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PubMed2005

Oxygen attenuates atelectasis-induced injury in the in vivo rat lung.

BACKGROUND: Atelectasis results in impaired compliance and gas exchange and, in extreme cases, increased microvascular permeability, pulmonary hypertension, and right ventricular dysfunction. It is not known whether such atelectasis-induced lung injury is due to the direct mechanical effects of lung volume reduction and alveolar collapse or due to the associated regional lung hypoxia. The authors hypothesized that addition of supplemental oxygen to an atelectasis-prone ventilation strategy would attenuate the pulmonary vascular effects and reduce the local levels of vasoconstrictor eicosanoids. METHODS: In series 1, anesthetized, atelectasis-prone mechanically ventilated rats were randomly assigned to one of six groups based on the inspired oxygen concentration and ventilated without recruitment. Series 2 was performed to determine the cardiac and pulmonary vascular effects of 21% versus 100% inspired oxygen. In series 3, computed tomography scans were performed after ventilation with a recruitment strategy (21% O2) or no recruitment strategy (21% O2 or 100% O2). In series 4, functional residual capacity was measured in animals where the gas was 21% or 100% O2. RESULTS: The partial pressure of arterial oxygen increased with increasing inspired oxygen, but the alveolar-arterial oxygenation gradient was also greater with higher inspired oxygen. Ventilation with 21% O2 (but not with 100% O2) was associated with progressive pulmonary vascular impedance and increased pulmonary vascular permeability. Prostaglandin F2alpha was increased by mechanical ventilation, especially without supplemental oxygen. Computed tomography scans demonstrated no atelectasis in recruited lungs, and atelectasis in nonrecruited lungs that was greater with supplemental oxygen. Increased atelectasis with 100% O2 (vs. 21% O2) was demonstrated by measurement of functional residual capacity. CONCLUSIONS: Although supplemental oxygen worsened atelectasis in this model, it prevented the pathologic effects of atelectasis, including microvascular leak and pulmonary hypertension. Atelectasis-induced lung injury seems to be mediated by hypoxia rather than by the direct mechanical effects of atelectasis.

Animals↗

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↗

PubMed2007

Atelectasis in the perioperative patient.

PURPOSE OF REVIEW: To report the impact of atelectasis on perioperative outcomes. Atelectasis occurs in the dependent parts of the lungs of most patients who are anesthetized. Development of atelectasis is associated with decreased lung compliance, impairment of oxygenation, increased pulmonary vascular resistance and development of lung injury. Here, we examine the etiology, contributing factors, consequences, diagnosis and treatment of atelectasis. RECENT FINDINGS: Atelectasis describes the state of absent air in alveoli attributable to collapse, but recent findings suggest that alveoli are filled with foam and fluid. It is now known that atelectasis plays an important role beyond abnormal gas exchange and that prevention or reversal of atelectasis in some populations of postoperative patients may improve outcome. SUMMARY: Atelectasis in the presence of preexisting lung disease or limited cardiopulmonary reserve may have significant consequences. Increasing understanding of the underlying nature of atelectasis and its contribution to acute lung injury will improve our approach to the prevention and management of atelectasis.

Aging↗

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↗

PubMed2003

An evaluation of pulmonary atelectasis and its re-expansion: hyperpolarized 3He MRI in the Yorkshire pig.

RATIONALE AND OBJECTIVES: Atelectasis, the collapse of small airways, is a significant clinical problem. We use hyperpolarized (HP) 3He magnetic resonance imaging (MRI), or HP 3He MRI, to describe atelectasis in the normal Yorkshire pig, the pig with atelectasis, and the pig with re-expansion of atelectasis. We compare HP 3He MRI findings with depictions of atelectasis by proton MRI. MATERIALS AND METHODS: During end-expiration in the anesthetized and paralyzed Yorkshire pig (n = 6), HP 3He gas produced by the optical pumping spin-exchange method, was delivered via an endotracheal tube. For two separate groups, atelectasis was either induced by Fogarty-catheter occlusion balloon inflation (n = 3), or lateral chest wall administration of sodium hydroxide (NaOH) (n = 3). MRI was performed at time zero, at 5, 9, 13, 15, and 19 minutes after atelectasis production, 30 minutes after balloon deflation, and 10 and 30 minutes after recruitment of atelectatic areas with increased tidal volumes and added positive end-expiratory pressure. High-resolution, cross-sectional MR images were procured, and comparison was made with the traditional proton MRI. RESULTS: Atelectatic areas by HP 3He MRI were easily distinguishable in both subject groups, and correlated with those located by proton MR. HP 3He MR images showed absence of ventilation, whereas proton MR images depicted dense, white areas. Re-expansion of atelectasis was well delineated by HP 3He MRI. CONCLUSION: HP 3He MRI may overcome many of the shortcomings of other well-established radiographic methods. HP 3He MRI is a novel, informative method for describing atelectasis and its re-expansion.

