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Pleural injury and subsequent loculation is characterized by acute injury, sustained inflammation and, when severe, pathologic tissue reorganization. While fibrin deposition is a normal part of the injury response, disordered fibrin turnover can promote pleural loculation and, when unresolved, fibrosis of the affected area. Within this review, we present a brief discussion of the current IPFT therapies, including scuPA, for the treatment of pathologic fibrin deposition and empyema. We also discuss endogenously expressed PAI-1 and how it may affect the efficacy of IPFT therapies. We further delineate the role of pleural mesothelial cells in the progression of pleural injury and subsequent pleural remodeling resulting from matrix deposition. We also describe how pleural mesothelial cells promote pleural fibrosis as myofibroblasts via mesomesenchymal transition. Finally, we discuss novel therapeutic targets which focus on blocking and/or reversing the myofibroblast differentiation of pleural mesothelial cells for the treatment of pleural fibrosis.

During pulmonary resections, removal of visceral pleura is frequently required, resulting in lung air leakage (LAL) and bleeding. Especially persistent LAL after pulmonary surgery has negative consequences. Current surgical procedures are ineffective in closing these visceral pleural injuries. Previously, the authors' laboratory has developed a novel and effective LAL sealant using tissue-engineered cell sheets harvested from temperature-responsive culture dishes. The clinical application of fresh fibroblast sheets (FSs) is limited by several problems related to the cell culture period, mass production, preservation, and transportation. Therefore, cryopreservation of FSs and feasibility of off-the-shelf FSs for repairing visceral pleural defects were investigated. Over 3 to 6 months, harvested skin-derived FSs in Dulbecco's modified Eagle's medium supplemented with 10% dimethyl sulfoxide were stored in an atmosphere of liquid nitrogen. The amounts of cytokines (basic fibroblast growth factor [bFGF] and vascular endothelial growth factor) released from frozen-thawed FSs were determined. bFGF levels were significantly elevated in frozen-thawed FSs compared with fresh FSs. After a visceral pleural injury model was created, a frozen-thawed skin-derived FS was transplanted directly to the defect. One month after transplantation, the frozen-thawed FS remained on the pleural surface, resulting in permanent closure, suggesting that cells in the off-the-shelf FS had the ability to proliferate and release various cytokines. Frozen-thawed FSs were useful for closing LALs during pulmonary surgery as an off-the-shelf technique and would be used as a pleural substitute.

