Low-volume ventilation of preinjured lungs degrades lung function via stress concentration and progressive alveolar collapse.

Mechanical ventilation can cause ventilation-induced lung injury (VILI). The concept of stress concentrations suggests that surfactant dysfunction-induced microatelectases might impose injurious stresses on adjacent, open alveoli and function as germinal centers for injury propagation. The aim of the present study was to quantify the histopathological pattern of VILI progression and to test the hypothesis that injury progresses at the interface between microatelectases and ventilated lung parenchyma during low-positive end-expiratory pressure (PEEP) ventilation. Bleomycin was used to induce lung injury with microatelectases in rats. Lungs were then mechanically ventilated for up to 6 h at PEEP = 1 cmH2O and compared with bleomycin-treated group ventilated protectively with PEEP = 5 cmH2O to minimize microatelectases. Lung mechanics were measured during ventilation. Afterward, lungs were fixed at end-inspiration or end-expiration for design-based stereology. Before VILI, bleomycin challenge reduced the number of open alveoli [N(alvair,par)] by 29%. No differences between end-inspiration and end-expiration were observed. Collapsed alveoli clustered in areas with a radius of up to 56 µm. After PEEP = 5 cmH2O ventilation for 6 h, N(alvair,par) remained stable while PEEP = 1 cmH2O ventilation led to an additional loss of aerated alveoli by 26%, mainly due to collapse, with a small fraction partly edema filled. Alveolar loss strongly correlated to worsening of tissue elastance, quasistatic compliance, and inspiratory capacity. The radius of areas of collapsed alveoli increased to 94 µm, suggesting growth of the microatelectases. These data provide evidence that alveoli become unstable in neighborhood of microatelectases, which most likely occurs due to stress concentration-induced local vascular leak and surfactant dysfunction.NEW & NOTEWORTHY Low-volume mechanical ventilation in the presence of high surface tension-induced microatelectases leads to the degradation of lung mechanical function via the progressive loss of alveoli. Microatelectases grow at the interfaces of collapsed and open alveoli. Here, stress concentrations might cause injury and alveolar instability. Accumulation of small amounts of alveolar edema can be found in a fraction of partly collapsed alveoli but, in this model, alveolar flooding is not a major driver for degradation of lung mechanics.

[A case of nontuberculous mycobacterium presenting as a mass and atelectasis with mediastinal and hilar lymph node enlargement].

With the development of testing technology, the diagnosis of nontuberculous mycobacterium (NTM) lung disease has gradually increased in recent years. Because the clinical characteristics of NTM are not typical, and its imaging manifestations are diverse and nonspecific, missed diagnosis and misdiagnosis are common. Etiological investigation is necessary for diagnosis. Conventional etiological investigations are very limited for the diagnosis of NTM. We reported a case of NTM lung disease presenting with a mass and atelectasis with mediastinal and hilar lymph node enlargement that resembled malignant tumors. The literature on this condition was reviewed to improve the clinician's understanding and broaden clinical thinking.

[Risk factors for pulmonary atelectasis in adults with tracheobronchial tuberculosis].

