PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ATELECTASIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1989

Shrinking pleuritis with lobar atelectasis, a morphologic variant of "round atelectasis".

Round atelectasis (shrinking pleuritis) is typically a localized process characterized by focal pleural scarring and subjacent peripheral atelectasis. We report three patients, studied at autopsy, with an unusual variant of round atelectasis, termed shrinking pleuritis with lobar atelectasis, which is characterized by lobar atelectasis, visceral pleural fibrosis involving multiple lobes, interlobar fibrous cords, pleural effusion, and nonspecific, persistent infiltrates on chest radiogram. The possible causes of shrinking pleuritis with lobar atelectasis in our patients were multiple and included environmental dust exposure, infection, uremia, and recurrent pleural effusions. Our findings support both the folding (pleural effusion) and fibrosing (pleural injury) theories of pathogenesis of round atelectasis and emphasize the spectrum of morphologic variability in this condition.

Aged↗
PubMed1994

[CT findings of peripheral atelectasis associated with pleural effusion: in association with the mechanism of rounded atelectasis formation].

The role of pleural effusion in the formation of rounded atelectasis (RA) was evaluated using CT in 159 patients with 210 pleural effusions. The forms of peripheral atelectasis associated with pleural effusion (PA-PE) were classified into five types: type 1: no atelectasis, type 2: flat or crescent type, type 3: convex type, type 4: mass-like type, type 5: consolidation type. Atelectasis (type 2-5) accounted for 78% (164/210) of all lesions. Type 2 was the commonest type of PA-PE, followed by type 5. Types 2 and 5 accounted for 79% (130/164) of all lesions with PA-PE. In most lesions of types 2 and 5, the collapsed pulmonary parenchyma re-expanded following decrease or disappearance of pleural effusion. Types 3 and 4 accounted for only 15% (25/164) and 5% (9/164), respectively. Most lesions of type 4 satisfied the criteria of CT findings of RA. Type 3 was similar to type 4 except for the obtuse angle between the collapsed pulmonary parenchyma and the pleura. As a consequence, it is reasonable to regard type 4 as RA, type 3 as the similar lesion of RA. Most lesions of types 3 and 4 were found in patients with small or moderate inflammatory exudate and pleural thickening, and most of them remained the same type in the follow-up studies. Three lesions of type 3 changed to type 4. This study showed that RA was mainly formed in the patients with inflammatory exudate and thickened pleura, rarely in the patients with transudate. It is concluded that inflammatory pleural effusion plays an important role in the formation of RA formation.

Adolescent↗
PubMed1987

Pathogenesis of shrinking pleuritis with atelectasis--"rounded atelectasis".

The pathogenesis of "shrinking pleuritis with atelectasis" or "rounded atelectasis" is discussed on the basis of 37 operated patients and on experiments on cadaver lungs. Peroperative dissections with microscopic examinations and the results of experiments with the cadaver lungs support the concept that the lesion is caused by an inflammatory reaction in the visceral layer of the pleura, caused by asbestos fibers. The inflammation occurs in stages, with deposition of connective tissue that shrinks and causes considerable atelectasis of the underlying pulmonary parenchyma. Compression of the lung due to fluid collecting in the pleural cavity involved was not noted.

Asbestos↗
PubMed1996

Types and mechanisms of pulmonary atelectasis.

Atelectasis is one of the most commonly encountered abnormalities in chest radiology and remains a daily diagnostic challenge. At times atelectasis can be overlooked, particularly when pulmonary opacification is minimal or absent, and at other times it might be interpreted as being some other form of intrathoracic pathology, particularly pneumonia. The direct signs of atelectasis are crowded pulmonary vessels, crowded air bronchograms, and displacement of the interlobar fissures. Indirect signs of atelectasis are pulmonary opacification; elevation of the diaphragm; shift of the trachea, heart, and mediastinum; displacement of the hilus; compensatory hyperexpansion of the surrounding lung; approximation of the ribs; and shifting granulomas. For descriptive purposes, atelectasis can be divided into the following types: segmental, lobar, or whole lung; subsegmental; platelike, linear, or discoid; round; and generalized or diffuse. Resorption atelectasis is caused by resorption of alveolar air distal to obstructing lesions of the airways; adhesive atelectasis stems from surfactant deficiency; passive atelectasis is caused by simple pneumothorax, diaphragmatic dysfunction, or hypoventilation; compressive atelectasis is due to tension pneumothorax, space-occupying intrathoracic lesions, or abdominal distention; cicatrization atelectasis stems from pulmonary fibrosis; and gravity-dependent atelectasis is the result of gravity-dependent alterations in alveolar volume. Whenever signs of volume loss are present on a chest radiograph, the radiograph should be interpreted as showing atelectasis. By understanding the various mechanisms leading to atelectasis, and by considering the underlying conditions, the radiologist should be able to develop an appropriate list of the possible causes of atelectasis. The diagnosis of atelectatic pneumonia should be based upon the presence of clinical signs and symptoms of pneumonia coupled with the identification of pathogenic bacteria in sputum, tracheal aspirates, or protected bronchoalveolar lavage or bronchial brush specimens rather than on the radiographic identification of atelectasis alone.

