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At least 19 recordsLinked to original sources
PubMed1992

Ultrathin fiberoptic bronchoscopy for airway toilet in neonatal pulmonary atelectasis.

Pulmonary atelectasis is often seen in young infants with respiratory disease and it may contribute to increased ventilatory requirements and the development of chronic lung disease such as bronchopulmonary dysplasia. Standard management consists of postural drainage (chest physiotherapy and suction) and selective intubation with suction of a major bronchus. This report describes a new approach consisting of removal of bronchial secretions under direct vision via ultrathin fiberoptic bronchoscopy, without interruption of mechanical ventilation. The procedure was performed safely in ten cases and resulted in significant rapid improvement in the infants' respiratory condition and in complete resolution of the atelectasis in eight cases. In two infants, partial improvement was seen. No adverse effects of the procedure were encountered. It is concluded that this approach is a safe and potentially valuable therapeutic maneuver in the management of pulmonary atelectasis in sick intubated neonates.

Bronchoscopy↗
PubMed1996

Effect of modulators of hypoxic pulmonary vasoconstriction on the response to inhaled nitric oxide in a neonatal model of severe pulmonary atelectasis.

Hypoxic pulmonary vasoconstriction (HPV) is an intrinsic mechanism that facilitates ventilation to perfusion matching and preservation of oxygenation. We investigated the neonatal HPV response from extensive atelectasis and tested the hypothesis that (I) the resulting hypoxemia is corrected by inhaled nitric oxide (NO); (2) the "pulmonary steal" of blood away from hypoxic area is further improved by modulators of the HPV. Intratracheal injection of steel beads in 32 piglets (7 to 20 days) resulted in atelectasis of 50% to 75% of the lungs. The piglets were then randomized to receive saline (control), indomethacin (IND) 2 mg/kg, doxapram (DOX) 0.5 mg/kg/h or almitrine (ALM) 4 micrograms/kg/min. After 30 minutes, all animals were subjected to NO at 40 ppm. Atelectasis resulted in severe impairment in oxygenation (PaO2 - 105 +/- 6 mm Hg, AaDO2 = 536 +/- 9 mm Hg; shunt fraction = 31% +/- 2%) and moderate pulmonary hypertension. Mean pulmonary artery pressure (PAP) increased to 35 +/- 0.8 mm Hg. NO reduced pulmonary vascular resistance (PVR) from 128 +/- 14 mm Hg/kg/mL/min to 74 +/- 9 mm Hg/kg/mL/min and improved gas exchange (PaO2 = 180 +/- 50 and AaDO2 = 438 +/- 50 mm Hg). Following the development of atelectasis, the peripheral chemoreceptor agonists (ALM and DOX) did not modify gas exchange and had no significant cardiovascular effect. ALM and DOX failed to enhance the response to NO. IND did not alter HPV, but prevented the improvement in gas exchange associated with NO-induced pulmonary vasodilation.

Administration, Inhalation↗
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↗
PubMed1987

Recurrent pulmonary atelectasis as a manifestation of familial Mediterranean fever.

Recurrent attacks of pulmonary atelectasis were the leading sign of familial Mediterranean fever in a young man of Jewish-Georgian extraction. His mother suffered from the more common manifestations of the disease. Treatment with colchicine caused a complete disappearance of his attacks. However, when challenged by discontinuing colchicine therapy for eight days, another, documented attack of pulmonary atelectasis occurred. To our knowledge, this is the first case of familial Mediterranean fever presenting with recurrent pulmonary atelectasis.

Adult↗
PubMed1984

The effects of pulmonary atelectasis and reexpansion on lung cellular immune defenses.

Pulmonary atelectasis predisposes the lung to infection. This condition may be partly due to impaired cellular immune response of the collapsed lung segment. We postulated that atelectasis may affect alveolar macrophage (AM) antibacterial function. To test this hypothesis, atelectasis was induced in the right upper lobes of piglet lungs. Alveolar macrophages harvested by bronchoalveolar lavage of collapsed segments for up to 24 hours showed progressive depression of their phagocytic activity against Pseudomonas aeruginosa in vitro. However, their intracellular bactericidal activity did not change. Reexpansion of the atelectatic lobes with mechanical ventilation and 100% oxygen supplementation for four hours after six hours of atelectasis resulted in reversal of the impaired AM phagocytic activity. These observations presented insight into the mechanisms of susceptibility to lung infection in pulmonary atelectasis and the potential for its reversal.

Animals↗
PubMed1987

[Pulmonary atelectasis and massive pleural effusion. Echocardiography].

Pulmonary atelectasis can be detected by Two Dimensional Echocardiography (2D-E) when massive pleural effusion is present. A triangular mass, base toward the mediastinum and apex moving freely in the pleural cavity, is shown by 2D-E either in an apical modified view in left pleural effusions or in a subcostal modified view in right pleural effusions. The texture of the mass is liver-like. Three cases are reported by way of example. Differential diagnosis with other masses, such as pleural or pericardial metastasis, is discussed.

Child↗
PubMed2002

Peripheral pulmonary atelectasis and oxygentation impairment following coronary artery bypass grafting.