Objective: To investigate the risk factors for pulmonary atelectasis in adults with tracheobronchial tuberculosis(TBTB). Methods: Clinical data of adult patients (≥18 years old) with TBTB from February 2018 to December 2021 in Public Health Clinical Center of Chengdu were retrospectively analyzed. A total of 258 patients were included, with a male to female ratio of 1∶1.43. The median age was 31(24, 48) years. Clinical data including clinical characteristics, previous misdiagnoses/missed diagnoses before admission, pulmonary atelectasis, the time from symptom onset to atelectasis and bronchoscopy, bronchoscopy and interventional treatment were collected according to the inclusion and exclusion criteria. Patients were divided into two groups according to whether they had pulmonary atelectasis. Differences between the two groups were compared. Binary logistic regression was used to analyze the risk factors for pulmonary atelectasis. Results: The prevalence of pulmonary atelectasis was 14.7%, which was most common in the left upper lobe (26.3%). The median time from symptom onset to atelectasis was 130.50(29.75,358.50)d, and the median time from atelectasis to bronchoscopy was 5(3,7)d. The median age, the proportion of misdiagnosis of TBTB before admission, and the time from symptom onset to bronchoscopy in the atelectasis group were higher than those without atelectasis, and the proportion of receiving bronchoscopy examination and interventional therapy previously, and the proportion of pulmonary cavities were lower than those without atelectasis (all P<0.05). The proportions of cicatrices stricture type and lumen occlusion type in the atelectasis group were higher than those without atelectasis, while the proportions of inflammatory infiltration type and ulceration necrosis type were lower than those without atelectasis (all P<0.05). Older age (OR=1.036, 95%CI: 1.012-1.061), previous misdiagnosis(OR=2.759, 95%CI: 1.100-6.922), longer time from symptom onset to bronchoscopy examination (OR=1.002, 95%CI: 1.000-1.005) and cicatrices stricture type (OR=2.989, 95%CI: 1.279-6.985) were independent risk factors for pulmonary atelectasis in adults with TBTB (all P<0.05). Of the patients with atelectasis who underwent bronchoscopy interventional therapy, 86.7% had lung reexpansion or partial reexpansion. Conclusions: The prevalence of pulmonary atelectasis is 14.7% in adult patients with TBTB. The most common site of atelectasis is left upper lobe. The TBTB type of lumen occlusion is complicated by pulmonary atelectasis in 100% of cases. Being older, misdiagnosed as other diseases, longer time from onset of symptoms to bronchoscopy examination, and being the cicatrices stricture type are factors for developing pulmonary atelectasis. Early diagnosis and treatment are needed to reduce the incidence of pulmonary atelectasis and increase the rate of pulmonary reexpansion.

Adaptive radiotherapy in locally advanced esophageal cancer with atelectasis: a case report.

BACKGROUND: To the best of our knowledge, no study has reported mediastinal shift accompanied with obstructive atelectasis due to bulky primary esophageal tumor components treated with adaptive radiotherapy and concurrent chemotherapy. CASE PRESENTATION: Here we report the case of a 65-year-old male patient diagnosed with locally advanced thoracic esophageal squamous cell cancer, clinical T4bN1M0, stage IVA. Bronchoscopy and computed tomography (CT) revealed an almost complete obstruction of the lumen of the left bronchus due to compression by bulky primary esophageal tumor components. On admission, the patient presented with dyspnea and decreased arterial oxygen saturation. Chest radiography and CT on admission revealed mediastinal shift with left atelectasis, as opposed to findings from the chest radiography performed 26 days before admission. Because of the patient's overall good condition, we recommended definitive chemoradiotherapy instead of palliative bronchial stent placement. After obtaining the patient's consent, chemoradiotherapy was initiated on the following day and it comprised three-dimensional conformal radiotherapy with 60 Gy in 30 fractions with concurrent administration of cisplatin and 5-fluorouracil. During chemoradiotherapy, tumor location was monitored with cone-beam CT and chest radiography. Chemoradiotherapy on day 8 revealed no evidence of the mediastinal shift. CT simulation was reperformed to adjust the radiotherapy fields to account for geometrical changes induced by the absence of the mediastinal shift. Subsequently, the mediastinal shift and bronchial obstruction did not recur during the course of chemoradiotherapy. The patient completed the planned radiotherapy with concurrent and adjuvant chemotherapy, and no non-hematological grade ≥ 3 adverse events were observed. Complete response was confirmed 7 months after initiating chemoradiotherapy. Currently, no disease recurrence, dysphagia, or respiratory symptoms have been reported at 13 months after initiating chemoradiotherapy. CONCLUSIONS: In this study, a bulky primary esophageal tumor caused mediastinal shift due to ipsilateral bronchial obstruction. The close follow-up for monitoring resolution of the mediastinal shift during the course of chemoradiotherapy enabled adequate dose delivery to targets, thus reflecting the geometrical changes induced by the absence of the mediastinal shift. Adaptive radiotherapy technique was crucial for favorable patient outcomes in this challenging clinical situation.

Diffuse Large B-Cell Lymphoma Arising from the Lesion of Chronic Lobar Atelectasis.