Animals↗

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↗

PubMed1996

Radiographic manifestations of lobar atelectasis.

In this article we review the plain radiographic and computed tomographic manifestations of lobar atelectasis. The progression of lobar atelectasis from mild to marked volume loss is emphasized. Common combinations of lobar and whole lung atelectasis are also discussed. Radiographic features that help distinguish lobar atelectasis from pleural thickening, pleural effusion, and mediastinal masses are outlined. Where appropriate, selected examples of segmental atelectasis are also presented. The recognition of lobar atelectasis is important, particularly in cases stemming from obstructing endobronchial tumors. Since all signs of volume loss are not present in any given case, knowing as many signs of lobar atelectasis as possible is useful. Careful analysis of the chest radiograph and subtle alterations in the fissures and hilar vascularity aids in differentiating lobar atelectasis from other intrathoracic processes.

Humans↗

PubMed1996

Atelectasis and pulmonary shunting during induction of general anaesthesia--can they be avoided?

BACKGROUND: Gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. A major cause of this disorder appears to be atelectasis and consequently pulmonary shunt. After re-expansion, atelectasis reappears very slowly if 30% oxygen in nitrogen is used, but much faster if 100% oxygen is used. The aim of the present study-was to evaluate if early formation of atelectasis and pulmonary shunt may be avoided if the lungs are ventilated with 30% oxygen in nitrogen instead of 100% oxygen during the induction of general anaesthesia. METHODS: Twenty-four adult patients with healthy lungs scheduled for elective surgery were investigated. During induction of anaesthesia, the lungs were manually ventilated via a face mask, using either 30% oxygen in nitrogen (group 1, n = 12) or 100% oxygen (group 2, n = 12). Atelectasis was estimated by computed x-ray tomography and ventilation-perfusion distribution with the multiple inert gas elimination technique, both awake and during general anaesthesia with mechanical ventilation. RESULTS: No atelectasis was present in the awake subjects. After induction of anaesthesia, the mean amount of atelectasis was minor (0.2 +/- 0.4 cm2) in group 1 and considerably greater (8.0 +/- 8.2 cm2) in group 2 (P < 0.001). The pulmonary shunt was 0.3 +/- 0.7% of cardiac output in the awake subjects. This value increased to 2.1 +/- 3.8% in group 1 and to 6.5 +/- 5.2% in group 2 (P < 0.05). The indices of VA/Q mismatch showed no difference between the two groups. CONCLUSION: During induction of general intravenous anaesthesia in patients with healthy lungs, gas composition plays an important role for atelectasis formation and the establishment of pulmonary shunt. By using a mixture containing 30% oxygen in nitrogen, the early formation of atelectasis and pulmonary shunt may, at least in part, be avoided.

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↗

PubMed2002

A comparison of intrapulmonary percussive ventilation and conventional chest physiotherapy for the treatment of atelectasis in the pediatric patient.

