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A 19-year-old with blunt trauma and repeated nose blowing presented with orbital emphysema and orbital compartment syndrome. Orbital emphysema is the abnormal presence of air within the orbit, typically secondary to trauma. Most cases will resolve with observation alone, however orbital compartment syndrome is a feared complication that necessitates urgent decompression. A superior fornix, trans-conjunctival approach was safely utilized to decompress the orbit while avoiding unwanted complications. Various decompression techniques have previously been described, most of which describe trans-palpebral approaches. The key safety benefit to the trans-conjunctival approach is direct visualization of the needle tip adjacent to the superior fornix, therefore posterior to the equator of the globe. With the needle positioned parallel to the curvature of the globe at the equator, the posterior sclera surface curves away from the tip, rendering it difficult to pierce the globe. In addition, the needle needs to be advanced only 3-4 millimeters and traverses only the conjunctiva and Tenon's to enter the central surgical space - the most direct route to the air pocket. The trans-conjunctival approach lowers the risk of damage to eyelid neurovascular structures and is less painful.

Orbital emphysema is an abnormal presence of air in the orbit. It usually arises after blunt trauma or periorbital surgery. When it occurs after dacryocystorhinostomy, usually it is reported as a benign condition. We present a case of a severe orbital emphysema secondary to transcanalicular diode laser-assisted dacryocystorhinostomy. The day after the surgery, the examination revealed crepitant periorbital swelling, general restriction of extraocular motility, visual loss and intraocular pressure of more than 70 mmHg. A computed tomography showed a massive orbital emphysema. An emergency decompression, using a 25-gauge needle attached to an empty syringe lacking a plunger was performed, achieving a quick decrease of intraocular pressure and pain and swelling improvement. Then, in this case, orbital decompression by passive airflow using a needle without a plunger was an effective treatment method to resolve a serious orbital emphysema after transcanalicular laser-assisted dacryocystorhinostomy.

This is a case description of a male patient found to have orbital and intracranial emphysema, specifically with air in his cavernous sinuses bilaterally following penetrating trauma to the medial orbit from a goat's horn. There were no orbital or skull base fractures. Although the presence of traumatic intracranial emphysema is not uncommon, it is typically the result of direct communication of the cranial vault with the paranasal sinuses in the setting of associated fracture or, alternatively, from direct penetration and inoculation. We present a rare case of orbital emphysema with traumatic intracranial emphysema without these previously described associations and postulate a mech``anism behind its development.

Although orbital emphysema is a recognized complication of orbital fractures involving any of the paranasal sinuses, it may develop without any fracture. A 23-year-old man presented with sudden left periorbital swelling during weight lifting in a fitness facility. On the left side, there was periorbital swelling with crepitus in palpation of subcutaneous tissue and conjunctival congestion. Computed tomography showed no fractures in the orbit. The patient was hospitalized. He was treated with empiric antibiotics and non-steroidal antiinflammatory drugs. In three days, the swelling and crepitus had almost disappeared. Seven days later, orbital emphysema had completely resolved.

Context: There are few short-term mouse models of chronic obstructive pulmonary disease (COPD) mimicking the human disease. In addition, p38 is recently recognized as a target for the treatment of COPD. However, the precise mechanism how p38 contributes to the pathogenesis of COPD is still unknown., Objective: We attempted to create a new mouse model for COPD by intra-tracheal administration of a mixture of lipopolysaccharide (LPS) and cigarette smoke solution (CSS), and investigated the importance of the p38 mitogen-activated protein kinase (p38) pathway in the pathogenesis of COPD., Methods: Mice were administered LPS + CSS once a day on days 0-4 and 7-11. Thereafter, CSS alone was administered to mice once a day on days 14-18. On day 28, histopathological changes of the lung were evaluated, and bronchoalveolar lavage fluid (BALF) was subjected to western blot array for cytokines. Transgenic (TG) mice expressing a constitutive-active form of MKK6, a p38-specific activator in the lung, were subjected to our experimental protocol of COPD model., Results: LPS + CSS administration induced enlargement of alveolar air spaces and destruction of lung parenchyma. BALF analyses of the LPS + CSS group revealed an increase in expression levels of several cytokines involved in the pathogenesis of human COPD. These results suggest that our experimental protocol can induce COPD in mice. Likewise, histopathological findings of the lung and induction of cytokines in BALF from MKK6 c.a.-TG mice were more marked than those in WT mice., Conclusion: In a new experimental COPD mouse model, p38 accelerates the development of emphysema.