Pulmonary lymphoma is rare, accounting for < 1% of primary lung cancers. Most primary pulmonary lymphomas (PPL) are low-grade mucosa-associated lymphoid tissue (MALT)-type, and among PPL, diffuse large B-cell lymphoma (DLBCL) is extremely rare. In contrast, there has been an increase in the incidence of DLBCL among patients with autoimmune disorders and recurrent or chronic bacterial infection. A subset of DLBCL has been reported to develop through transformation of preexisting or concurrent MALT. The respiratory symptoms are non-specific, and the chest X-ray findings demonstrate the presence of interstitial and mixed alveolar infiltrates, nodular lesions, and localized homogeneous consolidations; the diagnosis of pulmonary DLBCL is thus challenging and often leads to a misdiagnosis or delayed diagnosis. We herein report a case of DLBCL which was assumed to have arisen from the lesion of chronic atelectasis that was successfully diagnosed by endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). A 74-year-old woman with diffuse bronchiectasis and chronic atelectasis of the left lower lobe suffered from productive cough and high fever. Increased airway filling with mucoid secretion was repeatedly observed within the area of atelectasis with bronchiectasis, and left lower lobe atelectasis developed. Subsequently, the hilar and mediastinal lymph nodes gradually became enlarged, and DLBCL was pathologically confirmed. In the present case, DLBCL was considered to have arisen in the lesion of chronic atelectasis. Physicians should recognize that DLBCL may develop at the site of chronic atelectasis during disease course of diffuse bronchiectasis, and thus DLBCL may be misdiagnosed as superimposed infection of chronic atelectasis.

Relationship between a High-inspired Oxygen Concentration and Dorsal Atelectasis in High-energy Trauma Patients.

We performed a retrospective cohort study of 911 high-energy trauma patients who underwent chest CT scans at least twice after admission. We hypothesized that in high-energy trauma patients, a high-inspired oxygen concentration delivered after admission results in dorsal atelectasis. The study's primary outcome was dorsal atelectasis formation diagnosed based on CT images. We defined dorsal atelectasis as the presence of atelectasis at ≥ 10 mm thick on CT images. We defined high-inspired oxygen concentration as >60% oxygen delivered between two CT scans. Four hundred sixty-five patients (51.0%) developed atelectasis according to the second CT scan, and 338 (37.1%) received a high-inspired oxygen concentration. A univariate analysis showed that the rate of the high-inspired oxygen concentration in the atelectasis group was significantly higher than that in the non-atelectasis group (43.4% vs. 30.1%, p<0.001). However, a logistic regression analysis showed that there was no significant relationship between the oxygen concentration and the formation of dorsal atelectasis (OR: 1.197, 95%CI: 0.852-1.683, p=0.30). Age, the Injury Severity Score, BMI, and smoking were found to be risk factors of dorsal atelectasis formation in high-energy trauma patients. There was no relationship between the oxygen concentration and atelectasis formation in our series of high-energy trauma patients.

[Diagnosis and treatment value of bedside pulmonary ultrasound for atelectasis in patients after cardiac surgery].

Objective: To investigate the value of bedside pulmonary ultrasound in the diagnosis and treatment of atelectasis in patients after cardiac surgery. Methods: A total of 45 patients developed respiratory failure within 1 week after cardiovascular surgery from April 2017 to April 2018 were enrolled in this study. Among them, 27 were male and 18 were female, mean age was (47±5) years. The postoperative pulmonary ultrasound and chest CT findings were collected, and the consistency, efficacy evaluation, timeliness and safety value of pulmonary ultrasound and chest CT diagnosis were compared. The consistency of the two diagnostic methods was checked based on the Kappa consistency test. Results: A total of 87 foci of atelectasis were diagnosed in 45 patients, including 29 foci of complete atelectasis and 58 foci of incomplete atelectasis. Thoracic CT examination confirmed 44 cases of atelectasis (positive rate 97.8%), and 42 cases (93.3%) were found with atelectasis with ultrasound test. The two methods were consistent in the diagnosis of atelectasis (Kappa value was 0.741, P<0.05). In the evaluation of the atelectasis, the results of the two examination methods were completely consistent, and the pulmonary ultrasound couldcheck the lung recruitment in real time. Ultrasound examination after lung recruitment showed that the total ventilation score of 42 patients decreased significantly when compared with that before treatment ((18.3±3.6) vs (26.6±3.8), t=10.229, P<0.05). There was no significant difference in the safety between the two examination methods. The time the bedside pulmonary ultrasound used was significantly shorter than that in the chest CT. Conclusions: The accuracy of bedside pulmonary ultrasound in assessing atelectasis after cardiovascular surgery is consistent with chest CT, it brings dynamic monitoring of lung status and assessment of lung recruitment by changes in lung ventilation scores. The inspection takes a short time and is worth promoting.

