Cause Of Atelectasis Research Articles

Синдром ятагана: подходы к диагностике и ведению

В статье представлен клинический случай синдрома ятагана у 3-летней девочки. Заболевание манифестировало в месячном возрасте с бледности, периорального цианоза и эпизода апноэ. Ребенок госпитализирован для дальнейшего обследования. У девочки наблюдался пери­оральный цианоз, SpO2 90 %, частота дыхательных движений 36/мин. Аускультативно в легких пуэрильное дыхание, ­ослабленное справа по передней поверхности грудной клетки. Сердечные тоны ритмичные, систолический шум 2/6 вверху левого края грудины и 4/6 в межлопаточной области слева. При эхокардиографии диагностированы некритическая коарктация аорты, дефект межпредсердной перегородки. При рентгенографии органов грудной клетки в области правого легочного поля интенсивная тень от верхушки до уровня V ребра с нечеткими краями. Тень сердца смещена вправо. Что у ребенка: декстрокардия, декстрапозиция, пневмония, ателектаз, тимомегалия? При бронхоскопии обнаружена обструкция бронхов верхней и средней доли правого легкого с густой мокротой белого цвета. Проведена санация. После бронхоскопии нормализовалась сатурация, но, несмотря на ликвидацию причины ателектаза, контрольная рентгенография оставалась без изменений. Проведена компьютерная томография органов грудной полости с контрастированием. У ребенка диагностирован синдром ятагана в сочетании с коарктацией аорты и аберрантной правой подключичной артерией. В возрасте 2,5 мес. выполнена баллонная дилатация коарктации аорты. В возрасте 2 лет проведена хирургическая коррекция — устранение аномального дренажа легочных вен и пластика дуги аорты. Интраоперационная анатомия: мезокардия, правые отделы сердца дилатированы, нижняя доля правого легкого гипоплазирована. Наша пациентка фактически не имела симптомов, характерных для синдрома ятагана, поскольку отсутствовали признаки сердечной недостаточности, девочка не болела респираторными заболеваниями. Диагноз в грудном возрасте был установлен благодаря эпизоду аспирации, но ателектаз и мезокардия помешали визуализации характерной рентгенологической картины синдрома ятагана. Поэтому полное исследование с использованием компьютерной томографии с контрастированием является обязательным для таких пациентов.

Posterior basal segments atelectasis in descending necrotizing mediastinitis

We have observed that patients with descending necrotizing mediastinitis show bilateral lower lobes atelectasis before pleural effusion that finally forms empyema. Successful treatment of mediastinitis emphasizes optimal early drainage of neck, mediastinum, and antibiotic therapy. Methods: Exploratory study to determine the presence of segmental atelectasis as incipient sign of mediastinitis. We studied patients from August 2018 to July 2019 with tomographies. Results: We evaluated 25 patients operated due to Mediastinitis at our hospital, from August 2018 to July 2019. Ten (40%) were females and 15 (60%) were male patients. Twenty-one (84%) patients showed atelectasis and 4 (16%) did not have atelectasis. Of the patients that showed atelectasis, 17 (81%) were bilateral, 2 (9.5%) were right sided, and 2 (9.5%) were left sided. We also analyzed the occurrence of pleural effusion in this group. Fifteen (60%) patients had pleural effusion and 10 (40%) did not. Of the total patients with pleural effusion 11 (73.3%) were bilateral, 3 (20%) of the right side, and 1 (6.6%) of the left side. Conclusions: Atelectasis is a sign that we can find in most patients that will develop empyema and we assume that it is associated with lymph nodes inflammation, but it is necessary to develop other protocols to confirm that hilar lymph congestion is the cause of atelectasis. As atelectasis of lower lobes is a sign of imminent sepsis, we always decide to do mediastinal drainage when we find them associated with neck abscess. We are proposing a modification of the endo classification to decide surgery

Is postoperative atelectasis following lumbar fusion more prevalent among patients with chronic opioid use?

ObjectiveChronic opioid use (COU) remains on the rise globally, acting as a marker for patient morbidity and a risk factor for adverse health outcomes. Opioid use is a risk factor for respiratory depression, which may lead to dysfunctional breathing, a known cause of atelectasis. The objective of this study was to determine whether COU is associated with increased rates of postoperative atelectasis among patients undergoing lumbar fusion. Materials & MethodsThree State Inpatient Databases were used to identify patients who underwent an elective lumbar fusion through an anterior, posterior or circumferential approach in Florida, Kentucky and New York between 2013−2015. Patients with COU and those with postoperative atelectasis were identified using ICD diagnosis codes. Three operative groups were created and subsequently matched using propensity scores in order to provide comparable cohorts for analysis. Three-to-one propensity score matching was conducted using the variables of age, sex, race, number of chronic diagnoses and geographic state of admission. Multivariable logistic regressions were used to examine the relationship between COU and postoperative atelectasis. ResultsA total of 3618 lumbar fusions were identified. Atelectasis was noted in 1.33 % of NCOU patients and 2.32 % of COU patients. On multivariable analysis, while controlling for the Elixhauser Mortality Index and patient insurance status, COU was significantly associated with atelectasis in posterior lumbar fusion (OR = 2.27; CI: 1.09–4.72; p = 0.028) and circumferential lumbar fusion (OR = 4.68; CI: 1.52–14.45; p = 0.007). The Elixhauser Mortality Index was also significantly associated with atelectasis in posterior lumbar fusion (OR = 1.08; CI: 1.04–1.11; p < 0.001) and circumferential lumbar fusion (OR = 1.09; CI: 1.03–1.16; p = 0.002). ConclusionHigher rates of postoperative atelectasis were found among patients with COU following posterior and circumferential lumbar fusions. The Elixhauser Mortality Index was also independently associated with atelectasis. Knowledge of these risks may allow for earlier identification and intervention in patients who are at risk.