The critical care management of pleural air leaks can be challenging in all patients, but particularly in patients on mechanical ventilation. To investigate the effect of central airway pressure and pleural pressure on pulmonary air leaks, we studied orotracheally intubated mice with pleural injuries. We used clinically relevant variables - namely, airway pressure and pleural pressure - to investigate flow through peripheral air leaks. The model studied the pleural injuries using a pressure-decay maneuver. The pressure-decay maneuver involved a 3 sec ramp to 30 cmH 2 0 followed by a 3 sec breath hold. After pleural injury, the pressure-decay maneuver demonstrated a distinctive airway pressure time history. Peak inflation was followed by a rapid decrease to a lower plateau phase. The decay phase of the inflation maneuver was influenced by the injury area. The rate of pressure decline with multiple injuries (28 ± 8 cmH 2 0/sec) was significantly greater than a single injury (12 ± 3 cmH 2 O/sec) (P < 0.05). In contrast, the plateau phase pressure was independent of injury surface area, but dependent upon transpulmonary pressure. The mean plateau transpulmonary pressure was 18 ± 0.7 cm H 2 O. Finally, analysis of the inflation ramp demonstrated that nearly all volume loss occurred at the end of inflation (P < 0.001). We conclude that the air flow through peripheral lung injuries was greatest at increased lung volumes and limited by peripheral airway closure. In addition to suggesting an intrinsic mechanism for limiting flow through peripheral air leaks, these findings suggest the utility of positive end-expiratory pressure and negative pleural pressure to maintain lung volumes in patients with pleural injuries., (© 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Pleural loculation affects about 30,000 patients annually in the United States and in severe cases can resolve with restrictive lung disease and pleural fibrosis. Pleural mesothelial cells contribute to pleural rind formation by undergoing mesothelial mesenchymal transition (MesoMT), whereby they acquire a profibrotic phenotype characterized by increased expression of α-smooth muscle actin and collagen 1. Components of the fibrinolytic pathway (urokinase plasminogen activator and plasmin) are elaborated in pleural injury and strongly induce MesoMT in vitro. These same stimuli enhance glycogen synthase kinase (GSK)-3β activity through increased phosphorylation of Tyr-216 in pleural mesothelial cells and GSK-3β mobilization from the cytoplasm to the nucleus. GSK-3β down-regulation blocked induction of MesoMT. Likewise, GSK-3β inhibitor 9ING41 blocked induction of MesoMT and reversed established MesoMT. Similar results were demonstrated in a mouse model of Streptococcus pneumoniae-induced empyema. Intraperitoneal administration of 9ING41, after the induction of pleural injury, attenuated injury progression and improved lung function (lung volume and compliance; P < 0.05 compared with untreated and vehicle controls). MesoMT marker α-smooth muscle actin was reduced in 9ING41-treated mice. Pleural thickening was also notably reduced in 9ING41-treated mice (P < 0.05). Collectively, these studies identify GSK-3β as a newly identified target for amelioration of empyema-related pleural fibrosis and provide a strong rationale for further investigation of GSK-3β signaling in the control of MesoMT and pleural injury., (Copyright © 2017 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Background: Prolonged air leak after pleural decortication is one of the most frequent complications., Objective: The aim of this study is to compare the effects of prolonged air leak between the digital chest drainage (DCD) system and the classic drainage system in patients with empyema class IIB or III (American Thoracic Society classification) in pleural decortication patients., Material and Methods: A total of 37 patients were enrolled in a prospective randomized control trial over one year, consisting of 2blinded groups, comparing prolonged air leak as a main outcome, the number of days until removal of chest drain, length of hospital stay and complications as secondary outcomes., Results: The percentage of prolonged air leak was 11% in the DCD group and 5% in the classic group (P=0.581); the mean number of days of air leak was 2.5±1.8 and 2.4±2.2, respectively (P=0.966). The mean number of days until chest tube removal was 4.5±1.8 and 5.1±2.5 (P=0.41), the length of hospital stay was 7.8±3.7 and 8.9±4.0 (P=0.441) and the complication percentages were 4 (22%) and 7 (36%), respectively (P=0.227)., Discussion: In this study, no significant difference was observed when the DCD was compared with the classic system. This was the first randomized clinical trial for this indication; thus, future complementing studies are warranted., (Copyright © 2016 Academia Mexicana de Cirugía A.C. All rights reserved.)

Objectives: Although an alveolar air leak (AAL) after pulmonary resection is a troublesome complication that diminishes a patient's quality of life and increases medical costs, current treatment and preventive methods for AAL are not effective. Therefore, we transplanted adipose-derived stem cells (ASCs) to the damaged visceral pleura to facilitate the regeneration of mesothelial cells and investigated the possibility of cell therapy as a treatment option for AAL., Methods: Stem cells were isolated and cultured from discarded fat tissues that were collected after liposuction procedures. Flow cytometry analysis was performed to evaluate their suitability as mesenchymal stem cells. Cultured stem cells were seeded onto polyglycolic acid (PGA) sheets and incubated for 5 days. Under general anaesthesia, 10 New Zealand rabbits underwent thoracotomies. After the visceral pleura was damaged, PGA sheets containing ASCs were transplanted into 5 rabbits (ASC group) and PGA sheets without cells were transplanted into the other 5 rabbits (control group). Rethoracotomies were performed after 4 weeks, and the transplanted areas in the visceral pleura were excised for analysis. Haematoxylin and eosin and Azan staining were performed. In addition, electron microscopic examinations were performed to investigate the ultrastructure of the regenerating mesothelium., Results: Cultured stem cells were positive for the surface proteins CD13, CD29, CD49d, CD90 and CD105, whereas they were negative for CD34, CD45 and human leukocyte antigen (HLA)-DR. The adhesions between the transplanted visceral pleura and parietal pleura were weaker in the ASC group than in the control group. On histological examination, the mesothelial cell monolayer of the visceral pleura was well preserved in the ASC group, whereas it was frequently lost in the control group. Electron microscopy demonstrated that the mesothelial cell monolayer and its abundant microvilli were well preserved in the ASC group, but were absent or disintegrated in the control group., Conclusions: Transplantation of ASCs to the damaged visceral pleura can contribute to the treatment and prevention of AAL by improving the regeneration of mesothelial cells., (© The Author 2014. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Percutaneous nephrolithotomy (PCNL) is presently the treatment of choice for large or multiple kidney stones or stones in the calyx. PCNL is generally safe and associated with low but indisputable complication rate. Pleural injury in PCNL is a rare but severe complication which can occur during or immediately after operation. Pleural injury may lead to chronic empyema thoracis. Until now no such case has been reported in literature., (2014 BMJ Publishing Group Ltd.)