Death due to atypical urinothorax following percutaneous nephrolithotomy.

Urinothorax is a cause of pleural effusion that is often missed due to its perceived rarity. Here, we present a case of urinothorax secondary to percutaneous nephrolithotomy resulting in lung collapse and death. This case highlights urinothorax as a cause of death, its biochemical profile, and diagnostic features on autopsy. A 39-year-old female presented to the ED with low back pain and dysuria. Abdominal and pelvic CT showed a large staghorn calculus in the right kidney which was then treated with percutaneous nephrolithotomy. On post-operative day (POD) 1, the patient was febrile, had decreased breath sounds, and complained of pain with deep inspiration. Chest x-ray revealed increased right pleural fluid. On POD 3, the patient continued to have difficulty breathing and was eventually found apneic. Resuscitation was unsuccessful. Autopsy revealed a collapsed right lung associated with a 1200 mL pleural effusion, which was cloudy, yellow, and smelled like urine. The cause of death was listed as complications of percutaneous nephrolitotomy, with urinothorax and collapse of lung. While rare, urinothoraces must be considered as a cause of pleural effusion due to risk of respiratory failure and death. Diagnosis relies on pleural fluid analysis and history, especially with regard to genitourinary obstruction and surgeries.

Effect of sugammadex on chest radiographic abnormality in the early postoperative period after video-assisted thoracoscopic lobectomy

Background/aim: Sugammadex, which offsets the effects of neuromuscular blocking agents (NMBs), has advantages over traditional reversal agents like pyridostigmine, as it enables fast and reliable recovery from neuromuscular blockade. This study compared the incidence of early postoperative chest radiographic abnormalities (CRA) between sugammadex (group S) and pyridostigmine (group P) following video-assisted thoracoscopic (VAT) lobectomy for lung cancer. Materials and methods: We performed a retrospective cohort analysis by reviewing the medical records of patients who underwent VAT lobectomy at a single university medical center. We defined the early postoperative CRA as a characteristic appearance on chest radiograph up to 2 days after surgery. Arterial blood gas analysis (ABGA), surgical time, anaesthesia time, extubation time, and the total dose of rocuronium were analysed. Postoperative nausea and vomiting (PONV) and pain scores were observed until 2 days after surgery. Results: A total of 257 patients underwent VAT lobectomy during the study period; 159 were included in the final analysis. Ninety patients received sugammadex while 69 received pyridostigmine. The incidence of early postoperative atelectasis was significantly lower in group S than in group P (26.7%, 95% CI: 17.5%‒35.8% and 43.5%, 95% CI: 31.8%‒55.2%, respectively, P = 0.013). The median dose of rocuronium was higher in group S than in group P (120 mg vs. 90 mg, P < 0.001). ABGA, extubation time, and PONV were similar in both groups. Conclusion: Sugammadex decreased the incidence of CRA in the early postoperative period despite higher NMB consumption.

Low-frequency ventilation during cardiopulmonary bypass for lung protection: A randomized controlled trial.

OBJECTIVE: Pulmonary dysfunction is a common complication in patients undergoing heart surgery. Current clinical practice does not include any specific strategy for lung protection. To compare the anti-inflammatory effects of low-frequency ventilation (LFV), as measured by nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) p65 pathway activation, for the entire cardiopulmonary bypass (CPB) vs both lungs left collapsed in patients undergoing coronary artery bypass grafting (CABG). METHODS: Two groups parallel randomized controlled trial. The primary outcome was inflammation measured by NF-κB p65 activation in pre- and post-CPB lung biopsies. Secondary outcomes were additional inflammatory markers in both biopsy tissue and blood. RESULTS: Thirty-seven patients were randomly allocated to LFV (18) and to both lungs left collapsed (19). The mean concentration of NF-κB p65 in the biopsies before chest closure (adjusted for pre-CPB concentration) was higher in the LFV group compared to both lungs left collapsed group but this was not significant (0.102, 95% confidence interval, -0.022 to 0.226, P = 0.104). There were no significant differences between groups in the other inflammatory markers measured in tissue and blood. CONCLUSIONS: In patients undergoing elective CABG, the use of LFV during CPB when compared to both lungs left collapsed does not seem to reduce inflammation in lung biopsies and blood.

Comparison of different registration landmarks for MRI-CT fusion in radiotherapy for lung cancer with post-obstructive lobar collapse.