Inflammatory myofibroblastic tumor of the lung: a rare cause of atelectasis in children

Although rare, inflammatory myofibroblastic tumor is the most common primary lung mass in children. We report the case of an 11-year-old boy investigated for persistent cough and dyspnea with complete left lung atelectasis mimicking pneumonia. CT and MRI showed an endobronchial mass of the left main bronchus. The boy underwent endoscopic resection of the tumor and histology was in favor of an inflammatory myofibroblastic tumor of the lung. This diagnosis should be suspected in children with recurrent pneumonia. The prognosis is good after complete resection.

Sudden generalized lung atelectasis during thoracotomy following thoracic lavage in 3 dogs

To describe sudden onset of generalized pulmonary atelectasis following thoracic lavage in 3 dogs. Thoracic lavage was performed following ligation of a patent ductus arteriosus in case 1, prior to closure of a large traumatic full thickness wound in the chest wall in case 2, and during investigation of an idiopathic spontaneous pneumothorax in case 3. In each case anesthesia and surgery were uneventful until thoracic lavage was performed, after which sudden generalized pulmonary atelectasis was observed. The atelectasis was visualized and was associated with oxyhemoglobin desaturation, decreased end-tidal carbon dioxide partial pressure (ETCO(2)), and a marked increase in the peak inspiratory pressure (PIP) required to achieve visible lung inflation. Occlusion of the endotracheal tube and cervical trachea was directly eliminated as the cause of atelectasis in cases 1 and 2, and indirectly eliminated in case 3. Improvement in pulmonary function occurred in all cases in response to increased PIP ± positive end expiratory pressure (PEEP). Generalized atelectasis should be considered a possible complication of thoracic lavage performed during thoracotomy. In the cases presented here, it is suspected that pre-existing reduction in lung volume (due to inadequate ventilation, surgical compression, absorption atelectasis) was exacerbated by the addition of the lavage fluid to the thoracic cavity. This pre-existing lung collapse is believed to have resulted in reduction of lung volume and that further reduction below the critical closing volume occurred following instillation of saline into the thorax resulting in the subsequent development of generalized atelectasis. The performance of regular arterial blood gas analyses and different ventilation protocols may have prevented the marked atelectasis that was observed in these cases.

Is Atelectasis Following Aortocoronary Bypass Related to Temperature?

To determine the frequency of acute postoperative atelectasis in patients undergoing aortocoronary bypass with either normothermic (warm) or hypothermic (cold) technique. Prospective, randomized study comparing two groups. University-affiliated hospital. Three hundred thirty-one patients (166 cold and 165 warm) undergoing isolated aortocoronary bypass. Chest radiographs were obtained preoperatively, on the day of surgery, and subsequently as clinically indicated until discharge from the hospital. Radiologist (blinded to the patient allocation into warm or cold group) scored the atelectasis from 0 to 3 based on its severity. Regression analysis was used to determine if there was any difference in the atelectasis scores between the two groups. Mean daily postoperative atelectasis scores were not different between the cold and warm groups. The number of patients requiring chest radiographs was similar in both groups. The percent of patients with abnormal chest radiographs was similar in both groups. The temperature of cardioplegia has no effect on the development of atelectasis following aortocoronary bypass, and therefore temperature-related cold injury is not a major cause of atelectasis following this type of surgery.

Imaging Evaluation of Obstructive Atelectasis

Segmental or lobar atelectasis is a common radiographic finding in patients with bronchial obstruction. Although in many cases the presence and cause of atelectasis can be ascertained from the plain chest radiograph, computed tomography (CT) often provides valuable additional information, particularly with regard to the precise location and extent of the obstructing process. CT also can be used to differentiate between benign and malignant causes of obstructive atelectasis. After administration of intravenous contrast material, CT may distinguish a proximal obstructing tumor from collapsed lung or adjacent mediastinal structures. In some patients, magnetic resonance imaging (MRI) can provide comparable and/or complementary information. In this article, we review the major applications of CT and MRI, as well as the capabilities and limitations of both techniques, in the evaluation of patients with obstructive atelectasis.