Intrapleural processing of prourokinase (scuPA) in tetracycline (TCN)-induced pleural injury in rabbits was evaluated to better understand the mechanisms governing successful scuPA-based intrapleural fibrinolytic therapy (IPFT), capable of clearing pleural adhesions in this model. Pleural fluid (PF) was withdrawn 0-80 min and 24 h after IPFT with scuPA (0-0.5 mg/kg), and activities of free urokinase (uPA), plasminogen activator inhibitor-1 (PAI-1), and uPA complexed with α-macroglobulin (αM) were assessed. Similar analyses were performed using PFs from patients with empyema, parapneumonic, and malignant pleural effusions. The peak of uPA activity (5-40 min) reciprocally correlated with the dose of intrapleural scuPA. Endogenous active PAI-1 (10-20 nM) decreased the rate of intrapleural scuPA activation. The slow step of intrapleural inactivation of free uPA (t1/2(β) = 40 ± 10 min) was dose independent and 6.7-fold slower than in blood. Up to 260 ± 70 nM of αM/uPA formed in vivo [second order association rate (kass) = 580 ± 60 M(-1)·s(-1)]. αM/uPA and products of its degradation contributed to durable intrapleural plasminogen activation up to 24 h after IPFT. Active PAI-1, active α2M, and α2M/uPA found in empyema, pneumonia, and malignant PFs demonstrate the capacity to support similar mechanisms in humans. Intrapleural scuPA processing differs from that in the bloodstream and includes 1) dose-dependent control of scuPA activation by endogenous active PAI-1; 2) two-step inactivation of free uPA with simultaneous formation of αM/uPA; and 3) slow intrapleural degradation of αM/uPA releasing active free uPA. This mechanism offers potential clinically relevant advantages that may enhance the bioavailability of intrapleural scuPA and may mitigate the risk of bleeding complications.

While performing thoracoscopic wedge resection of the lung, the location of the lesion is generally identified by visual inspection or palpation. When difficulty in identification of the lesion by thoracoscopy is anticipated, preoperative marking is performed. However, complications and technical difficulties plague current marking techniques. To overcome this problem, we designed a new, safe and easy marking technique that avoids pleural puncture, called the intrathoracic stamping method.

Elevated concentrations of plasminogen activator inhibitor-1 (PAI-1) are associated with pleural injury, but its effects on pleural organization remain unclear. A method of adenovirus-mediated delivery of genes of interest (expressed under a cytomegalovirus promoter) to rabbit pleura was developed and used with lacZ and human (h) PAI-1. Histology, β-galactosidase staining, Western blotting, enzymatic and immunohistochemical analyses of pleural fluids (PFs), lavages, and pleural mesothelial cells were used to evaluate the efficiency and effects of transduction. Transduction was selective and limited to the pleural mesothelial monolayer. The intrapleural expression of both genes was transient, with their peak expression at 4 to 5 days. On Day 5, hPAI-1 (40-80 and 200-400 nM of active and total hPAI-1 in lavages, respectively) caused no overt pleural injury, effusions, or fibrosis. The adenovirus-mediated delivery of hPAI-1 with subsequent tetracycline-induced pleural injury resulted in a significant exacerbation of the pleural fibrosis observed on Day 5 (P = 0.029 and P = 0.021 versus vehicle and adenoviral control samples, respectively). Intrapleural fibrinolytic therapy (IPFT) with plasminogen activators was effective in both animals overexpressing hPAI-1 and control animals with tetracycline injury alone. An increase in intrapleural active PAI-1 (from 10-15 nM in control animals to 20-40 nM in hPAI-1-overexpressing animals) resulted in the increased formation of PAI-1/plasminogen activator complexes in vivo. The decrease in intrapleural plasminogen-activating activity observed at 10 to 40 minutes after IPFT correlates linearly with the initial concentration of active PAI-1. Therefore, active PAI-1 in PFs affects the outcome of IPFT, and may be both a biomarker of pleural injury and a molecular target for its treatment.

