Subpleural Emphysema Research Articles

Subpleural emphysema as a rare initial manifestation of an iatrogenic tracheal penetration: a case report

BackgroundIatrogenic tracheal injury is a rare but potentially morbid condition and often poses a diagnostic challenge due to its rarity and the lack of specific clinical findings. Because a delayed diagnosis is associated with a higher mortality, a prompt diagnosis is essential. We report a case of an iatrogenic tracheal injury detected by subpleural emphysema as a rare initial manifestation.Case presentationA 75-year-old woman was diagnosed with stage IA2 right lung cancer. During the surgery, visceral subpleural emphysema developed along the lung surface up to the interlobar fissure followed by subcutaneous emphysema in the anterior neck. Suspecting a tracheal injury, we aborted the surgery. Fiberoptic bronchoscopy revealed a longitudinal laceration on the membranous part of the distal trachea without esophageal involvement, consistent with a level II injury. Conservative management was chosen and she had a successful recovery.ConclusionsIatrogenic tracheal injury could initially manifest as visceral subpleural emphysema. Once subpleural emphysema is observed during surgery, a prompt diagnostic workup of the tracheal injury should be performed.

Lung Ultrasound in the Diagnosis of COVID-19 Pneumonia: Not Always and Not Only What Is COVID-19 "Glitters".

Background: In the current coronavirus disease-2019 (COVID-19) pandemic, lung ultrasound (LUS) has been extensively employed to evaluate lung involvement and proposed as a useful screening tool for early diagnosis in the emergency department (ED), prehospitalization triage, and treatment monitoring of COVID-19 pneumonia. However, the actual effectiveness of LUS in characterizing lung involvement in COVID-19 is still unclear. Our aim was to evaluate LUS diagnostic performance in assessing or ruling out COVID-19 pneumonia when compared with chest CT (gold standard) in a population of SARS-CoV-2-infected patients.Methods: A total of 260 consecutive RT-PCR confirmed SARS-CoV-2-infected patients were included in the study. All the patients underwent both chest CT scan and concurrent LUS at admission, within the first 6–12 h of hospital stay.Results: Chest CT scan was considered positive when showing a “typical” or “indeterminate” pattern for COVID-19, according to the RSNA classification system. Disease prevalence for COVID-19 pneumonia was 90.77%. LUS demonstrated a sensitivity of 56.78% in detecting lung alteration. The concordance rate for the assessment of abnormalities by both methods increased in the case of peripheral distribution and middle-lower lung location of lesions and in cases of more severe lung involvement. A total of nine patients had a “false-positive” LUS examination. Alternative diagnosis included chronic heart disease (six cases), bronchiectasis (two cases), and subpleural emphysema (one case). LUS specificity was 62.50%. Collateral findings indicative of overlapping conditions at chest CT were recorded also in patients with COVID-19 pneumonia and appeared distributed with increasing frequency passing from the group with mild disease (17 cases) to that with severe disease (40 cases).Conclusions: LUS does not seem to be an adequate tool for screening purposes in the ED, due to the risk of missing some lesions and/or to underestimate the actual extent of the disease. Furthermore, the not specificity of LUS implies the possibility to erroneously classify pre-existing or overlapping conditions as COVID-19 pneumonia. It seems more safe to integrate a positive LUS examination with clinical, epidemiological, laboratory, and radiologic findings to suggest a “virosis.” Viral testing confirmation is always required.

A case of parietal subpleural emphysema during thoracoscopic surgery for pneumothorax

A case of parietal subpleural emphysema during thoracoscopic surgery for pneumothorax

