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A rare cause of subcutaneous emphysema is described which developed in two patients after epidural anaesthesia. Only two case reports could be found in literature describing similar conditions. The anaesthesia is performed using the "loss of resistance" technique with injection of air for the identification of the epidural space. Possible explanations for the development of the emphysema are discussed.
Scrotal emphysema is mostly iatrogenic and posttraumatic in origin. It usually occurs after surgical operation in the inguinal or the retroperitoneal areas. Three cases of scrotal emphysema secondary to chest problems and one case of scrotal inflation with a syringe and needle are reported. The literature is reviewed and the management is discussed.
PURPOSE: We investigated the association of carbon dioxide absorption with the approach (transperitoneal versus extraperitoneal) and other factors during laparoscopy. MATERIALS AND METHODS: Carbon dioxide elimination during laparoscopic renal surgery was retrospectively calculated in 63 patients. RESULTS: Carbon dioxide elimination increased with time. Multiple factorial analysis revealed that subcutaneous emphysema and the extraperitoneal approach were independently associated with a greater increase in carbon dioxide elimination. Pneumothorax and pneumomediastinum were more common during extraperitoneal procedures. CONCLUSIONS: Carbon dioxide absorption during laparoscopic renal surgery increases with time, and is greatest in patients treated through an extraperitoneal approach and in those with subcutaneous emphysema. Nonetheless, with attentive ventilatory management adverse sequelae of hypercapnia can be avoided.
Cervical mediastinic emphysema usually does not demand emergency procedures: nevertheless its ethiology must be promptly assessed though his achievement may prove less than easy owing the vague clinical presentation and to the limits imposed by regional topography. Among the possible etiologic factors one should take into account the rare abdominal source too. Indeed the cervical region is connected to the retroperitoneal space through a virtual "visceral space" via the thoracic cavity and some diaphragmatic break-throughs variable in size. The communication allows, in some pathologic conditions, the unopposed circulation of air and fluids. Our interest in the topic is due to the occurrence of a cervical mediastinic emphysema in a patient suffering from a colonic perforation.
In children, subcutaneous emphysema and pneumomediastinum are produced by bronchopulmonary infections, increased transalveolar pressure, bronchotracheal foreign bodies, and anesthetic or dental procedures. The case of a child with subcutaneous emphysema and pneumomediastinum after tonsillectomy and adenoidectomy is reported. The etiopathogenesis is discussed and the literature is reviewed.
Subcutaneous emphysema and pneumomediastinum have many causes. Generally they course without severe pathophysiological complications and severe respiratory complications are rare. However, cases with progressive dyspnea should be treated with tracheostomy or superficial incisions. A case is reported of a patient who underwent hip surgery under general anesthesia with tracheal intubation and later presented progressive dyspnea with subcutaneous emphysema and neuromediastinum. Tracheostomy yielded satisfactory results.
Subcutaneous peripharyngeal emphysema and pneumomediastinum are rare complications in postoperative patients after several types of surgery (orthognathic, laryngeal, tracheotomy and oropharyngeal). We report a case of subcutaneous and peripharyngeal emphysema after bilateral tonsillectomy in a 43-year-old male. Air or anesthetic gases spread to the neck, mediastinum, abdomen, or pleural cavity.
Patients with mediastinal emphysema and free air in the cervical region often present to an emergency medicine department, where an otolaryngologist-head and neck surgeon may be consulted for a surgical opinion. These occasions underscore the necessity that the disease be thoroughly understood and that conservative management be executed. Two patients with asthma, a 16-year-old boy and a 20-year-old man, were found on roentgenograms to have retropharyngeal free air and mediastinal emphysema. They were treated conservatively, and both recovered rapidly.
The recent development of laparoscopic cholecystectomy has introduced the technique of laparoscopy to the general surgical community. As increasing numbers of laparoscopic cholecystectomies are performed, increasing numbers of complications directly related to laparoscopy will result. A case of subcutaneous emphysema and hypercarbia without pneumothorax is reported in a patient undergoing laparoscopic cholecystectomy. Etiology, evaluation, and therapy for subcutaneous emphysema associated with laparoscopy are reviewed.
BACKGROUND & OBJECTIVE: Although thoracoscopic laser ablation therapy has been hailed as an effective surgical treatment for diffuse emphysema, no one has as yet made an in-depth study of the efficacy of this treatment. This investigation was undertaken to research the effects of laser pneumoplasty on an animal model of emphysema. STUDY DESIGN/MATERIALS AND METHODS: Eight weeks after elastase treatment, the rats' left lungs were irradiated using contact Nd:YAG laser. Pulmonary function tests were performed 4 weeks after irradiation and the lungs were prepared for histologic examination. RESULTS: Dense fibrous scars beneath the pleura were observed at 4 weeks after irradiation. Although mean linear intercept values of irradiated lungs were not much lower than those in the non-irradiated elastase-treated group, laser irradiation caused a significant decrease in lung volume. While there was no significant difference in quasistatic compliance, elastic recoil pressure of the lung increased to control levels at total lung capacity volume. CONCLUSION: We conclude that laser therapy does not cause normalization of compliance, or improvement in the deeper part of the emphysematous lung, but rather a peripheral volume reduction and "encasement effect" on the lungs as a result of fibrotic scars.