Humans↗
PubMed2004

Pulmonary atelectasis: a frequent alternative diagnosis in patients undergoing CT-PA for suspected pulmonary embolism.

The purpose of the study was to evaluate the prevalence of atelectasis as an alternative diagnosis in patients who underwent computed tomographic pulmonary angiography (CT-PA) for suspected pulmonary embolism (PE), and to contrast the pathophysiology of pulmonary atelectasis and PE, both of which are associated with dyspnea and hypoxemia. We retrospectively identified 144 consecutive emergency department patients (n=49) and inpatients (n=95) admitted between July 2001 and June 2002 who were evaluated with CT-PA for suspected PE. There were 98 women and 46 men with a mean age of 58 years (range 27-95 years). Each CT report was reviewed for PE, the words "atelectasis," "collapse," and/or "volume loss," findings known to predispose to atelectasis, and alternative diagnoses. CT scans of those with PE and those with atelectasis were reviewed. Each case was categorized into one of three groups, as follows: group 1, PE; group 2, atelectasis of three or more segments and no PE; group 3, neither PE nor atelectasis. PaO2 was documented, when available (n=115), with PaO2 >100 mmHg recorded as 100 mmHg. Reports for group 3 were reviewed for alternative diagnoses. Thirteen percent of the study population (19/144, group 1) had PE, and two of them had concomitant atelectasis; mean PaO2 was 69 mmHg (range 38-100 mmHg). Nineteen percent of the study population (27/144, group 2) had atelectasis of three or more segments without PE; mean PaO2 was 73 mmHg (range 45-100 mmHg). Sixty-eight percent of the study population (98/144, group 3) had neither PE nor atelectasis; mean PaO2 was 79 mmHg (range 36-100 mmHg). There was a significant difference in the PaO2 between groups 1 and 3 (Student's t-test), with group 2 intermediate. Seventy percent of group 2 (19/27) had at least one finding predisposing to atelectasis: central bronchial abnormality (n=6), moderate or larger pleural effusion (n=11), pleural mass, pneumothorax, elevated hemidiaphragm, and severe kyphosis (the last four all n=1 each), versus 16% (3/19) of group 1 ( P<0.05). Sixty-three percent of group 3 (62/98) had one or more alternative diagnoses on CT that explained the patient's symptoms as follows: pneumonia (28%, 27/98), other lung disease (18%, 18/98), congestive heart failure (13%, 13/98), and malignancy (13%, 13/98). Pulmonary atelectasis was common in patients undergoing CT-PA for suspected PE, equaling pneumonia as the most common alternative diagnosis. Most patients with atelectasis had predisposing findings on CT. Pulmonary atelectasis and PE cause similar symptoms by different mechanisms of ventilation-perfusion mismatch.

Adult↗
PubMed1996

Atelectasis and chest wall shape during halothane anesthesia.

BACKGROUND: Anesthesia produces atelectasis in the dependent areas of the lungs by mechanisms that remain unknown. It has been proposed that anesthesia produces a cephalad shift in the end-expiratory position of the diaphragm, which compresses the lungs and produces atelectasis. This study tested the hypothesis that the extent of atelectasis is correlated with the cephalad displacement of the dependent portion of the diaphragm produced by halothane anesthesia in healthy young human subjects. METHODS: Twelve volunteers (mean age 34 yr) were studied while awake and during approximately 1.2 minimum alveolar concentration halothane anesthesia. Chest wall configuration was determined using images of the thorax obtained by three-dimensional fast computed tomography. Functional residual capacity was measured by a nitrogen dilution technique. Measurements were performed during quiet breathing in all subjects and after paralysis with 0.1 mg/kg vecuronium and mechanical ventilation in six subjects. Atelectasis was assumed to be present in regions of the lung that showed radiographic attenuation values similar to solid organs such as the liver. RESULTS: Atelectasis in dependent lung regions was not apparent in scans performed while the subjects were awake. Anesthesia with spontaneous breathing increased the volume of atelectasis measured at end-expiration by more than 1 ml in 9 of 12 subjects. For all subjects, the volume of atelectasis was 29 +/- 10 ml (M +/- SE), representing 0.67 +/- 0.23% of the total thoracic volume. The distribution of atelectasis varied along the cephalocaudal axis, with less atelectasis in more cephalad transverse sections. Paralysis and mechanical ventilation significantly decreased the volume of atelectasis present at end-expiration. There was no correlation between the average amount of cephalad displacement of the most dependent region of the diaphragm and the amount of atelectasis, nor was there any correlation between the amount of atelectasis and anesthesia-induced changes in the end-expiratory position of any chest wall structure. CONCLUSIONS: The dependent lung atelectasis produced by halothane anesthesia does not appear to be related to changes in the position of any single chest wall structure in these healthy young subjects, but rather to an interaction of several factors that remain to be identified.