We report a case of a 21-year old male with an asymptomatic solitary costal exostosis incidentally detected on a chest X-ray. The exostosis originated from the costochondral junction of the left fourth rib and protruded into the thoracic cavity. Exploratory thoracoscopy showed that the exostosis had scratched the adjacent pericardium and visceral pleura. A 5.5-cm long rib segment including the exostosis was excised. This report describes that the thoracoscopic findings of an asymptomatic costal exostosis originate from the costochondral junction, demonstrating that this condition may cause more extensive thoracic organ injury than expected.

Enternal nutritional support, a frequently applied technique for providing nutrition and energy, played a pivotal role in the treatment of high risk patients. However, severe complications induced by malposition of nasogastric tube caused great danger and even death to the patients. In this case report, we present a patient with severe acute respiratory distress syndrome (ARDS) induced by bronchopleural fistula (BPF) due to malposition of nasogastric tube. Repeated lung lavage combined with extracorporeal membrane oxygenation (ECMO) was performed after transferring to the ICU of our hospital. Finally, the patient recovered and discharged 7 days after admission.

Purpose: Massive earthquakes are harmful to humankind. This study of a historical cohort aimed to investigate the difference between earthquake-related crush thoracic traumas and thoracic traumas unrelated to earthquakes using a multi-detector Computed Tomography (CT)., Methods: We retrospectively compared an earthquake-exposed cohort of 215 thoracic trauma crush victims of the Sichuan earthquake to a cohort of 215 non-earthquake-related thoracic trauma patients, focusing on the lesions and coexisting injuries to the thoracic cage and the pulmonary parenchyma and pleura using a multi-detector CT., Results: The incidence of rib fracture was elevated in the earthquake-exposed cohort (143 vs. 66 patients in the non-earthquake-exposed cohort, Risk Ratio (RR) = 2.2; p<0.001). Among these patients, those with more than 3 fractured ribs (106/143 vs. 41/66 patients, RR=1.2; p<0.05) or flail chest (45/143 vs. 11/66 patients, RR=1.9; p<0.05) were more frequently seen in the earthquake cohort. Earthquake-related crush injuries more frequently resulted in bilateral rib fractures (66/143 vs. 18/66 patients, RR= 1.7; p<0.01). Additionally, the incidence of non-rib fracture was higher in the earthquake cohort (85 vs. 60 patients, RR= 1.4; p<0.01). Pulmonary parenchymal and pleural injuries were more frequently seen in earthquake-related crush injuries (117 vs. 80 patients, RR=1.5 for parenchymal and 146 vs. 74 patients, RR = 2.0 for pleural injuries; p<0.001). Non-rib fractures, pulmonary parenchymal and pleural injuries had significant positive correlation with rib fractures in these two cohorts., Conclusions: Thoracic crush traumas resulting from the earthquake were life threatening with a high incidence of bony thoracic fractures. The ribs were frequently involved in bilateral and severe types of fractures, which were accompanied by non-rib fractures, pulmonary parenchymal and pleural injuries.