BACKGROUND: Severe pulmonary oxygenation impairment occurred in some patients with pleurotomy during the harvest of the internal mammary artery graft followed by coronary artery bypass grafting (CABG). Peripheral pulmonary atelectasis in the postoperative chest X-ray was detected in these patients. We studied the efficacy of intraoperative positive end-expiratory airway pressure (PEEP) therapy for the prevention of postoperative pulmonary oxygenation impairment. METHODS: The pleural cavity was intraoperatively opened in 40 patients with solitary CABG procedure performed during 5 years since January 1992. These patients were divided into two groups. Intraoperative PEEP therapy, which is initiated just after pleurotomy, was not used in 32 patients before May, 1996 (control group) and used for recent 8 patients with pleurotomy (PEEP group). The mean age of patients was 60 years old in the control group and 68 in the PEEP group. RESULTS: Respiratory insufficiency (A-aDO2 >400 mmHg and RI >1.5) was detected in 6 patients in the control group. Three out of these 6 patients required long-term mechanical respiratory support over a week. No respiratory insufficiency occurred in patients of the PEEP group. Values of PaO2, A-aDO2, respiratory index and shunt ratio were significantly worse in the control group than in the PEEP group. CONCLUSIONS: In conclusion, PEEP therapy may prevent pulmonary atelectasis and oxygen impairment after CABG.

Aged↗
PubMed1999

Comparable postoperative pulmonary atelectasis in patients given 30% or 80% oxygen during and 2 hours after colon resection.

BACKGROUND: High concentrations of inspired oxygen are associated with pulmonary atelectasis but also provide recognized advantages. Consequently, the appropriate inspired oxygen concentration for general surgical use remains controversial. The authors tested the hypothesis that atelectasis and pulmonary dysfunction on the first postoperative day are comparable in patients given 30% or 80% perioperative oxygen. METHODS: Thirty patients aged 18-65 yr were anesthetized with isoflurane and randomly assigned to 30% or 80% oxygen during and for 2 h after colon resection. Chest radiographs and pulmonary function tests (forced vital capacity and forced expiratory volume) were obtained preoperatively and on the first postoperative day. Arterial blood gas measurements were obtained intraoperatively, after 2 h of recovery, and on the first postoperative day. Computed tomography scans of the chest were also obtained on the first postoperative day. RESULTS: Postoperative pulmonary mechanical function was significantly reduced compared with preoperative values, but there was no difference between the groups at either time. Arterial gas partial pressures and the alveolar-arterial oxygen difference were also comparable in the two groups. All preoperative chest radiographs were normal. Postoperative radiographs showed atelectasis in 36% of the patients in the 30%-oxygen group and in 44% of those in the 80%-oxygen group. Relatively small amounts of pulmonary atelectasis (expressed as a percentage of total lung volume) were observed on the computed tomography scans, and the percentages (mean +/- SD) did not differ significantly in the patients given 30% oxygen (2.5% +/- 3.2%) or 80% oxygen (3.0% +/- 1.8%). These data provided a 99% chance of detecting a 2% difference in atelectasis volume at an alpha level of 0.05. CONCLUSIONS: Lung volumes, the incidence and severity of atelectasis, and alveolar gas exchange were comparable in patients given 30% and 80% perioperative oxygen. The authors conclude that administration of 80% oxygen in the perioperative period does not worsen lung function. Therefore, patients who may benefit from generous oxygen partial pressures should not be denied supplemental perioperative oxygen for fear of causing atelectasis.

Adult↗
PubMed1994

[Blood flow pattern in pulmonary atelectasis with color Doppler flow imaging].

Blood flow pattern in the lesion was evaluated in 4 patients with pulmonary atelectasis by color Doppler flow imaging synchronized electrocardiography. The pulsatile signal and triphasic signal were detected, whereas the continuous signal was not. It seemed that in pulmonary atelectasis the pulsatile signal was the blood flow signal in the pulmonary artery and the triphasic signal was the blood flow signal in the pulmonary vein.

Aged↗
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↗
PubMed1993

A model of pulmonary atelectasis in rats: activation of alveolar macrophage and cytokine release.

Although atelectasis frequently occurs after surgery and trauma, and such patients have elevated body temperatures, the mechanism of temperature elevation secondary to atelectasis is unknown. Moreover, a small animal model has not been available to study the pathophysiology of pulmonary atelectasis. The purpose of this study, therefore, was to develop a model of pulmonary atelectasis in rats. Because interleukin-1 (IL-1) and tumor necrosis factor (TNF), both potent pyrogens, are produced by macrophages during infection and inflammation, our aim was also to determine whether alveolar macrophages produce IL-1 or TNF in response to atelectasis. Whole-lung atelectasis was produced in rats by ligating the left main stem bronchus while maintaining ventilation of the right lung. After a 1-h period of atelectasis, alveolar macrophages were harvested from the right and left lungs and incubated for 24 h, and the supernatants were assayed for IL-1 and TNF. Both IL-1 and TNF levels of macrophage cultures from the atelectatic lung were significantly increased compared with the control lung. These results suggest that increased IL-1 or TNF production by alveolar macrophages may be responsible for fever caused by atelectasis.

Animals↗