Acute and chronic bovine pulmonary edema and emphysema in Uruguay

ABSTRACT: An outbreak of pulmonary edema and emphysema with acute and chronic cases is reported in a farm in Uruguay. In a herd of 40 Hereford steers, 20 died. The deaths began four days after a change of paddock, from an old pasture of Avena sativa to a lush growing pasture of the same grass. Acutely affected animals showed severe dyspnea, sialorrhea, cough, and subcutaneous edema, and died within 72 hours. Chronically affected steers showed dyspnea, respiratory noises, weight loss, and intolerance to exercise. The deaths began four days after the change of paddock. Ten days after the first death, the steers were withdrawn from the pasture, but continued dying throughout the following 40 days. Twenty animals died and six were necropsied. Grossly, the lungs were diffusely armed and glistening, with reddish and crepitant cut surface, and presented alveolar septae sharply distended by edema and emphysema. There was subpleural emphysema with air blebs distributed across the pleural surface. Presence of Dictyocaulus viviparus was observed in three steers. In some animals, the trachea was diffusely reddish with presence of pink foam; in some others, there was bloody liquid in the tracheal lumen. Histologic examination showed severe diffuse alveolar and interstitial emphysema, hyaline membranes adhered to the alveolar wall, thickening of the interlobular septae with proliferation of type II pneumocytes, and moderate-to-severe multifocal histiocytic, neutrophilic and eosinophilic infiltrate. In the trachea, there was submucosal hemorrhage and moderate multifocal eosinophilic and lymphocytic infiltrate. The steers with chronic signs presented similar lung lesions, but multifocal pulmonary fibrosis and cardiac dilatation were also observed. The diagnosis of acute bovine pulmonary emphysema and edema (ABPE) was based on the occurrence of the disease after introduction of the herd in a lush green pasture, on the characteristic gross and histologic lesions, and on the absence of other toxic or infectious agents causing similar lesions. Cattle raisers should be alert to the risks of occurrence of this disease after the introduction of the herds into paddocks with green and lush pastures.

Spontaneous pneumothorax from cryptococcal pneumonia in systemic sclerosis: a case report

IntroductionSpontaneous pneumothorax is usually found in people with systemic sclerosis who have extensive pulmonary fibrosis with enlarged sub-pleural blebs. We report a case of spontaneous pneumothorax caused by cryptococcal pneumonia in a patient with systemic sclerosis with minimal sub-pleural emphysema.Case presentationA 49-year-old Thai man with underlying limited cutaneous systemic sclerosis presented with acute low-grade fever, progressive dyspnea and right pleuritic chest pain for five days. Our patient had pulmonary fibrosis with bronchiectasis of both lower lungs related to this underlying disease. He received only low-dose steroid therapy, without any immunosuppressant. A chest radiograph revealed right lung pneumothorax with cloudy yellow color pleural fluid. Cryptococcal pneumonia was diagnosed by positive identification of the cryptococcal antigen in the serum and pleural fluid. His symptoms improved after intercostal drainage and fluconazole therapy.ConclusionInfection can exacerbate symptoms in patients with systemic sclerosis with sub-pleural emphysema, thereby triggering a spontaneous pneumothorax. Pleural fluid--present but not initially seen because of the pneumothorax--could be a clue to a pre-existing pulmonary infection.

Circulation of bovine respiratory syncytial virus in Brazil

cent (Campalans and Arns 1997). BRSV was isolated for the first time in Brazil in 1996, from nasotracheal secretions of calves with respiratory disease in the south of the country (Arns and others 2003). This short communication describes the characterisation of a new strain of BRSV in Brazil isolated from a one-year-old calf with severe respiratory signs. The calf showed anorexia, apathy, fever, an abundant seromucous nasal discharge, intense dyspnoea, tracheal and pulmonary sounds, and pain in the ventral thoracic region. Despite supportive treatment, the animal did not recover and was euthanased five days after the onset of clinical signs. Postmortem examination revealed interstitial multifocal pneumonia, extensive consolidated areas, severe interstitial and subpleural emphysema, intense thickening of the interlobular walls, non-catarrhal pleuritis and marked hypertrophy of the right ventricle. For immunohistochemistry (IHC) analysis, samples of lung tissue were fixed in 4 per cent paraformaldehyde (SigmaAldrich), embedded in paraffin wax, cut in 4 μm thick sections and mounted on microscope slides. The IHC was carried out at the Royal Veterinary and Agricultural University, Copenhagen, Denmark. After a pretreatment with 0·018 per cent protease, the sections were blocked with 5 per cent normal pig serum, and then incubated overnight at 4°C with a biotinylated polyclonal bovine serum against BRSV. The sections were then incubated with 0·9 per cent streptavidin (Dako), followed by 0·9 per cent biotinylated alkaline phos-

Detection of Brazilian bovine respiratory syncytial virus strain by a reverse transcriptase-nested-polymerase chain reaction in experimentally infected calves