The registration of the two sets of images based on the spine and pulmonary artery landmarks and the geometric center difference of the mean displacement in the X, Y, and Z directions (X, Y, and Z represent the directions of the body from left to right, superior to inferior, and anterior to posterior) between their MRI-CT fusions were compared, respectively. Fifty-five lung cancer patients with post-obstructive lobar collapse were enrolled in this study. Before radiation, two sets of simulating images according to the spine and the pulmonary artery registrations were obtained for each patient using MRI-CT fusion. The differences of mean displacement in the X, Y, and Z directions based on spine and pulmonary artery landmarks were of -0.29, 0.25, and 0.18 cm, respectively. The mean displacements of the pulmonary artery based images in the three directions were smaller than that in the spine registration images (P < 0.05). By the method of pulmonary artery landmark, MRI-CT has better registration accuracy and can better help confirm the target volume.

Sudden, Unexpected Death Due to Pseudo-Meigs Syndrome: A Case Report and Review of the Literature.

Meigs syndrome is the triad of ascites, hydrothorax, and benign ovarian tumor (mostly fibroids). It is a diagnosis of exclusion, and the characteristic symptoms disappear after resection of the tumor. Instead, in Pseudo-Meigs syndrome, the triad includes a nonfibroma ovarian tumor. The latter may consist of benign tumors (ie, of fallopian tube or uterus, struma ovarii, and ovarian leiomyomas) but can also comprise ovarian or metastatic gastrointestinal malignancies.The authors describe a case of sudden death in a 43-year-old woman, with no noteworthy reported history of present illness or medical history and in apparently good health before death.The autopsy showed a picture of bilateral hydrothorax with lung collapse, ascites, and a large left-sided ovarian mass, approximately 15 cm in diameter. Histopathological examinations revealed an ovarian epithelial malignancy (cystadenocarcinoma). There was also lung atelectasis with accompanying thrombosis of small and medium blood vessels. The combination of autopsy and histological findings allowed us to establish the diagnosis of Pseudo-Meigs syndrome, undiagnosed antemortem, resulting in death due to pulmonary and thrombotic complications. Our subsequent review of the literature found no case reports of undiagnosed Pseudo-Meigs syndrome presenting as sudden death, highlighting the uniqueness of the case presented herein.

Management of superior vena cava syndrome in critically ill cancer patients.

PURPOSE: The purpose of this study is to describe the management and outcome of critically ill cancer patients with Superior Vena Cava Syndrome (SVCS). METHODS: All cancer patients admitted to the medical intensive care unit (ICU) of the Saint-Louis University Hospital for a SVCS between January 2004 and December 2016 were included. RESULTS: Of the 50 patients included in the study, obstruction of the superior vena cava was partial in two-thirds of the cases and complete in one-third. Pleural effusion was reported in two-thirds of the patients, pulmonary atelectasis in 16 (32%), and pulmonary embolism in five (10%). Computed tomography of the chest showed upper airway compression in 18 (36%) cases, while echocardiography revealed 22 (44%) pericardial effusions. The causes of SVCS were diagnosed one (0-3) day after ICU admission, using interventional radiology procedures in 70% of the cases. Thirty (60%) patients had hematological malignancies, and 20 (40%) had solid tumors. Fifteen (30%) patients required invasive mechanical ventilation, seven (14%) received vasopressors, and renal replacement therapy was implemented in three (6%). ICU, in-hospital, and 6-month mortality rates were 20, 26, and 48%, respectively. The cause of SVCS was the only factor independently associated with day 180 mortality by multivariate analysis. Patients with hematological malignancies had a lower mortality than those with solid tumors (27 versus 80%) (odds ratio 0.12, 95% confidence interval (0.02-0.60), p < 0.01). CONCLUSION: Airway obstruction and pleural and pericardial effusions contributed to the unstable condition of cancer patients with SVCS. The vital prognosis of SVCS was mainly related to the underlying diagnosis.

Atelectasis after airway extubation during veno-arterial extracorporeal membrane oxygenation support.