We applied the rapid imaging capability of echo planar MR pulse sequences and hyperpolarized (3)He ventilation imaging to observe the dynamic distribution of gas in the lungs during breathing. Findings in five normal volunteers (age 19-53 years) and four patients with severe smoking-related emphysema (age 56-71 years) were compared. All studies were performed on a 1.5 T whole body scanner using a 30 cm Helmholtz surface coil and 0.5 l of 20-40% polarized (3)He mixed with 1-2 l nitrogen. Our echo planar imaging pulse sequence allowed acquisition of each image in 0.04 s, with a pixel size of 7 mm(2) (TR = 40.5 ms, TE = 12.1 ms, flip angle = 22 degrees, echo train length = 32, matrix = 32 x 64, field of view = 225 x 450 mm, slice thickness = 10 mm). Imaging was performed in the transaxial plane repeatedly at 3, 10 or 20 evenly spaced levels, immediately before and during breathing of the gas mixture. In normal subjects during the first breath, (3)He appeared throughout each slice first in the mid lungs, then in the lower lungs, then in the upper lungs, with slightly greater signal in the dependent posterior regions. In patients with emphysema, sequential filling of different lung regions was seen during the first breath, with delayed filling of other regions observed during rebreathing and room air washout. We conclude that subsecond dynamic (3)He MR ventilation imaging can reveal normal and abnormal ventilation phenomena not seen with conventional scintigraphic methods, and offers another approach to the study of ventilation physiology and pathophysiology.
Familial idiopathic nonarteriosclerotic cerebral calcification (FINCC) constitutes a rare but pathologically well defined disorder. Thus far, central nervous system symptoms and signs have been the only recorded expression of this disease. Autosomal dominant and autosomal recessive inheritance have both been postulated as cause. We describe three sibs who had symmetrical cerebral calcifications, but three also had cirrhosis and pulmonary emphysema; two had congenital cerebral aneurysms. All were male and of short stature; they also had delayed development and seizures, and two had other neurologic deficits. One sib died at age 3 years of hepatic failure and portal hypertension. Ruptured cerebral aneurysms led to the death of the other two boys at ages 8 and 13 years. The cerebral calcifications symmetrically involved the basal ganglia and thalami, the dentate nucleus, and the cortical and subcortical areas of the cerebrum. The liver was studied by sequential biopsies in two of the children and in all three by autopsy. Fatty degeneration and portal fibrosis preceded a periportal and micronodular cirrhosis. Severe bilateral pulmonary emphysema was present in one sib at age 12 years, whereas all three had bullae and cysts at autopsy. Ruptured left middle cerebral artery aneurysms were demonstrated in two sibs, and one also had aneurysms of the anterior and posterior communicating arteries. We conclude that in this family FINCC is a complex pleiotropic mendelian mutation, either of autosomal or X-linked recessive nature, whose basic pathogenesis remains unknown but may involve a metabolic defect. This form of FINCC may be a previously undescribed syndrome or a form of FINCC in which extraneural manifestations were previously overlooked.
Diffusion MRI of hyperpolarized (3)He shows that the apparent diffusion coefficient (ADC) of (3)He gas is highly restricted in the normal lung and becomes nearly unrestricted in severe emphysema. The nature of this restricted diffusion provides information about lung structure; however, no direct comparison with histology in human lungs has been reported. The purpose of this study is to provide information about (3)He gas diffusivity in explanted human lungs, and describe the relationship between (3)He diffusivity and the surface area to lung volume ratio (SA/V) and mean linear intercept (L(m)) measurements--the gold standard for diagnosis of emphysema. Explanted lungs from patients who were undergoing lung transplantation for advanced COPD, and donor lungs that were not used for transplantation were imaged via (3)He diffusion MRI. Histological measurements were made on the same specimens after they were frozen in the position of study. There is an inverse correlation between diffusivity and SA/V (and a positive correlation between diffusivity and L(m)). An important result is that restricted (3)He diffusivity separated normal from emphysematous lung tissue more clearly than the morphometric analyses. This effect may be due to the smaller histologic sampling size compared to the MRI voxel sizes.
A single dose of crystalline, porcine pancreatic elastase injected intratracheally into hamsters induces widespread alveolar enlargement with subpleural bullae. A uniformly severe lesion is consistently induced by 0-2 mg elastase per 100 g body weight and with negligible mortality. Compared with controls, which showed no lesion, elastase-damaged lungs show a highly significant (P less than or equal to 0-001) increase in alveolar size and a decrease in internal surface area. Taken with the associated physiological abnormalities, these findings closely simulate human emphysema of the panlobular (panacinar) type. Histologically it appears that elastase converts the fine elastic fibres in alveolar walls and pleura into thickened, nodular fibres which may also be broken along their length. With higher doses of elastase, i.e., 0-5 mg/100 g body weight, many pulmonary arteries showed segmental loss of inner and outer elastic laminae, usually with thrombosis on the overlying endothelium. The mechanism of this thrombosis is unclear. These experiments suggest that damage to elastic fibres may be an important element in the development of human panacinar emphysema, and that the damage could be one pathogenetic mechanism which produces damage of elastic fibres.
