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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↗
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↗
PubMedDate not supplied

Analysis of frequency of pulmonary atelectasis in patients undergoing pectoralis major musculocutaneous flap reconstruction.

The incidence of pulmonary atelectasis following head and neck surgery is not well reported. This study retrospectively evaluated the incidence of pulmonary atelectasis in 161 head and neck cancer patients, with 152 being evaluable. There were 90 patients evaluated following pectoralis musculocutaneous flap reconstruction with their effective flap size and 71 nonflap patients as a control group. Clinical findings were correlated to radiographic scores. Of pectoralis musculocutaneous flap patients screened for preexisting pulmonary disease (PEPD), nine of 45 (20%) demonstrated pulmonary atelectasis in the first 24 hours compared with 10 of 39 or 25.6% nonflap controls. Major pulmonary atelectasis was not found in the pectoralis musculocutaneous flap patients by scoring criteria, and in only one of 39 (2.6%) nonflap patients. In flaps larger than 40 cm2, the incidence was eight of 37 (21.6%), with no major pulmonary atelectasis noted. Only one of nine (11.1%) patients with radiographic pulmonary atelectasis exhibited clinical symptoms (three of 10 or 30% control). In patients with PEPD and pectoralis musculocutaneous flaps, 22 of 45 (48.9%) had evidence of pulmonary atelectasis in contrast to 13 of 32 or 40.6% controls. There were two of 45 (4.4%) who had major pulmonary atelectasis with zero of 32 in the nonflap group. For flaps larger than 40 cm2, the incidence was 19 of 39 (48.7%) with two of 39 (5.1%) scored as major pulmonary atelectasis. The clinical correlation for this group and the major pulmonary atelectasis group was each approximately 50% compared to 15.4% for nonflap patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Comorbidity↗
PubMed2000

Atelectasis formation during anesthesia: causes and measures to prevent it.

Pulmonary gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. This results in decreased oxygenation of blood. A major cause is collapse of lung tissue (atelectasis), which can be demonstrated by computed tomography but not by conventional chest x-ray. Collapsed lung tissue is present in 90% of all subjects, both during spontaneous breathing and after muscle paralysis, and whether intravenous or inhalational anaesthetics are used. There is a correlation between the amount of atelectasis and pulmonary shunt. Shunt does not increase with age. In obese patients, larger atelectatic areas are present than in lean ones. Finally, patients with chronic obstructive lung disease may show less or even no atelectasis. There are different procedures that can be used in order to prevent atelectasis or to reopen collapsed lung tissue. The application of positive end-expiratory pressure (PEEP) has been tested in several studies. On the average, arterial oxygenation does not improve markedly, and atelectasis may persist. Further, reopened lung units re-collapse rapidly after discontinuation of PEEP. Inflation of the lungs to an airway pressure of 40 cm H2O, maintained for 7-8 seconds (recruitment or "vital capacity" manoeuvre), re-expands all previously collapsed lung tissue. During induction of anaesthesia, the use of a gas mixture, that includes a poorly absorbed gas such as nitrogen, may prevent the early formation of atelectasis. During ongoing anaesthesia, pulmonary collapse reappears slowly if a low fraction of oxygen in nitrogen is used for the ventilation of the lungs after a previous VC-manoeuvre. On the other hand, ventilation of the lungs with pure oxygen results in a rapid reappearance of atelectasis. Thus, ventilation during anaesthesia should be done if possible with a moderate fraction of inspired oxygen (FIO2, e.g. 0.3-0.4). Alternatively, if the lungs are ventilated with a high inspiratory fraction of oxygen, the use of PEEP may be considered. In summary, atelectasis is present in most humans during anaesthesia and is a major cause of impaired oxygenation. Avoiding high fractions of oxygen in inspired gas during induction and maintenance of anaesthesia may prevent formation of atelectasis. Finally, intermittent "vital capacity"-manoeuvres together with PEEP reduces the amount of atelectasis and pulmonary shunt.

Anesthesia, General↗
PubMed1996

Atypical manifestations of pulmonary atelectasis.