Objective: To assess the effect of the anterior surgical approach for thoracolumbar spine tuberculosis and analyzed the causes of the surgical complications and the countermeasures., Methods: From Jan 1996 to Dec 2005, 120 patients with thoracolumbar spine tuberculosis underwent operations through the anterior approach either following the primary diagnosis (115 cases) or for recurrence (5 cases)., Results: Intraoperative pleural rupture occurred in 4 cases, and rupture of the external iliac vein occurred 1 case. Three patients had damages of the T12 dorsal ramus. One patient developed venous embolism of the lower extremity after the operation, two had paralytic ileus and 1 had false diabetes insipidus. Of the 5 recurrent patients, 1 died due to alcoholic cirrhosis and acute liver failure, 1 received a third operation for loosened internal fixation, and 1 had recurrence due to extensive drug resistance (XDR)., Conclusion: Standardized antituberculous therapy is fundamental for preventing the recurrence of tuberculosis, and individualized antituberculous therapy adjustment according to the results of bacterial culture and drug sensitivity tests can be the most effective means for preventing drug resistance and reducing tuberculosis recurrence.

Objective: Pneumothorax caused by damaged pleura represents the biggest obstacle in awake coronary artery bypass grafting. In order to safely perform this surgery, a new technique was developed to close the damaged pleura., Methods: A rub-and-spray method was employed using polyglycolic acid nonwoven fabric and fibrin glue. At first, some fibrinogen solution was rubbed on the edge of the pleural defect and then the PGA fabric was placed and the fibrinogen and thrombin solutions were sprayed. Using a thorax model, the burst pressure caused by positive pressure and the influence of negative pressure, moisture, time, continuous respiratory movement and pleural defect size were examined. In an animal experiment using pigs, the duration spent on repair was measured and any air leakage from the pleura was also identified., Results: In the thorax model, the burst pressure was 355.9+/-55.8 mmHg with positive pressure and no significant difference in negative pressure, moisture, time and respiratory moment was identified. However, there was a significant difference in the defect size. In the animal model, repair was easily achieved regardless of the defect size or location and air leakage was not seen after repair. The average duration of repair was 21.0s., Conclusions: The present method achieved a strong closure with sufficient durability. Since the fabric is soft and flexible and suturing is not required, moving and fragile pleura can be easily repaired regardless of the defect location and size. Once established, the present method may be used in other forms of awake thoracic surgery or reconstruction of the thorax.

Objective: The occurrence of intraoperative air leaks is an unavoidable complication during pulmonary surgeries. However, current surgical methods are generally ineffective in closing these visceral pleural defects, resulting in a decreased quality of life for patients. Here, we examined novel tissue engineered cell sheets for the closure of pleural defects in a porcine model., Methods: Skin biopsies were harvested from juvenile swine and tissue sheets composed of dermal fibroblasts were created using ex vivo culture on temperature-responsive dishes. After creating a visceral pleural injury model, the tissue engineered autologous dermal fibroblast sheets were transplanted directly to the defects without the use of sutures or additional adhesive agents, such as fibrin glue., Results: The tissue engineered autologous dermal fibroblast sheets attached directly to the lung surface providing an immediate seal against up to 25 cm H2O of airway pressure. Four weeks after transplantation, the dermal fibroblast sheets remained present on the pleural surface, providing permanent closure. The dermal fibroblast sheets were also responsive to changes in lung volume due to mechanical ventilation. No recurrences of air leaks were observed throughout the follow-up period., Conclusions: This study presents the development of an effective sealant for visceral pleural defects using autologous cells that have the flexibility to respond to expansion and contraction during respiration.

Objective: Animal models are indispensable for the development of new therapeutic methods for the closure of alveolar air leakage. However, it is difficult to create a uniform pleural defect model. The purpose of this study was to establish an appropriate animal model for assessing the efficacy and histotoxicity of synthetic sealants for lung surgery., Methods: Nine beagle dogs were used to evaluate the pleural defect model in comparison with conventional resection procedures. A donut-shaped silicon ring with an inner diameter of 15 mm was placed on the pleura, and 0.1 mL of cyanoacrylate was dropped into the ring. A pleural defect was created by sliding a microtome blade just beneath the polymerized cyanoacrylate. Hemostasis was performed by pressure with a sponge., Results: Morphologically, round areas of the pleura were uniformly resected with our procedure. The resected tissue consisted of pleura and thin underlying lung parenchyma. Among the results from 3 surgeons, there were no significant differences in the mean time required for hemostasis (P = .69), the mean thickness of the resected tissue (P = .13), and the mean amount of air leakage from the resected area (P = .19). No penetration of cyanoacrylate into the lung parenchyma was evidenced by immunofluorescence microscopy. Histologically, when the pleura was resected without using cyanoacrylate, a thick fibrocellular layer extended to the lung parenchyma. Furthermore, severe fibrosis was observed when electrocautery was used for hemostasis. However, when the pleura was resected using cyanoacrylate, the normal alveolar structure was preserved., Conclusions: Our uniform pleural defect model using cyanoacrylate may be feasible for the evaluation of synthetic sealants for alveolar air leakage.

