acutely during their hospitalization.     

Reexpansion pulmonary edema.

A case of pulmonary edema following reexpansion of a collapsed lung due to pneumothorax is described and illustrated. The importance of recognizing this relatively uncommon phenomenon is stressed. The development of such edema can be prevented by avoiding application of sudden and excessive negative pleural pressures during the evacuation of a pneumothorax or a pleural effusion. The edema generally occurs in a lung that has been collapsed for more than three days. The importance of the duration of pulmonary collapse in the causation of edema is demonstrated in this patient.     

Bilateral reexpansion pulmonary edema following unilateral pleurocentesis

Acute ipsilateral pulmonary edema following reexpansion of the lung after pleurocentesis or pneumothorax is a well described entity. We report the unusual occurrence of bilateral pulmonary edema following unilateral pleurocentesis in a young male without heart disease. Various hypotheses regarding the mechanism of reexpansion pulmonary edema include increased capillary permeability due to hypoxic injury, decreased surfactant production, altered pulmonary perfusion and mechanical stretching of membranes. This case suggests that forces leading to ipsilateral reexpansion pulmonary edema also affect the contralateral lung.     

Reexpansion pulmonary edema]

Reexpansion pulmonary edema is an uncommon complication which sometimes occurs after evacuation of a large amount of air or fluid from the pleural space. We report two cases that illustrate the diversity of the clinical expression, severe in one case and latent in the other. The pathophysiology of reexpansion pulmonary edema remains obscure. Increased pulmonary capillary permeability, favored by previous atelectatic parenchyma and rapid reexpansion appears to be the main cause. Treatment is basically preventive. Curative treatment is based on adequate oxygenation and circulation. Lower aspiration pressure and oxygenation were sufficient in our patients. Severe clinical prognosis has been reported in the literature with a 15 to 20% mortality despite use of mechanical ventilation in particularly serious situations.     

Reversible cardiogenic shock due to chest tube compression of the right ventricle

A 62-year-old woman developed shock immediately after the insertion of a right-sided chest tube. A chest roentgenogram showed the chest tube to be overlying the heart and possibly compressing the right ventricle. An animal model was developed to replicate this clinical situation. Using a domestic goat model pulmonary artery, peripheral arterial catheters were inserted along with a right sided chest tube placed to suction. A second chest tube guided by a flexible fiberoptic bronchoscope placed within its lumen was positioned between the right ventricle and the sternum of the animals. Thirteen paired measurements in three goats (average of 4.3 measurements per animal) of cardiac output, heart rate, and mean arterial blood pressure were made at baseline and after chest tube placement over the right ventricle. The data were analyzed using a paired t test statistic. Compared with baseline measurements, there was a significant decrease in cardiac output (p less than 0.001) and mean arterial pressure (p less than 0.001) as well as an increase in heart rate (p = 0.0056) after placement of the chest tube across the right ventricle. We conclude that a misplaced chest tube compressing the right ventricle can impede cardiac output and lead to a low cardiac output state. Physicians inserting chest tubes in patients should be aware of this potential complication as it is easily treated by withdrawal of the chest tube.     

The importance of early detection and therapy of reexpansion pulmonary edema

Three cases are reported of unilateral pulmonary edema, two following rapid reexpansion after prolonged tension pneumothorax, with total collapse of the right lung and one after reexpanded atelectasis following left intrabronchial obstruction. In all cases decrease of blood pressure and tachycardia not responding to intravenous fluid substitution were already present within the first 15 min after chest drainage or after removal of the intrabronchial obstruction. The preexistent dyspnea failed to improve. A cloudy opacity of the reexpanded lung was found immediately after drainage in 2 cases. After immediate application of a continuous positive airway pressure mask no more extensive therapy was necessary in one patient. The two others in whom treatment was begun with more than 1 hour delay required artificial ventilation and adrenergics for 2 and 4 days, respectively.     

Pneumothorax

Spontaneous pneumothoraces can occur without obvious underlying lung disease (primary) or in patients with known underlying lung disease (secondary). Management guidelines for spontaneous pneumothorax have been published by major professional organizations, but awareness and application among clinicians seems poor. First episodes of primary spontaneous pneumothorax can be managed with observation if the pneumothorax is small. If the pneumothorax is large or if the patient is symptomatic, manual aspiration via a small catheter or insertion of a small-bore catheter coupled to a Heimlich valve or water-seal device, should be performed. In general, definitive measures to prevent recurrence are recommended after the first recurrence of the pneumothorax, and can be achieved by medical (e.g. talc) or surgical (video-assisted thoracic surgery) pleurodesis. Secondary pneumothoraces should be treated with chest tube drainage followed by pleurodesis after the first episode to minimize any risk of recurrence. Traumatic pneumothoraces may be occult (not seen on an initial CXR) or non-occult. The majority are treated by placement of a chest tube. Selected patients may be treated conservatively, with approximately 10% of these patients eventually requiring chest tube placement. Iatrogenic pneumothoraces have a myriad of causes with transthoracic lung needle biopsy being most common. Transthoracic needle biopsy-related pneumothoraces have CT findings that can predict their occurrence and the need for chest tube placement. Iatrogenic pneumothoraces, regardless of cause, may be managed by observation or small bore chest tube placement, depending upon patient stability and the size of the pneumothorax.     