A reverse transcriptase (RT)-nested-polymerase chain reaction (PCR) was standardised to detect bovine respiratory syncytial virus (BRSV), using a Brazilian isolate, in three experimentally infected calves. This followed initial tests in infected chicken embryo related (CER) cells. One animal had lesions, characterized by interstitial multifocal pneumonia, severe interstitial and subpleural emphysema, and lung consolidated areas. Lung and tracheal tissues collected 6 days after infection were analysed by RT-nested-PCR. Primers, specific for the BRSV G and F glycoproteins genes, yielded amplification fragments of 371 and 481 bp, respectively, from the RNA of the cell-propagated virus. Using RNA extracted from organs of infected calves, RT-nested-PCR amplified the fragment of the G gene in all tracheal samples, but in only two of three lung samples analysed. These results suggest that RT-nested-PCR could be a promising assay for diagnosis and epidemiological analysis of BRSV in Brazil.

The incidence of senile plaques and multiple infarction in aged Macaque brain

IN 1980, shortly after I moved from the Oregon Primate Center to the Wisconsin primate Center, I noticed that the Wisconsin Center had almost 80 animals >20 years of age. This, of course, was the heritage of Dr. Harry Harlow who started a large-scale rhesus monkey colony near the end of the 1940s and early 1950s. Because the Wisconsin Center traditionally focused more on behaviorally oriented research studies that were not terminal experiments, many of animals were retired to a breeding colony. The aged animals have been supported by the set-aside program of the National Institute on Aging for aged animals. We record life span using only those which die spontaneously; those used in experimental studies are not included. For example, in 1980 we had 70 monkeys >20 years. By 1992, about 80 animals were about 20 years. Many monkeys die between 20 and 30 years of age, but an occasional monkey lives to 35-36 years of age, and maximum longevity is about 36 years. In a population of monkeys >20 years approximately 15 can be expected to die annually. How does this compare with humans? The rhesus monkey reaches reproductive age at 3-4 years and menopause is by 25-26 years; histologic examination shows a tremendous decrease of ovarian foUiculogencsis; by 31 years old, there is literally no folliculogenesis. The oldest monkey to givc birth at the Wisconsin Center was 27 years. In comparison to the human age for menopause of 50 years, it is 25 years in the rhesus monkey. The geriatric signs in these '~post-menopausar' monkeys 2026 years of age include drier skin, telangiectasias, tooth decay, muscle atrophy, a decrease in body weight, cataracts, and many bone and joint problems. Cataracts may be a very good sign of aging in the rhesus monkey; severe ones are seen at about 26 years. What is the cause of death for these monkeys? Many have subpleural emphysema, we see it in about 20% of monkeys by 19 years of age. Coronary sclerosis but not atherosclerotic plaque, is quite a prevalent change in the heart, although we do not see stenosis (5). Histologically, the muscle layer in the media is decreased and replaced with fibrous tissues, so blood flow is decreased. We have found 18 monkeys >20 years with cancer of the colon in 20 years; unlike the human, it is mostly in the cecum. Histologically, these tumors are similar to those in humans, a mucus producing adenocarcinoma. We have accumulated about 51 brains from monkeys >25 years of age; they were not behaviorally characterized. We have seen no evidence of atrophy in the cortex nor does the brain weight decline-----even up to 36 years. In the aging human, Alzheimer's disease and multiple infarction are the major causes of dementia. Although we have no behavioral data for dementia in these mon-

RADIOLOGIC CONSIDERATIONS IN THE ADULT RESPIRATORY DISTRESS SYNDROME TREATED WITH POSITIVE END EXPIRATORY PRESSURE (PEEP)

Radiographic changes with ARDS are similar to alveolar pulmonary edema in the typical case, although early changes may also be nodular in a small number of cases. These may last about 4 days. Following early alveolar changes the later ARDS findings evolve into a diffuse interstitial pattern, and if the patient survives without complications, the chest x-ray may eventually clear completely. PEEP therapy may cause no x-ray changes or may manifest an apparent hyperinflation appearance to the chest x-ray. PEEP may result in barotrauma changes to the lungs manifested by vesicular rarefactions, lucent lines streaking toward the hilus, radiolucent halos around vessels, pneumatocele formation, and subpleural emphysema manifested by blebs or lucent lines on the chest x-ray. Barotrauma pulmonary changes preceded more serious complications such as pneumothorax, mediastinal emphysema and extrathoracic gas collection.