Adult↗
PubMed2000

Incidence and significance of lobar atelectasis in thoracic surgical patients.

Lobar atelectasis, defined by complete lobar collapse and mediastinal shift on chest roentgenogram, represents one extreme form of postoperative atelectasis. We have evaluated the incidence and clinical significance of lobar atelectasis in a thoracic surgical patient group. A retrospective review was done of patients who underwent pulmonary resection over a 2-year period to determine patient characteristics, contributing comorbidities, and associated perioperative care factors. Lung resections were performed for both benign and malignant disease through open or video-assisted techniques. One hundred eighty patients had pulmonary resection, 101 males and 79 females, and they were divided into three groups: I, no complications (112 patients, 62%); II, complications unrelated to lobar atelectasis (60 patients, 33%); and III, complications of lobar atelectasis (8 patients, 5%). There was one death in the series, in the lobar atelectasis group (III). Mean age for the entire group was 64.5 +/- 12.5 years; however, patients in Groups II (67.3 years) and III (69.6 years) were significantly older than in Group I (P < 0.02). Mean hospital length of stay in Group I was 6 +/- 3 days, whereas that in Group II was 13 +/- 12 days (P < 0.001), and in Group III it was 27 +/- 31 days (P < 0.001). In addition, patients who developed lobar atelectasis were more likely to be male (88% vs 48%, P = 0.034), had a longer ICU length of stay (P < 0.001), were more likely to have two or more comorbidities (P < 0.05), and had a lower forced expiratory volume in 1 second (2.34 +/- 0.90 vs 1.96 +/- 0.63). All patients in the lobar atelectasis group were operated on for malignancy, but this was not significantly different from the other groups. None of the 16 patients who had thoracoscopy developed lobar atelectasis, but this also was not a significant finding. We conclude that severe postoperative atelectasis occurs as lobar atelectasis in approximately 5 per cent of patients who undergo pulmonary resection and significantly adds to the intensive care unit and hospital length of stay. The etiology of lobar atelectasis appears to be multifactorial and warrants further study to define mechanisms of occurrence and their prevention.

Aged↗
PubMed1979

Pulmonary atelectasis and other respiratory complications after cardiopulmonary bypass and investigation of aetiological factors.

Radiological evidence of pulmonary complications and possible aetiological factors were investigated in 50 consecutive patients after heart operations with cardiopulmonary bypass. Atelectasis was the most frequent pulmonary complication except for small pleural effusions, with an incidence of 64 per cent. Several types of atelectasis frequently co-existed, with a predominance of the less extensive plate and subsegmental forms. The incidence of atelectasis was the same on each side and the site of atelectasis was basal in three quarters of the patients. Preoperative clinical and catheter data were unrelated to the incidence of atelectasis. There was a significant positive correlation between a short cardiopulmonary bypass time and plate atelectasis, between a large fluid load after bypass and segmental atelectasis, between re-operation for bleeding and subsegmental atelectasis and between post-operative gastric dilation and atelectasis. The type of operation, the use of the intra-aortic balloon and the length of postoperative respiratory ventilation were unrelated to the incidence of atelectasis. The mechanism of development of atelectasis is discussed.

Adult↗
PubMed2002

Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem.

UNLABELLED: Perturbation of respiratory mechanics produced by general anesthesia and surgery is more pronounced in morbidly obese (MO) patients. Because general anesthesia induces pulmonary atelectasis in nonobese patients, we hypothesized that atelectasis formation would be particularly significant in MO patients. We investigated the importance and resorption of atelectasis after general anesthesia in MO and nonobese patients. Twenty MO patients were anesthetized for laparoscopic gastroplasty and 10 nonobese patients for laparoscopic cholecystectomy. We assessed pulmonary atelectasis by computed tomography at three different periods: before the induction of general anesthesia, immediately after tracheal extubation, and 24 h later. Already before the induction of anesthesia, MO patients had more atelectasis, expressed in the percentage of the total lung area, than nonobese patients (2.1% versus 1.0%, respectively; P < 0.01). After tracheal extubation, atelectasis had increased in both groups but remained significantly more so in the MO group (7.6% for MO patients versus 2.8% for the nonobese; P < 0.05). Twenty-four hours later, the amount of atelectasis remained unchanged in the MO patients, but we observed a complete resorption in nonobese patients (9.7% versus 1.9%, respectively; P < 0.01). General anesthesia in MO patients generated much more atelectasis than in nonobese patients. Moreover, atelectasis remained unchanged for at least 24 h in MO patients, whereas atelectasis disappeared in the nonobese. IMPLICATIONS: We compared the resolution over time of pulmonary atelectasis after a laparoscopic procedure by performing computed tomography scans in two different groups of patients: 1 group had 10 nonobese patients, and in the other group there were 20 morbidly obese patients.

Adult↗