Veno-arterial extracorporeal membrane oxygenation (VA ECMO) is used in cardiopulmonary failure patients to provide temporary assisted circulation. Usually, prolonged intubation and invasive mechanical ventilation are required in patients with ECMO support. We report on two cases of patients who had no pre-existing injuries of the affected lung, underwent VA ECMO support after open-heart surgery and received airway extubation (AE) or awake ECMO with the recovery of left ventricular ejection fraction. Atelectasis happened after AE and non-invasive positive pressure ventilation attenuated the atelectasis of one patient. The atelectasis of the other patient was corrected 10 hours after weaning from ECMO. Both patients were discharged successfully. Awake VA ECMO for post-cardiac surgery patients should be performed with prudence and needs further research.

Normal spectrum of pulmonary parametric response map to differentiate lung collapsibility: distribution of densitometric classifications in healthy adult volunteers.

OBJECTIVES: Pulmonary parametric response map (PRM) was proposed for quantitative densitometric phenotypization of chronic obstructive pulmonary disease. However, little is known about this technique in healthy subjects. The purpose of this study was to describe the normal spectrum of densitometric classification of pulmonary PRM in a group of healthy adults. METHODS: 15 healthy volunteers underwent spirometrically monitored chest CT at total lung capacity (TLC) and functional residual capacity (FRC). The paired CT scans were analyzed by PRM for voxel-by-voxel characterization of lung parenchyma according to 4 densitometric classifications: normal lung (TLC ≥ -950 HU, FRC ≥ -856 HU); expiratory low attenuation area (LAA) (TLC ≥ -950 HU, FRC < -856 HU); dual LAA (TLC<-950 HU, FRC < -856 HU); uncharacterized (TLC < -950 HU, FRC ≥ -856 HU). RESULTS: PRM spectrum was 78 % ± 10 % normal lung, 20 % ± 8 % expiratory LAA, and 1 % ± 1 % dual LAA. PRM was similar between genders, there was moderate correlation between dual LAA and spirometrically assessed TLC (R = 0.531; p = 0.042), and between expiratory LAA and VolExp/Insp ratio (R = -0.572; p = 0.026). CONCLUSIONS: PRM reflects the predominance of normal lung parenchyma in a group of healthy volunteers. However, PRM also confirms the presence of physiological expiratory LAA seemingly related to air trapping and a minimal amount of dual LAA likely reflecting emphysema. KEY POINTS: • Co-registration of inspiratory and expiratory computed tomography allows dual-phase densitometry. • Dual-phase co-registered densitometry reflects heterogeneous regional changes in lung function. • Quantification of lung in healthy subjects is needed to set reference values. • Expiratory low attenuation areas <30 % could be considered within normal range.

Overcoming inactivation of the lung surfactant by serum proteins: a potential role for fluorocarbons?

In many pulmonary conditions serum proteins interfere with the normal adsorption of components of the lung surfactant to the surface of the alveoli, resulting in lung surfactant inactivation, with potentially serious untoward consequences. Here, we review the strategies that have recently been designed in order to counteract the biophysical mechanisms of inactivation of the surfactant. One approach includes protein analogues or peptides that mimic the native proteins responsible for innate resistance to inactivation. Another perspective uses water-soluble additives, such as electrolytes and hydrophilic polymers that are prone to enhance adsorption of phospholipids. An alternative, more recent approach consists of using fluorocarbons, that is, highly hydrophobic inert compounds that were investigated for partial liquid ventilation, that modify interfacial properties and can act as carriers of exogenous lung surfactant. The latter approach that allows fluidisation of phospholipid monolayers while maintaining capacity to reach near-zero surface tension definitely warrants further investigation.

Hyperpolarized gas diffusion MRI for the study of atelectasis and acute respiratory distress syndrome.

Considerable uncertainty remains about the best ventilator strategies for the mitigation of atelectasis and associated airspace stretch in patients with acute respiratory distress syndrome (ARDS). In addition to several immediate physiological effects, atelectasis increases the risk of ventilator-associated lung injury, which has been shown to significantly worsen ARDS outcomes. A number of lung imaging techniques have made substantial headway in clarifying the mechanisms of atelectasis. This paper reviews the contributions of computed tomography, positron emission tomography, and conventional MRI to understanding this phenomenon. In doing so, it also reveals several important shortcomings inherent to each of these approaches. Once these shortcomings have been made apparent, we describe how hyperpolarized (HP) gas MRI--a technique that is uniquely able to assess responses to mechanical ventilation and lung injury in peripheral airspaces--is poised to fill several of these knowledge gaps. The HP-MRI-derived apparent diffusion coefficient (ADC) quantifies the restriction of (3) He diffusion by peripheral airspaces, thereby obtaining pulmonary structural information at an extremely small scale. Lastly, this paper reports the results of a series of experiments that measured ADC in mechanically ventilated rats in order to investigate (i) the effect of atelectasis on ventilated airspaces, (ii) the relationship between positive end-expiratory pressure (PEEP), hysteresis, and the dimensions of peripheral airspaces, and (iii) the ability of PEEP and surfactant to reduce airspace dimensions after lung injury. An increase in ADC was found to be a marker of atelectasis-induced overdistension. With recruitment, higher airway pressures were shown to reduce stretch rather than worsen it. Moving forward, HP MRI has significant potential to shed further light on the atelectatic processes that occur during mechanical ventilation.