Subpleural emphysema complicating staphylococcal and other pneumonias

Our observations suggest that the radiologic images of so-called "pneumatoceles" are caused by subpleural emphysema, an accumulation of air between the visceral pleura and the pulmonary parenchyma. For this reason the term "subpleural emphysema" seems to be more appropriate than "pneumatocele." Air from the respiratory tree escapes into the interstitial interlobular tissue and flows under the pleura, detaching it and collapsing the parenchyma. By histologic examination it can be demonstrated that the interlobular spaces contain "air corridors" linked to the subpleural air cavity. Air accumulating beneath the pleura can coalesce to form large bullae, resulting in complete pleural detachment. The lesion is capable of sudden change, including rapid resolution. Secondary infection and its associated reaction, however, may alter thin-walled vesicles into thick-walled, rigid, semipermanent cysts.

Certain effects of positive pressure respiration on the circulatory and respiratory systems

Experimental studies were carried out on dogs anesthetized with pentobarbital sodium to determine the effect of long periods of pressure breathing alone and when combined with acute hemorrhage or trauma of the hind limbs. The following results were obtained: 1. 1. Continuous positive pressure respiration with a pressure of 20 cm. of water. 2. a. Five of nine animals survived three hours of continuous positive pressure respiration, but, in the case of the other four, fatal apnea developed. 3. b. The apnea caused by a continuous positive respiratory pressure of 20 cm. of water was not affected by large doses of atropine but was abolished by bilateral vagotomy. 4. c. Continuous positive pressure respiration had a variable effect on the femoral arterial pressure and on the heart rate. It slowed and deepened the respirations. It elevated the jugular venous pressure, the renal venous pressure, the pulmonary arterial pressure, and the pulmonary venous pressure. It decreased the diameter of the heart and thoracic inferior vena cava but increased the diameter of the abdominal vena cava. It dilated the tracheobronchial tree. 5. d. Three of eight animals survived two hours of continuous positive pressure respiration after a hemorrhage of 30 c.c. per kilogram of body weight in five minutes, but in the case of the other five animals either apnea or circulatory failures developed. 6. e. Three hours of continuous positive pressure respiration did not cause either pneumothorax or mediastinal emphysema in a single case, but in all of a group of five animals acute parenchymal and subpleural emphysema developed. 7. 2. Intermittent positive pressure respiration with a pressure of 20 cm. of water. 8. a. All of a group of five animals withstood three hours of intermittent positive pressure respiration without difficulty. 9. b. Intermittent positive pressure respiration produced considerable fluctuation of the femoral arterial pressure with a decrease of the mean pressure. It elevated the jugular venous pressure, the pulmonary venous pressure, the renal venous pressure, and the pulmonary arterial pressure. It decreased the diameter of the heart and thoracic inferior vena cava but increased the diameter of the abdominal vena cava and the tracheobronchial tree. It slowed and deepened the respirations but had no consistent effect on the heart rate. 10. c. Three of five animals survived, without difficulty, two and a half hours of intermittent positive pressure respiration following a hemorrhage of 30 c.c. per kilogram of body weight in five minutes. In the case of the other two, eirculatory failure developed and the animals were given 10 c.c. of blood per kilogram of body weight with such improvement that they were then able to complete the experiment. 11. d. Splenectomized animals were unable to withstaud even a small hemorrhage (10 to 20 c.c. per kilogram of body weight) during intermittent positive pressure respiration. 12. e. Trauma to the hind limbs during intermittent positive pressure respiration proved fatal to all four animals. It was demonstrated that the pressure breathing was a definite factor in hastening their death. 13. f. Three hours of intermittent positive pressure respiration with a pressure of 15 cm. of water did not cause either pneumothorax or mediastinal emphysema in a single case, but in all of a group of three animals acute parenchymal and subpleural emphysema developed.

Annular Shadows in the Lungs Caused by Subpleural Emphysema

Annular Shadows in the Lungs Caused by Subpleural Emphysema