The aim of this study was to determine whether lipopolysaccharide-induced elastase release from recruited neutrophils in the hamster lung would induce emphysema, measured by mean linear intercept (Lm) and bronchial mucus cell hyperplasia (BMCH), scored in tissue sections stained with periodic acid-Schiff. Lipopolysaccharide (LPS) was instilled transorally twice a week for up to 5 weeks in hamsters. At 4 weeks after seven LPS instillations, Lm amounted to 87.6 +/- 1.2 microns, while it was 68.3 +/- 1.5 microns after seven saline instillations (P less than 0.01). At 6 months after the sixth LPS instillation, the Lm of these lungs was 83.3 +/- 1.6 microns, indicating irreversible tissue destruction. LPS-treated hamsters showed marked to severe BMCH, which was most evident in large intrapulmonary airways. Instillations of highly selective inhibitor of hamster PMN elastase resulted in 50 per cent inhibition of LPS-induced emphysema. The development of BMCH was inhibited by approximately 35 per cent by this agent. To study the response in time of cellular infiltration after a single LPS instillation, the lungs of groups of four hamsters were lavaged at different time points. PMN recruitment showed peak values at 4 and 48 h after LPS instillation and returned to baseline values at 96 h. Simultaneous intratracheal instillation of LPS and anti-TNF alpha antiserum resulted in a considerable reduction of neutrophil influx into bronchoalveolar spaces in the first 6 h after instillation.
Persistent pulmonary interstitial emphysema (PPIE) is a chronic form of pulmonary interstitial emphysema. The disease is histologically distinguished by large cysts and giant cells. Our patient was a female twin who was born at 31 weeks of gestation with a birth weight of 1,450 g. A chest X-ray at 2 hr after delivery was normal. At 12 hr, respiratory distress developed, and nasal continuous positive airway pressure (CPAP) was initiated. A chest film revealed left-sided pneumothorax. A chest tube was inserted, and the baby continued on nasal CPAP for 5 days. Her chest X-ray on postnatal day 4 showed diffuse cystic changes in the left lung. Thoracic computed tomography revealed multiple thick-walled cysts, the largest measuring 3 cm in diameter. Our case confirms that localized PIE may occur in preterm infants who have been treated with nasal CPAP only. Since this method is being used increasingly to avoid mechanical ventilation and in the postextubation period, it is very important that clinicians be aware of its complications.
The effects of low levels of air pollution and weather conditions on the number of patients admitted to hospitals for exacerbation of chronic bronchitis or emphysema (n = 2807) was studied in Helsinki during a 3-year period, 1987-1989. The daily number of admissions via the emergency room was significantly associated with prevailing levels of sulfur dioxide (SO2) and nitrogen dioxide (NO2) in Poisson regressions controlled for weather, season, time trends, and day of the week, whereas the total number of admissions (via the emergency room and otherwise) was not significantly associated with these pollutants. The effect of SO2 was observed only among those under 65 years old; a significant peak of admissions was seen during the same day (RR, 1.31 for a 2.7-fold increase in SO2; 95% CI, 1.01-1.70; P = 0.039), and another after a 3-day lag (RR, 1.39; 95% CI, 1.05-1.86; P = 0.021). The effect of NO2 was strongest after a 6-day lag and was significant only among those over 64 years old (RR, 1.31; 95% CI, 1.03-1.66; P = 0.022). The average of mean 24-hr concentrations of NO2 was 39 micrograms/m3 (0.021 ppm) and that for SO2 was 19 micrograms/m3 (0.0067 ppm). No relationship was found between admissions and the concentrations of total suspended particulates (TSP) or ozone (O3), the temperature, or the relative humidity. However, the number of admissions among those over 64 years of age was significantly lower, irrespective of temperature, during the summer than during other seasons. The mean daily concentration of O3 was fairly low (22 micrograms/m3 or 0.011 ppm), but that of TSP was high, 76 micrograms/m3. the mean temperature was low, +4.7 degrees C. These results suggest that SO2 and NO2 concentrations lower than those given as guidelines in many countries, and lower than previously shown, may increase the incidence of symptoms in some patients with chronic bronchitis or emphysema.
Emphysema is a slowly progressive degenerative lung disease involving fragmentation and depletion of elastic fibers, loss of lung elastance, and architectural destruction with ectasia, tortuosity, and loss of bronchioles irrespective of localization or morphological type. Occurring under physiological conditions, predominantly in geriatrics, matrix laxity and destructive parenchymal lesions are indicative of a pathological loss of tissue tensile strength attributable to bioengineering or structural fatigue in repetitively stressed tissues. The occurrence of severe premature emphysema in inherited connective tissue diseases and under some experimental and iatrogenic conditions is supportive evidence. Experiments advocating unrestrained proteolysis as a cause or pathogenic factor are invalid, being based on a false premise and assumed causality.