Background: Epidemiological research and meta-analyses of published data have shown that biomass smoke (BS) is a risk factor for chronic obstructive pulmonary disease (COPD). However, the link between BS and COPD lacks experimental confirmation., Objectives: To verify whether BS can induce pathologic changes and systemic oxidative stress, which may be relevant to the development of emphysema and chronic bronchitis in rats., Methods: Rats were exposed to BS, cigarette smoke (CS), or clean air (sham) for 14 weeks. During the exposure, the O2, SO2, and CO levels were monitored. Pathological changes in the lungs, systemic oxidative stress, and inflammation biomarkers, together with GSTM1 and GSTP1 mRNA expression in the lung were measured. The glutamate-cysteine ligase catalytic subunit (GCLC) protein expression in the lung was measured using immunohistochemistry and western blotting., Results: The O2, CO, and SO2 levels were 20.31 ± 0.03%, 981.72 ± 64.76, and 2.59 ± 0.26 mg/m(3) for the BS group, respectively, while their levels in the CS group were 20.28 ± 0.15%, 745.56 ± 30.83, and 12.64 ± 0.591 mg/m(3) respectively. As with the rats exposed to CS, the BS rats showed an increased number of inflammatory cells in the bronchoalveolar lavage fluid, an increased pulmonary mean linear intercept and a decreased pulmonary mean alveolar number. Characteristics of chronic bronchitis and peribronchial fibrosis were also found in the BS-exposed rat lungs. Reduced body weight, systemic oxidative stress, and increased GCLC protein expression in the lungs were observed in the rats exposed to BS and CS., Conclusions: BS can cause emphysema and chronic bronchitis similar to that caused by CS, which is accompanied by systemic oxidative stress and inflammation.

Background: Smoking causes lung endothelial cell apoptosis and emphysema. Derived from bone marrow, circulating endothelial progenitor cells (EPCs) maintain vascular integrity by replacing and repairing damaged endothelial cells. Smoking influences the number of circulating EPCs. Recruitment of EPCs from bone marrow to peripheral blood depends on the interaction of c-Kit/soluble c-Kit ligand (sKitL). We hypothesized that smoking might influence c-Kit(+) EPCs/sKitL interaction in bone marrow in the development of smoking-related emphysema. In this study, we used a cigarette smoke extract (CSE)-induced emphysema model., Methods: Mice were injected intraperitoneally with PBS/CSE and sacrificed at day 28. Lung function and pathology of lung tissue were measured to characterize the model. Expressions of c-Kit in the lung tissue were assayed. Bone marrow cells were isolated by red blood cell lysis. EPCs/c-Kit(+) EPCs in nonred blood cells were analyzed by flow cytometry. Expressions of KitL and MMP-9, and activity MMP-9 in bone marrow were measured., Results: Our data demonstrated that gene and protein expressions of c-Kit were decreased in the lung tissue in this model. Compared with the control group, the number of bone marrow nonred blood cells was unchanged following CSE treatment, while the depletion of bone marrow EPCs/c-Kit(+) EPCs was significant. The level of sKitL was reduced in the bone marrow in the model. The reduction of sKitL was associated with deregulated KitL expression and decreased MMP-9 activity., Conclusions: The interaction between c-Kit and sKitL in bone marrow EPCs, a critical step in endothelial repair, is negatively affected in a CSE-induced emphysema model.

A 36-year-old man with Crouzon syndrome was referred post-operatively with unilateral painful limitation of eye movements and proptosis following removal of bilateral malar and orbital rim implants. Further investigation revealed right inferior orbital emphysema, caused by the intra-operative entrance of hydrogen peroxide through a suspected perforation of the orbital septum. The symptoms settled with conservative management.

Gram-negative bacterial endotoxin lipopolysaccharide (LPS) administration has been used as an animal model of sepsis-related acute lung injury and adult respiratory distress syndrome (ALI/ARDS). This paper describes the lung histology following lung injury induced by the intraperitoneal (i.p.) administration of endotoxin to rats, in comparison with earlier findings. ALI was induced by the i.p. administration of Esherichia coli LPS 2 (n = 8) or 3 (n = 5) mg/kg, whereas physiological saline was administered to the control animals (n = 5). Eighteen hours after the LPS injections, the animals were euthanized. The lungs and heart were removed in one block for histological study (hematoxylin and eosin [H&E], periodic acid-Schiff [PAS], Mason's trichrome; light microscopy). The lung tissue injury (bronchial wall, vessels, alveoli, interstitium) was graded via a scoring system (0 to 3+). The control animals showed intact lung tissue. Ten of the 13 LPS group had bronchus-associated lymphoid tissue (BALT) hyperplasia. Pathological signs of ALI/ARDS, diffuse alveolar damage (DAD) and emphysema, were observed in 5 and 8 cases, respectively. LPS injection induces primarily BALT hyperplasia and also the less characteristic DAD. This rat model is suitable for the investigation not only of ALI/ARDS but also of BALT hyperplasia occurring as a consequence of chronic pulmonary inflammatory processes.