Recognizing atelectasis has always been a challenge. Atypical patterns further our knowledge of this subject. The lung has two mechanisms to help keep the lobes inflated: collateral ventilation and trapped nitrogen both tend to inflate the lungs when the airways are obstructed. Peripheral upper-lobe atelectasis resembles apical pleural fluid. Instead of collapsing superomedially, the upper lobe collapses posterolaterally, marginated by either the middle lobe or the superior segment of the lower lobe. This pattern may also be produced by segmental atelectasis of the apical-posterior segments of the upper lobe. Combined right-upper- and middle-lobe atelectasis usually stems from malignancy and violates Felson's double lesion sign. Upper-lobe atelectasis may produce a localized pneumothorax (pneumothorax ex vacuo), analogous to the vacuum joint phenomenon. Conversely, a large pneumothorax may cause torsion of an upper-lobe bronchus, leading to atelectasis. It is important to distinguish between these two conditions in order to choose the appropriate treatment-bronchoscopy in the former and chest tube drainage in the latter. Round atelectasis is a form of peripheral atelectasis that is variable in size and is thought to occur either when the lung collapses around a cleft in the presence of a pleural effusion or when shrinkage of a pleural scar pinches the adjacent lung. Round atelectasis has many features of plate atelectasis and may represent a special form of this condition.

Bronchoscopy↗
PubMed2002

The effect of increased FIO(2) before tracheal extubation on postoperative atelectasis.

UNLABELLED: General anesthesia promotes pulmonary atelectasis, which can be eliminated by a vital capacity (VC) maneuver (inflation of the lungs to 40 cm H(2)O for 15 s). High-inspired oxygen concentration favors recurrence of atelectasis. Therefore, 100% oxygen before tracheal extubation may contribute to atelectasis. To evaluate whether the use of 100% oxygen before extubation increases the amount of postoperative atelectasis, we studied 30 adults scheduled for elective surgery of the extremities. Ten minutes before the presumed end of surgery, patients were randomly assigned to (a) a fraction of inspired oxygen (FIO(2)) = 1.0 (n = 10), (b) VC maneuver + FIO(2) = 1.0 (n = 10), or (c) VC maneuver + FIO(2) = 0.4 (n = 10). The amount of atelectasis was measured by computed tomography scan, and oxygenation was studied by arterial blood gas analysis. Data were analyzed by one-way analysis of variance with Bonferroni correction. Results are presented as mean +/- SD; P < 0.05 was considered significant. In the VC maneuver + FIO(2) = 0.4 group, postoperative atelectasis was smaller (2.6% +/- 1.1% of total lung surface, P < 0.05) than in the FIO(2) = 1.0 group (8.3% +/- 6.2%) and in the VC maneuver + FIO(2) = 1.0 group (6.8% +/- 3.4%). Oxygen 100% at the end of general anesthesia promotes postoperative atelectasis. A safety margin in terms of oxygenation during tracheal extubation is essential, and further studies should therefore evaluate whether atelectasis formation could be prevented despite the use of 100% oxygen. IMPLICATIONS: For safety reasons, it is common to ventilate patients with 100% oxygen before tracheal extubation. This study demonstrates that this practice favors postoperative atelectasis.

Adolescent↗
PubMed2003

Bronchoscopy for atelectasis in the ICU: a case report and review of the literature.

Fiberoptic bronchoscopy has become a commonplace procedure in ICUs. Despite the fact that one of the most common indications for bronchoscopy is the presence of retained secretions and atelectasis, there is little research dedicated to its safety and utility in this clinical situation. This article presents a case of an intubated trauma victim who had undergone numerous bronchoscopic procedures, with varying degrees of success, for retained secretions and atelectasis. This review then seeks to answer the following three main questions regarding bronchoscopy in critically ill patients: (1) Is bronchoscopy effective in resolving atelectasis? (2) Is bronchoscopy superior to other means of resolving atelectasis? (3) Is bronchoscopy safe in critically ill patients? The patient was a 28-year-old man with no significant medical history who presented to the emergency department after his car was hit by a dump truck. He was found to have multiple leg fractures and a splenic rupture, and he was taken to the operating room for an exploratory laparotomy, splenectomy, and reduction of his fractures. He was then brought to the surgical ICU intubated, sedated, and receiving mechanical ventilation. Over the next 6 h, he developed progressive hypoxemia and diffuse, bilateral alveolar infiltrates on a chest radiograph (CXR). Four days postoperatively, a routine CXR revealed total atelectasis of his right upper lobe (RUL). Emergent bronchoscopy was performed, and a large mucus plug obscuring the RUL bronchus was removed. Follow-up CXR demonstrated resolution of the atelectasis. The next day, RUL atelectasis was again seen on his CXR. A repeat bronchoscopic examination and BAL failed to reveal any plug. A follow-up CXR showed continued atelectasis. Over the next week, the patient underwent daily bronchoscopy for atelectasis with variable degrees of improvement. Over the next 3 weeks, his pulmonary status improved until he was eventually extubated, and 1 month after hospital admission he was discharged to rehabilitation.