Non-lobar atelectasis generates inflammation and structural alveolar injury in the surrounding healthy tissue during mechanical ventilation.

INTRODUCTION: When alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation. METHODS: A total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with FIO2 = 1.0, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (VT) = 10 ml/kg and positive end-expiratory pressure (PEEP) = 3 cmH2O (VT10/PEEP3); and 2) VT = 20 ml/kg and PEEP = 0 cmH2O (VT20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n = 12); tissue cytokines (n = 12); and micro-computed tomography (microCT; n = 2). An additional six, non-ventilated, healthy animals were used as controls. RESULTS: Atelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm3. There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the VT20/ZEEP than VT10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1ß and cytokine-induced neutrophil chemoattractant-1 between regions. CONCLUSIONS: The present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue.

Lung ultrasonography may provide an indirect estimation of lung porosity and airspace geometry.

BACKGROUND: Echographic vertical artifacts (B-lines) in chest ultrasonography have often been associated with pathological patterns. A scientifically sound explanation of these artifacts has not yet been proposed. OBJECTIVES: The 'spongy' nature of the lung in its liquid and solid components and the changes that take place in peripheral airspace (PAS) geometry might be the key point to understanding these phenomena. METHODS: Six excised right rabbit lungs were obtained. Each lung underwent direct ultrasound evaluation in two different conditions: at complete tissue elastic recoil volume and at pulmonary expansion volume achieved by applying a constant positive pressure of 12 cm H2O. Lung volumes and densities were reported in both conditions. Histological examination was performed on three naturally collapsed lungs and on three lungs under positive pressure inflation after having been fixed in formalin solution. RESULTS: Mean volumes of naturally collapsed lungs and fixed expanded lungs were 11.2 ± 0.36 and 44.83 ± 3.03 ml, respectively. Mean densities were 0.622 ± 0.016 and 0.155 ± 0.007 g/ml, respectively. Ultrasound evaluation of collapsed lungs showed dense vertical artifacts and a 'white lung' pattern, while the evaluation of expanded lungs showed hyperechoic line and horizontal artifacts of reflection. Histological evaluation showed a different PAS geometry in collapsed lungs caused by alveolar size reduction and shape changes with unfolded and closed units modifying the peripheral porosity of the frothy nature of the lung. CONCLUSIONS: Airspace geometry, frothy nature and porosity are the determinants of the different behavior of ultrasound interacting with the subpleural lung parenchyma. Chest ultrasound may thus be interpreted as an indirect 'estimator' of lung porosity.

Bovine thoracoscopy: surgical technique and normal anatomy.

OBJECTIVE: To describe a surgical technique for thoracoscopy and report visible anatomy within the thoracic cavity of standing cattle. STUDY DESIGN: Prospective study. ANIMALS: Adult clinically healthy Holstein-Friesian cows (n = 15). METHODS: Each cow had four thoracoscopic examinations. Initially, the left hemithorax was examined after passive lung collapse, then again 24 hours later after CO2 insufflation. The right hemithorax was examined 24 hours later after passive lung collapse and again 24 hours later after CO2 insufflation. RESULTS: CO2 insufflation did not significantly improve visibility within the pleural space. Collapsed lung, aorta, esophagus, diaphragm, and azygos vein were readily viewed; however, the pericardial region was not consistently visible. Minor laceration of the lung occurred in 1 cow with adhesions, otherwise there were no intra- or postoperative complications. All cows recovered without signs of discomfort. No local swelling or emphysema occurred at the portals. CONCLUSIONS: Thoracoscopy can be safely performed on healthy standing cattle.