Ethmoidal pneumocele is a rare condition with little known about its etiology. We report a 5-year-old boy who had recurrent right orbital cellulitis, non-axial proptosis, and inferolateral globe displacement. Initial radiological investigations demonstrated an ethmoidal mucocele. There was complete resolution of inflammatory signs with endoscopic drainage of the mucocele; however, repeat CT revealed a residual pneumocele with continued proptosis and lateral displacement of the globe. This case illustrates the potential for chronic sinusitis and iatrogenic drainage of an ethmoidal mucocele to progress to a pneumocele.

Orbital emphysema due to orbital trauma is a well-known occurrence. Visual loss due to orbital emphysema, however, is an uncommon phenomenon. A case of unilateral orbital emphysema following door-handle trauma with subsequent proptosis, painful ophthalmoplegia and compressive optic neuropathy resulting in compromised vision is presented in an 8-year-old male child. Conservative management, including intravenous corticosteroids, failed to resolve the patient's symptoms and compressive optic neuropathy. Surgical intervention to evacuate orbital emphysema resulted in prompt resolution of symptoms, including recovery of vision. A review of the medical literature revealed that only few isolated cases of orbital emphysema with compressive optic neuropathy have been reported previously, with no reports due to door-handle trauma.

The authors investigated whether autologous bone marrow mononuclear cell (BMC) transplantation via the left and right main bronchi would mitigate elastase-induced pulmonary emphysema in rabbits. Four weeks after elastase administration, rabbits also receiving BMCs showed significantly better pulmonary function (FVC, FEV100, FEVPEF) and smaller alveolar airspaces, as indicated by a smaller mean linear intercept, than those receiving porcine pancreatic elastase (PPE) (200 U/kg) alone via the left and right main bronchi. BMCs also significantly reduced cell counts in bronchoalveolar lavage fluid, the incidence of apoptotic (TUNEL-positive) cells and matrix metalloproteinase (MMP)-2 expression, while increasing numbers of proliferative (Ki-67-positive) cells. Thus, BMCs may inhibit the progression to emphysema by attenuating inflammation, MMP-2 expression, and apoptosis, while enhancing alveolar cell proliferation.

Disruption of the extracellular matrix is believed to play an important role in the pathogenesis of emphysema. Prior studies have demonstrated that transgenic mice expressing the human tissue collagenase, matrix metalloproteinase 1 (MMP-1), develop emphysema. MMP-1 is a protease with substrate specificity for fibrillar collagen. Type I and III collagens, which are the most abundant proteins within the lungs, are the primary substrates for MMP-1. To assess if type I collagen was indeed the site of action for MMP-1 in these transgenic mice, hybrid mice were generated by crossing the MMP-1 transgenic mice with mice that had degradation-resistant type I collagen. The hybrid mice demonstrated an identical emphysematous phenotype as the MMP-1 transgenic mice, indicating that the degradation of type I collagen was not essential to the development of emphysema in these mice. Immunohistochemical studies in control mice demonstrated that collagen fibers in the alveolar walls and ducts of the normal mouse lungs consist mainly of type III collagen. In the transgenic and hybrid mice, the emphysematous changes, which developed, were associated with a marked decrease in type III collagen in these alveolar structures. These results indicate that MMP-1 generated the emphysematous phenotype via the degradative effect on type III collagen, which is a vital structural element of the alveolar walls. This is the first study to show that a matrix metalloproteinase may cause emphysema via its effects on a specific collagen subtype. As such, it should provide important insight into the mechanisms of this disease in humans.

Knowledge about the regional deposition of aerosol particles is essential in order to perform efficient inhalation therapy or to minimize health risks due to environmental or occupational aerosol particles. In this study, 2 techniques were used to measure thoracic deposition and to differentiate between bronchial and alveolar deposition. The first technique was the clearance-derived regional deposition (CRD) technique and the second the single-breath regional deposition (SBRD) technique. Deposition was measured in 12 patients with alpha1-antitrypsin deficiency and symptoms of moderate to severe chronic obstructive pulmonary disease (COPD) using monodisperse test particles with aerodynamic diameters of 2, 3, and 4 microm. In CRD, the kinetic of particle clearance within the first 24 hours after inhalation was used to determine bronchial and alveolar deposition. In SBRD, the longitudinal distribution of deposited inert test particles was used to calculate the particle fraction deposited within and distal to the dead space. Both techniques delivered very similar mean values for total and alveolar deposition. Due to controlled slow and deep inhalations, alveolar deposition was as much as 50%. Therefore, SBRD can be considered as an easy tool to study alveolar deposition in patients.

Emphysema is a pulmonary disease that may be exacerbated by inhaled particles. Over the years, many animal models of emphysema have been developed that may be useful in studying the effects of inhaled particles on humans with emphysema. Models have been described in many species, and many approaches have been described for inducing emphysema. Emphysema in humans is a parenchymal component of chronic obstructive pulmonary disease and frequently coexists in a complex with disease of the airways such as bronchitis. Animal models of emphysema usually recapitulate only one or a few aspects of this complex disease. Thus, the emphysema model must be selected carefully in order to answer specific questions about the interactive effects of particles and emphysema.