Intrapleural fibrinolysins have been used to treat pleural loculations. However, the efficacy of clinically available agents has recently been questioned, providing a rationale for investigation of new interventions. Single-chain urokinase plasminogen activator resists inhibition by serpins, and repeated, daily intrapleural administration of this agent prevents intrapleural loculation more effectively than complexes of this proenzyme with its receptor (Idell S, Mazar A, Cines D, Kuo A, Parry G, Gawlak S, Juarez J, Koenig K, Azghani A, Hadden W, McLarty J, Miller E. Am J Respir Crit Care Med 166: 920-926, 2002). Understanding of the protective mechanism and intrapleural processing remains unclear. We speculated that single-chain urokinase could induce sustained local fibrinolysis and protection by selective administration either before, during, or following loculation after pleural injury induced by tetracycline in rabbits. Enzymography, immunoassays, histology, immunohistochemistry, morphology, and morphometry were used to test the efficacy, duration of protective effect, and processing of single-chain urokinase. Intrapleural single chain urokinase prevented loculation at 72 h after injury (P < 0.01) if given either before or during adhesion formation and was converted to two-chain high-molecular-weight urokinase, which remained active for at least 24 h within pleural fluids. The effect was dose dependent, and established loculations at 72 h after tetracycline-induced injury were reversed at 96 h by single-dose treatment. Single-chain urokinase bound and saturated intrapleural plasminogen activator inhibitory (PAI)-1-like activity and urokinase-related immunoreactivity of the mesothelium was comparable in treatment or vehicle-control groups. Adhesions recurred by 2 wk after treatment with recurrence of excess local PAI activity. Single-chain urokinase induces sustained local fibrinolysis and reversibly prevents pleural loculation for up to 48 h after intrapleural administration after tetracycline-induced injury.

We report a case of cerebral arterial air embolism that was followed by a brain computed tomographic scan and magnetic resonance imaging during the first week after onset. A 73-year-old man was admitted for treatment of pleural dissemination that was a recurrence after right lower bilectomy for advanced lung cancer. Thirty minutes after an anti-drug administration through the chest drainage tube, he lost consciousness shortly after coughing. A bubble in the inferior sagittal sinus was observed on the day of the stroke, which then disappeared within 24 hours. It seems that the anti-cancer agent evoked inflammation at the visceral pleura and the subject inhaled massive air flow into the systemic circulation.

We report three patients who had intrapleural insertion of an intended thoracic epidural catheter. These misplaced catheters were used for local anesthetic administration. Bupivacaine injection via these catheters in two cases was effective for reducing postoperative pain. We conclude that if an intended thoracic epidural catheter is found to be in the intrapleural cavity at the time of surgery and if correct replacement of the catheter into the epidural space is not believed to be feasible after surgery, then the administration of local anesthetic through the intrapleural catheter could be considered as a potential alterative analgesic method.

Single-injection paravertebral block offers adequate unilateral analgesia for thoracic and upper abdominal surgery. This technique is easy to learn but there is a risk, albeit low, of pleural puncture. The aim of the study was to determine whether sonographic measurements of the distances from the skin to the transverse process and to the parietal pleura are useful for calculating the required depth of needle insertion. Before puncture of the paravertebral space, the distances from the skin to the transverse process and to the parietal pleura were measured by sonography. The deviation of the needle from the horizontal plane was measured and an angle correction for the insertion depth was calculated. Twenty-two women undergoing elective unilateral breast surgery were studied. Sonographic visualization of the transverse process and the parietal pleura and measurement of their distances from the skin was successful in all women. Puncture of the paravertebral space failed in one obese woman. There was a very close correlation between needle insertion depth from the skin to the transverse process and the distance measured by ultrasound if angle correction was used (adjusted r2=0.95). Similarly, there was excellent correlation between the angle-corrected ultrasound distance from the skin to the parietal pleura and the distance from the skin to the paravertebral space (adjusted r2=0.92).