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.

Right to left shunt in patients with acute myocardial infarction: A proposed mechanism

Bedside catheterization of femoral and pulmonary arteries allowed serial measurement of pulmonary arterial pressure, cardiac output and percent right to left shunt in 25 patients with (1) acute myocardial infarction with minimal or no evidence of heart failure, (2) severe heart failure, (3) shock, or (4) shock and heart failure. There was positive correlation between mean cardiac output and percent right to left shunt ( r = +0.64, P < 0.01) but no significant correlation between mean shunt flow and pulmonary arterial pressure (when cardiac output was held constant). Deep breathing or intermittent positive pressure breathing resulted in significant decreases in right to left shunt flow. These observations are explained on the basis of atelectasis of dependent lung units and maximal dilatation of vessels to superior lung zones. Increases in blood flow are accommodated by recruitment of more dilatable vessels in the lower pulmonary lobe, hence explaining the relation between right to left shunt and pulmonary flow. Increases in left atrial pressure would be expected to result in less perfusion to dependent zones (decreasing right to left shunt flow) and increased formation of intraalveolar edema (increasing right to left shunt flow), thus explaining the lack of correlation between pulmonary arterial pressure and right to left shunt flow. Prolonged static position, overzealous use of analgesic agents and rapid shallow ventilation patterns are important causes of atelectasis, right to left shunt and arterial hypoxemia in patients with acute myocardial infarction.

NEW TREATMENT FOR ATELECTASIS OF THE NEWBORN

A SIMPLE method of treatment of one type of persistent atelectasis of the new-born infant will be presented. It is based on a familiar but frequently unrecognized cause of atelectasis in the premature infant. The treatment is patterned after that found effective for a somewhat similar physiological disturbance observed in the adult with steering wheel fractures of the sternum. The necessity of improved therapy in atelectasis of the newborn infant has been emphasized recently in a review of neonatal mortality by Bundesen 1 and co-workers. They found that abnormal pulmonary ventilation is the leading cause of death in the newborn, accounting for 47% of all deaths. The etiological concept upon which our treatment is based was presented by Wilson and Farber, 2 who noted that often in the newborn infant, and more frequently in the premature, a retraction of the chest wall occurred with each diaphragmatic contraction. They felt that

New treatment for atelectasis of the newborn.

A SIMPLE method of treatment of one type of persistent atelectasis of the new-born infant will be presented. It is based on a familiar but frequently unrecognized cause of atelectasis in the premature infant. The treatment is patterned after that found effective for a somewhat similar physiological disturbance observed in the adult with steering wheel fractures of the sternum. The necessity of improved therapy in atelectasis of the newborn infant has been emphasized recently in a review of neonatal mortality by Bundesen 1 and co-workers. They found that abnormal pulmonary ventilation is the leading cause of death in the newborn, accounting for 47% of all deaths. The etiological concept upon which our treatment is based was presented by Wilson and Farber, 2 who noted that often in the newborn infant, and more frequently in the premature, a retraction of the chest wall occurred with each diaphragmatic contraction. They felt that

Postoperative Atelectasis; Clinical Aspects and a Review of Cases

The surgical importance of atelectasis is obvious; it may complicate convalescence from any operation and it is the most commonly encountered pulmonary complication after abdominal operations. Interest in atelectasis is not new. Knowledge of postoperative atelectasis, however, has been acquired in comparatively recent years. SOME NOTEWORTHY CONTRIBUTIONS As long ago as 1850 Gairdner 1 presented the belief that atelectasis could be produced by obstructing a major bronchus with thick, viscid mucus. William Pasteur 2 in 1910 recognized and described the clinical features of this condition. Lee and Tucker 3 in 1925 were first to demonstrate by bronchoscopy the mechanism of postoperative atelectasis. The cause of atelectasis in his case was found to be complete obstruction of the bronchi of the atelectatic lung with thick, tenacious secretion. Lemon 4 in 1926, working with dogs, showed that secretion in the mouth was readily aspirated into the tracheobronchial tree in the course of

POSTOPERATIVE APNEUMATOSIS (ATELECTASIS) AND POSTOPERATIVE PNEUMONIA

Experimental and clinical study of postoperative apneumatosis and postoperative pneumonia, carried on for several years, has convinced me that these two complications represent two phases of the same morbid condition. The differences between them are differences only in degree, and they depend on the type and virulence, of their most frequent causative organism, the pneumococcus. Otherwise they have the same etiology and the same mechanism of production; they present a similar clinical evolution and they show similar pathologic changes. Furthermore, they are often superimposed in the same case and give rise to similar complications. The experimental work on atelectasis and lobar pneumococcic pneumonia carried on with the collaboration of Dr. Birnbaum, 1 in the Laboratory of Surgical Research at Cornell Medical College, led me to the following conclusions: 1. There is only one determining cause of atelectasis and that is bronchial obstruction. 2. This occlusion must be complete. 3. Neither