Emphysematous pyelonephritis and double cancers of the kidney and urinary tract are rare. We describe here a case of a diabetic man who had simultaneous renal cell carcinoma of the right kidney and transitional cell carcinoma of the right ureter complicated with emphysematous pyelonephritis within the tumour parenchyma of renal cell carcinoma. Imaging and pathology are demonstrated.

Previously, this laboratory has shown that intratracheally administered hyaluronic acid (HA) significantly reduces air-space enlargement in a hamster model of emphysema induced with pancreatic elastase. Whereas HA was given immediately following elastase in those initial studies, the current investigation determined the effect of instilling HA up to 2 h before or after intratracheal administration of elastase to hamsters. Both 1 and 2 mg HA, given 2 h before pancreatic elastase, significantly decreased (p < .05) air-space enlargement compared to controls (as measured by the mean linear intercept). Instillment of 2 mg HA, 1 h after pancreatic elastase, had a similar effect (p < .05). In contrast, 1 mg HA, given 1 or 2 h after pancreatic elastase, did not significantly affect the mean linear intercept. Against human neutrophil elastase, HA exhibited the same protective effect. While neutrophil elastase induced less air-space enlargement than pancreatic elastase, both 1 and 4 mg of HA, given 2 h prior to the enzyme, still produced a significant reduction (p < .05) in the mean linear intercept. HA exerted this effect despite the fact that it initiates a transient influx of neutrophils into the lung. Since HA does not slow the clearance of intratracheally instilled [14C] albumin from the lung, its mechanism of action may not involve physical interference with the movement of elastase through the lung, but may instead depend on interaction with elastic fibers. Evidence for an association between these two matrix constituents was provided by studies using fluorescein-labeled HA. Overall, these results further suggest that HA may be useful in preventing lung injury by elastases.

Emphysematous pyelonephritis, bilateral or in a solitary kidney, is a life-threatening condition that requires prompt diagnosis and early intervention. Reported mortality is high, despite desperate surgical measures often ending in loss of renal unit, but medical management, possibly combined with percutaneous drainage, is sometimes successful. We report two cases of emphysematous pyelonephritis, one bilateral and one in a solitary kidney, with successful conservative management. Predisposing factors were insulin-dependent diabetes mellitus and micronodular cirrhosis secondary to chronic alcoholism. Prompt sonographic diagnosis determined the success of conservative management. Escherichia coli was identified as causal factor. In the bilateral case the clinical picture improved within 48 h after control of diabetes and broad-spectrum antibiotic treatment. For the affected solitary kidney, percutaneous drainage and ureteric catheterization were required.

A 59-year-old man developed emphysematous cystitis 3 weeks after undergoing left orchiectomy because of suppurative epididymitis. The case is presented because of its unusual cause and to emphasize the high degree of suspicion required for the diagnosis.

Several attempts have been made to describe the relation that exists between tobacco smoke and emphysema, through different experimental models of the active smoker. Despite the negative effects that involuntarily inhaled tobacco smoke can have on the lung, no experimental model of the passive smoker has been proposed. In this study, an experimental model of the involuntary smoker is described and the following hypothesis proposed: Passive exposure to tobacco smoke produces morphological alterations in the rat lung, which are compatible with emphysema. Emphysema will be considered to have been caused when enlargement of the distal airspaces of the lung and lung tissue destruction are demonstrated. Sixty Wistar rats were used, divided into two groups: a control group and a group that was passively exposed to tobacco smoke for a period of 3 months. A morphometrical study of the lung was performed using a computerized system. To demonstrate enlargement of the distal airspaces of the lung, the following variables were quantified: alveolar chord and mean linear intercept index (Lm); tissue loss was demonstrated by means of the quantification of the variables: tissue density, internal alveolar perimeter (IAP), and wall thickness (WT). The elastic fiber was also quantified. The animals that were exposed to tobacco smoke displayed the following significant alterations (p < .05): an increase of the alveolar chord and of the Lm, a decrease of the IAP, WT, and tissue density, and a loss of the elastic component of the lung. On the basis of these findings, it is concluded that the rats that were exposed in a passive way to tobacco smoke display morphological pulmonary alterations that are compatible with the definition of emphysema.

If emphysema is identified early, much can be done to prevent or even reverse its progress. Smokers must be helped to stop smoking, and early, aggressive therapy with bronchodilators (plus corticosteroids, if needed) should be instituted. By preventing emphysema, the desperate cost of progressive respiratory insufficiency and curtailment of the pleasurable activities of daily living can be avoided.