A previously described infraclavicular brachial plexus block may be modified by using a more lateral needle insertion point, while the patient abducts the arm 45 degrees or 90 degrees. In performing the modified block on patients abducting 45 degrees, we often had problems finding the cords of the brachial plexus. Therefore, we designed an anatomic study to describe the ability of the recommended needle direction to consistently reach the cords. Additionally, we assessed the risk of penetrating the pleura by the needle. Magnetic resonance images were obtained in 10 volunteers. From these images, a virtual reality model of each volunteer was created, allowing precise positioning of a simulated needle according to the modified block, without exposing the volunteers to actual needle placement. In both arm positions, the recommended needle angle of 45 degrees to the skin was too shallow to reach a defined target on the cords. Comparing the two arm positions, target precision and risk of contacting the pleura were more favorable with the greater arm abduction. We conclude that when the arm is abducted to 90 degrees, a 65 degrees -needle angle to the skin appears optimal for contacting the cords, still with a minimal risk of penetrating the pleura. However, this needs to be confirmed by a clinical study.

Pleural injury results in the death of mesothelial cells and denudation of the mesothelial basement membrane. Repair of the mesothelium without fibrosis requires proliferation and migration of mesothelial cells into the injured area. We hypothesized that monocyte chemoattractant protein-1 (MCP-1) induces proliferative and haptotactic responses in pleural mesothelial cells (PMCs) and that the MCP-1 binding receptor CCR2 mediates the pleural repair process. We demonstrate that PMCs exhibited MCP-1-specific immunostaining on injury. MCP-1 induced proliferative and haptotactic responses in PMCs. PMCs express CCR2 in a time-dependent manner. Fluorescence-activated cell sorting analysis demonstrated that interleukin (IL)-2 upregulated CCR2 protein expression in PMCs, whereas lipopolysaccharide (LPS) downregulated the response at the initial period compared with that in resting PMCs. However, the inhibitory potential of LPS was lost after 12 h and showed a similar response at 24 and 48 h. Haptotactic migration was upregulated in PMCs that were cultured in the presence of IL-2. The increased haptotactic capacity of mesothelial cells in the presence of IL-2 correlated with increased CCR2 mRNA expression. PMCs cultured in the presence of LPS showed decreased haptotactic activity to MCP-1. Blocking the CCR2 with neutralizing antibodies decreased the haptotactic response of PMCs to MCP-1. These results suggest that the haptotactic migration of mesothelial cells in response to MCP-1 are mediated through CCR2, which may play a crucial role in reepithelialization of the denuded basement membrane at the site of pleural injury and may thus contribute to the regeneration of the mesothelium during the process of pleural repair.

Chemical pleurodesis using tetracycline is an accepted and commonly employed treatment of pneumothorax and pleural effusions. We describe a case of chemical burn of the pleura in a ventilated 41-year-old who came to thoracotomy after 3 days of continuous intrapleural infusion of tetracycline at another hospital. To our knowledge this has not been previously reported although other adverse effects of this procedure are documented. We suggest that damage to the pleura and underlying lung may occur if excessive amounts of tetracycline are used in attempted pleurodesis.