Sequential treatment of a simple pneumothorax

In a prospective investigation of isolated simple pneumothorax, the treatment of 35 patients with a total of 37 pneumothoraces was studied. A standardized sequential treatment approach was followed for evacuation of the pneumothorax and maintenance of lung reexpansion. The protocol involved catheter placement using a Seldinger technique, aspirations, and documentation of reexpansion by chest radiography and observation. Reaccumulation of air was treated with Heimlich valve attachment to the catheter at intrapleural pressure and further observation. Continued air leak following Heimlich valve attachment was treated with chest catheter suction using a Pleurovac at -20 cm H2O pressure. Chest tube thoracostomy was performed for continued failure of reexpansion. In 22 of the 37 pneumothoraces (59%) simple catheter aspiration maintained lung reexpansion without complications. In the remaining 15 pneumothoraces (41%), seven (47%) responded to Heimlich valve attachment, and three (20%) maintained expansion with chest catheter suction. Chest tube thoracotomy was required to maintain expansion in 33% (five) of those who failed catheter suction (14% of all pneumothoraces studied). Patients treated successfully with simple catheter aspiration were sent home. Patients requiring a Heimlich valve, chest catheter suction, or chest tube thoracostomy were hospitalized. Use of these catheter techniques resulted in lower cost and was associated with shorter hospitalizations than in chest tube thoracostomy. Our study suggests that sequential treatment of simple pneumothorax should be considered as a cost-effective and therapeutically successful alternative to immediate chest thoracostomy in selected cases.     

Evaluation of reexpansion pulmonary edema following unilateral pneumothorax in rabbits and the effect of superoxide dismutase

We investigated the lung injury that occurs following reexpansion of a unilateral pneumothorax and determined the effect of superoxide dismutase (SOD) infused immediately prior to reexpansion on this injury. After 7 days of at least 80% right pneumothorax, rabbits received intravenous infusions of either SOD (n = 7), heat-inactivated SOD (n = 1), or vehicle (n = 7) immediately before lung reexpansion. Lung injury was assessed by measuring the systemic white cell counts, pulmonary blood volumes, extravascular albumin, extravascular lung water, wet/dry weight ratios, and histology 2 h after reexpansion. The reexpanded lung showed increased extravascular albumin, extravascular lung water and wet/dry weight ratios with decreased blood volumes compared to the uninjured lung. SOD delayed the onset of leukopenia and neutropenia at 3 and 7 min after reexpansion, but the white cell counts had decreased to the same level in both groups by 30 min. SOD had no effect on the degree of injury after 2 h. While a single bolus of SOD given immediately before reexpansion delayed the onset of this injury, it did not affect the injury that subsequently developed in the lung.     

Unilateral pulmonary oedema due to lung re-expansion following pleurocentesis for spontaneous pneumothorax. The role of non-invasive continuous positive airway pressure ventilation

Re-expansion pulmonary oedema represents a rare complication of treatment of spontaneous pneumothorax with only a few cases documented in the current literature. We present the case of a 47-year-old male who presented a right-sided spontaneous pneumothorax and developed respiratory failure after chest tube drainage. The diagnosis of re-expansion pulmonary oedema was made and he was successfully treated with non-invasive continuous positive airway pressure ventilation. Since pathogenesis of re-expansion unilateral pulmonary oedema differs significantly from that of cardiogenic pulmonary oedema, the role of non-invasive continuous positive airway pressure ventilation is discussed as an additional therapeutic option.     

Bilateral spontaneous pneumothorax in systemic sclerosis--report of two cases

We describe 2 patients with systemic sclerosis who developed bilateral spontaneous pneumothoraces. Though unilateral spontaneous pneumothorax has been described, the problem has not been emphasized recently and the complication of bilateral spontaneous pneumothoraces has not been documented. Treatment of the pneumothorax is difficult and reexpansion of the lung is slow. This complication is associated with a poor prognosis as both patients had severe respiratory impairment and one died shortly afterwards.     

Reexpansion hypotension. A complication of rapid evacuation of prolonged pneumothorax

Three cases of hypotension are described that followed rapid evacuation of persistent unilateral pneumothorax. Common features included the presence of a pneumothorax for approximately one week before treatment commenced and profuse unilateral reexpansion edema, a rising hematocrit reading, hypotension, and anuria after evacuation of the pneumothorax in spite of a relatively normal pulmonary capillary wedge pressure. In one case, cardiac output was measured and found to be low (1.54 and 1.65 L/min/sq m), with a pulmonary capillary wedge pressure of 10 to 14 mm Hg. Death due to cardiovascular collapse occurred in one patient; ischemic colitis, acute renal failure, disseminated intravascular coagulation, and ischemic necrosis of both humeral heads occurred in another. The cases presented and the literature reviewed suggest that cardiovascular compromise was the end result of the combined effects of intravascular volume depletion and myocardial depression.     