Adult↗
PubMed2002

Pulmonary atelectasis after reconstruction with a rectus abdominis free tissue transfer.

BACKGROUND: Atelectasis is one of the most common postoperative complications encountered in head and neck surgery. Risk factors include preexisting pulmonary disease, the procedure performed, and the length of anesthetic. Regional flaps used to reconstruct defects in the head and neck predispose to radiographic atelectasis. The rectus abdominis myocutaneous flap is usually transferred as a free tissue transfer. Harvesting the flap results in abdominal wall pain and postoperative splinting that may contribute to an increased development of atelectasis. To our knowledge, this issue has not been previously examined. DESIGN: Retrospective review. RESULTS: Fifty-three patients underwent rectus abdominis myocutaneous free flap reconstruction following major ablative procedures for head and neck cancer. The flap size ranged from 5 x 7 to 25 x 27 cm. Most flaps were 8 x 15 cm. The cutaneous area transferred ranged from 35 to 600 cm(2) (mean, 120 cm(2)). These patients were compared with a group of 53 patients who were matched for age, sex, length of the procedure, and stage of disease. Postoperative atelectasis was radiographically detected in 37 (70%) of the patients who underwent rectus abdominis myocutaneous free flap reconstruction vs 41 (77%) of the controls. Major atelectasis was not encountered in any patient in either group. Patients with a larger cutaneous paddle (>120 cm(2)) had a higher atelectasis score than patients with smaller cutaneous paddles (< or =120 cm(2)) (P =.02). CONCLUSIONS: The incidence of radiographic postoperative atelectasis in patients undergoing rectus abdominis myocutaneous free tissue transfer is high. The degree of atelectasis is small, and the clinical correlation and relevance are minimal.

Head and Neck Neoplasms↗
PubMed1993

Re-expansion of atelectasis during general anaesthesia: a computed tomography study.

Formation of atelectasis is one mechanism of impaired gas exchange during general anaesthesia. We have studied manoeuvres to re-expand such atelectasis in 16 consecutive, anaesthetized adults with healthy lungs. In group 1 (10 patients), the lungs were inflated stepwise to an airway pressure (Paw) of 10, 20, 30 and 40 cm H2O. In group 2 (six patients), three repeated inflations up to Paw = 30 cm H2O were followed by one inflation to 40 cm H2O. Atelectasis was assessed by analysis of computed x-ray tomography (CT). In group 1 the mean area of atelectasis in the CT scan at the level of the right diaphragm was 6.4 cm2 at Paw = 0 cm H2O, 5.9 cm2 at 20 cm H2O, 3.5 cm2 at 30 cm H2O and 0.8 cm2 at 40 cm H2O. A Paw of 20 cm H2O corresponds approximately to inflation with twice the tidal volume. In group 2 the mean area of atelectasis was 9.0 cm2 at Paw = 0 cm H2O and 4.2 cm2 after the first inflation to 30 cm H2O. Repeated inflations did not add to re-expansion of atelectasis. The final inflation (Paw = 40 cm H2O) virtually eliminated the atelectasis. We conclude that, after induction of anaesthesia, the amount of atelectasis was not reduced by inflation of the lungs with a conventional tidal volume or with a double tidal volume ("sigg"). An inflation to vital capacity (Paw = 40 cm H2O), however, re-expanded virtually all atelectatic lung tissue.

Adult↗