Background: The Argon Beam Coagulator (ABC) and neodymium:yttrium-aluminum garnet (Nd:YAG) laser are used for lung tissue contraction. Assessing the damage of treated lung tissue is helpful in choosing devices for pulmonary volume reduction by pneumoplastic procedures., Methods: We assessed the damage of in vitro lung lobes resected at operation for pulmonary carcinoma. Samples were irradiated with noncontact Nd:YAG laser and ABC. One hundred forty-four samples obtained from 24 lobes were examined by light microscopy. The lung tissue showing destructive degeneration at the pleura and slight coagulation at the residual parenchyma was defined as showing "air leak pattern" based on a previously reported experiment of the air inflation test., Results: At the power of clinical use (Nd:YAG, 15 W; ABC, 80 W), most of the visceral pleura treated with the Nd:YAG laser was classified as presenting amorphous degeneration, and that treated with ABC showed destructive degeneration. Air leak pattern occurred in all samples treated with ABC. At the power of 40 W, ten (42%) of 24 visceral pleuras irradiated with the Nd:YAG laser were classified as presenting destructive degeneration, and of those irradiated with the ABC, 18 (75%) showed destructive degeneration (p < 0.05). Air leak patterns were found in 3 (13%) of the samples treated with the Nd:YAG laser and in 16 (63%) of those treated with the ABC (p < 0.05)., Conclusions: The ABC had more potential to damage the pleura and less potential to produce underlying parenchymal coagulation in the lung tissue than did the Nd:YAG laser. This information may be useful in the selection of devices for pulmonary volume reduction by pneumoplastic procedures.

Two hundred and fifty one cases of penetrating wounds of the chest were studied prospectively. Clinical evidence is presented to show that: basal intercostal drains are adequate to remove both air and fluid from within the pleural cavity; frequent chest radiographs are unnecessary and intercostal drains may be removed on clinical grounds alone; long term antibiotic prophylaxis is unnecessary; eight per cent of those undergoing initial observation will develop a delayed haemothorax or pneumothorax of sufficient size to require drainage; subcutaneous emphysema is of no prognostic significance in the symptomless patient with minimal intrapleural damage on admission; and outpatient follow up is not required.

Eighty-three cases of tracheopleuropulmonary injuries complicating enteral tube feeding are analyzed to identify the patterns of injury, and precipitating factors and ways to avoid them. Six new cases observed by the authors and 77 other cases cited in British literature between 1976 and 1987 are presented. In recent years, reports of this complication have been increasing, apparently in a geometrical progression: 8%, 18%, and 74% were reported between 1976 to 1979, 1980 to 1983, and 1984 to 1987, respectively. Sixty-one percent occurred in patients aged 60 years or older. Most of the patients (84%) were seriously ill, which compounded their complications. Seventy-four percent of all injuries were committed by house staff; the narrow bore tube with guide wire was used in 77% of cases. Less than reliable methods were used to confirm tube position in most instances. The presence of cuffed endotracheal tubes did not offer protection. The patients on mechanical ventilation tended to deteriorate if they developed a pneumothorax once the malpositioned tubes were removed. Of the cases reviewed for this report, 18 deaths occurred; 72% being directly related to the tube injuries. Lack of awareness, inadequate confirmatory methods, and insufficient supervision accounted for most of these preventable complications. Educating house/nursing staff in the use of the new tubes, closer supervision, and the application of equal measures of care and caution as employed in other invasive and potentially dangerous procedures are recommended to avoid disastrous outcome.

The investigation and surgical closure of a subarachnoid pleural fistula following direct trauma to the dorsal spinal theca and spinal cord are described and a review of the literature on spinal subarachnoid-pleural fistula is presented.

The inflammatory reaction that is caused by the placement of a tube in the pleural space persists after tube removal and may be observed on chest roentgenograms. One radiological presentation of this reaction is a lucent stripe, which represents localized iatrogenic pneumothorax in the track of the tube. The possibility that this stripe may represent a tubular track is not generally appreciated. We report two instances in which the three-dimensional tubular nature of the tracks is demonstrated. Failure to correlate such a stripe with roentgenograms showing the previous placement of the chest tube at the site of a track may lead to confusion and potentially serious misinterpretation.

The case of a child suffering from traumatic bilateral subarachnoid-pleural fistula is reported and the possible mechanisms responsible are discussed.

Pneumothorax following subclavian venipuncture is a well-known risk. Less well recognized is the potential for life-threatening bilateral pneumothoraces occurring at the time of subclavian vein catheterization in patients who have previously undergone median sternotomy. Inadvertent bilateral pleural entry at the time of sternotomy may result in a common pleural space which subsequently places the patient in special jeopardy when the complication of pneumothorax occurs. This report documents the successful management of this important sequence of complications associated with now widely applied therapeutic interventions.