Hemodynamic Effects of Noninvasive Ventilation in Patients with Venocapillary Pulmonary Hypertension

Background

The hemodynamic effects of noninvasive ventilation with positive pressure in patients with pulmonary hypertension without left ventricular dysfunction are not clearly established.

Objectives

Analyze the impact of increasing airway pressure with continuous positive airway pressure on hemodynamic parameters and, in particular, on cardiac output in patients with variable degrees of pulmonary hypertension.

Methods

The study included 38 patients with pulmonary hypertension caused by mitral stenosis without left ventricular dysfunction or other significant valvulopathy. The hemodynamic state of these patients was analyzed in three conditions: baseline, after continuous positive pressure of 7 cmH₂O and, finally, after pressure of 14 cmH₂O.

Results

The population was composed of predominantly young and female individuals with significant elevation in pulmonary arterial pressure (mean systolic pressure of 57 mmHg). Of all variables analyzed, only the right atrial pressure changed across the analyzed moments (from the baseline condition to the pressure of 14 cmH₂O there was a change from 8 ± 4 mmHg to 11 ± 3 mmHg, respectively, p = 0.031). Even though there was no variation in mean cardiac output, increased values in pulmonary artery pressure were associated with increased cardiac output. There was no harmful effect or other clinical instability associated with use application of airway pressure.

Conclusion

In patients with venocapillary pulmonary hypertension without left ventricular dysfunction, cardiac output response was directly associated with the degree of pulmonary hypertension. The application of noninvasive ventilation did not cause complications directly related to the ventilation systems.     

Incidence and risk factors of delayed pneumothorax after transthoracic needle biopsy of the lung

STUDY OBJECTIVES: To evaluate the incidence and clinical significance of delayed pneumothorax, and to analyze the influence of multiple variables on the rate of delayed pneumothorax associated with transthoracic needle biopsy (TTNB) of the lung. STUDY DESIGN: Prospective study. SETTING: Tertiary care university hospital. STUDY SUBJECTS: Adult patients underwent TTNB from June 2001 to June 2002. MEASUREMENTS AND RESULTS: Among the 458 patients included in this study, 280 fluoroscopic-guided, 21 CT-guided, and 157 ultrasonography-guided lung biopsies were performed. A follow-up chest radiograph was obtained immediately, and 3 h, 8 h, and 24 h after the biopsy procedure. Pneumothorax that had not developed up to 3 h but developed later was defined as a delayed pneumothorax. Patients with a symptomatic or enlarged pneumothorax were treated using a pigtail catheter or chest tube. Variables such as age, gender, lesion size, location, presence of an emphysematous change, biopsy guidance methods, and biopsy devices were analyzed. Pneumothorax developed in 100 of the 458 patients (21.8%), and delayed pneumothorax developed in 15 patients (3.3%). Seventeen patients, including 3 patients with delayed pneumothorax, required a pigtail catheter or a chest tube insertion. The pigtail catheter or chest tube insertion rate in delayed pneumothorax was 20% (3 of 15 patients). Female gender and the absence of an emphysematous change correlated with an increased rate of delayed pneumothorax (p < 0.05). Lesion size, location, biopsy guidance methods, devices, and underlying diseases were not correlated with the delayed pneumothorax rate. CONCLUSIONS: The incidence of delayed pneumothorax was 3.3% of all TTNBs. Female gender and the absence of an emphysematous change were identified as risk factors for delayed pneumothorax. Delayed pneumothorax is clinically important because of its considerable incidence and the necessity for pigtail catheterization or chest tube insertion in these patients.     

Effects of two chest tube clearance protocols on drainage in patients after myocardial revascularization surgery

The purpose of the study was to determine the effects of two methods of clot clearance on chest tube drainage in patients undergoing myocardial revascularization. Two hundred adult patients immediately after myocardial revascularization were randomly assigned to a specific chest tube manipulation group. The dependent variables were drainage, incidence of cardiac tamponade, incidence of surgical reentry, hemodynamic values, and number of manipulation episodes. Statistical analyses revealed no difference in any of the dependent variables when milking and stripping were used. Of the 200 patients, 78 did not require any manipulation of the chest tubes in the first 8 hours after surgery. One patient had signs of cardiac tamponade and six other patients required surgical reentry. Positioning of the connecting tube in a nondependent position assisted with the removal of drainage from the chest cavity. In conclusion, patients having myocardial revascularization did not need their chest tubes manipulated the first 8 hours after surgery. Visible drainage in the chest tube did not cause a lack of patency.     

Clinical analysis of reexpansion pulmonary edema

Twenty-one of 146 cases of spontaneous pneumothorax that were treated by thoracentesis or continuous low negative pressure suction drainage (-12 cm H2O) of the pleural space developed REPE. The rate of REPE was higher in patients 20 to 39 years of age than in those over the age of 40, and the rate progressively increased in proportion to the extent of pneumothorax, as assessed by roentgenographic criteria. It is postulated that age-related changes in the lung may afford some degree of protection against developing REPE. It is also suggested that the treatment of pneumothorax with thoracentesis and/or suction drainage in young patients, or in the face of a large pneumothorax, requires careful consideration in view of a relatively high incidence of REPE in such individuals.