OBJECTIVE: Compare intrapulmonary percussive ventilation (IPV) to conventional chest physiotherapy (CPT) and determine their effects on improving atelectasis and static compliance in pediatric patients. METHODS: We conducted a retrospective study of 46 patients who received IPV therapy with the Percussionator IPV-1 ventilator at frequencies of 180-220 cycles/min and pressures of 15-30 cm H(2)O. Medicated aerosol therapy with albuterol 2.5 mg in 6 mL normal saline solution was delivered with each IPV treatment. Baseline and subsequent chest radiographs were evaluated by a pediatric radiologist. We used an ordinal scoring system to measure the degree of atelectasis to evaluate chest radiographs (4 = complete collapse, 0 = complete resolution). Then we conducted a prospective, randomized, controlled study of intubated and mechanically ventilated patients to compare changes in atelectasis and static compliance. Baseline and daily chest radiographs were evaluated using the same scoring system as in the retrospective pilot evaluation. Patients were ventilated in the volume-controlled, synchronized intermittent mandatory ventilation mode, with tidal volumes of 6-10 mL/kg. Patients were randomized to CPT (clapping and vibration) or IPV at frequencies of 180-220 cycles/min and pressures of 15-30 cm H(2)O (equal to the peak pressures on the ventilator), with 6 mL of normal saline solution via medicated aerosol. Both treatments were given every 4 h and lasted 10-15 min. Static compliance measurements were calculated from exhaled tidal volumes and plateau pressures. RESULTS: In the retrospective study the median age of patients receiving IPV was 4.2 years and the median duration of IPV was 6.2 days. A change in atelectasis score from 3 to 1 (p < 0.001) was seen. In the randomized, controlled trial the median age of patients was 3.1 years. Atelectasis scores before treatment were comparable between the CPT and IPV groups (median 2.0 for both groups, p = 0.530). Atelectasis scores after treatment were unchanged in the CPT group (median 2.0, p = 0.421) but improved in the IPV group (median 1.0, p = 0.026). Treatment lasted an average of 6.2 days in the CPT group and 2.1 days in the IPV group (p = 0.018). Neither group showed any change in static compliance following treatment. CONCLUSIONS: In the retrospective study a clinically important improvement in atelectasis was seen in patients who received IPV therapy. In the controlled, clinical trial the IPV group showed more clinically important improvement in atelectasis than the CPT group. IPV is a safe and effective method of alternative airway clearance and can be used on patients with artificial airways.

Adolescent↗

PubMed1977

[Animal experiments on particulars of the time factor in the development and solving of pulmonary atelectasis caused by foreign body (author's transl)].

In literature are only older publications about the temporal beginning of the acute atelectasis after obstructive foreign body occlusion of the bronchial system which are operated at the open thorax. For this reason experiments on animals were made to find out the earliest beginning of an atelectasis by a simple bronchial occlusion as an imitation of a natural process of a foreign body aspiration. The alterations in each single phase of development showed regularly based on serial radiographies and by the autopsy macroscopic and microscopic that about 2 or 3 h after aspiration of an obstructive foreign body it will be reckoned with a complete atelectasis. Only now correlate the clinical result, the X-ray and the pathological-anatomical alterations. The histological picture of the complete atelectasis follows the macroscopic result only in longer temporal distance. Atelectasis occuring before the mentioned moment cannot be explained by an absorption of air from the alveolar tissue, but they depend on foreign body independent reflexes (= reflex contraction atelectasis). In other series of experiments the retroplasia of an atelectasis showed no regularity after the release of the bronchial occlusion, as the time of development, but it is possible to say that it takes more time of retroplasia the longer the atelectasis lasts. Dependent on that the respiratory exchange was jerky into the atelectatic lung after a resting period without prefering any lobes of lungs where localised atelectatic foci remain a longer time.

Animals↗

PubMed1990

Pulmonary atelectasis after reconstruction with pectoralis major flaps.

Forty-four patients were reviewed to determine the incidence of atelectasis following pectoralis major myocutaneous flap reconstruction of head and neck defects. Patients underwent tumor resection with subsequent pectoralis major myocutaneous flap reconstruction (flap group, n = 24) or another major head and neck procedure (control group, n = 20). Chest roentgenograms taken on the first postoperative day were scored for atelectasis by preestablished criteria. Sixty-five percent of control and 70% of flap patients demonstrated postoperative atelectasis roentgenographically. The flap patients with skin paddles larger than 40 cm2 had a 60% incidence of major atelectasis compared with 5% in control patients. The skin island area was strongly correlated with the atelectasis score in the flap group. These results suggest that atelectasis is common following pectoralis major myocutaneous flap reconstruction of head and neck defects. As well, decreased chest wall compliance after primary closure of large donor defects may contribute to the atelectasis observed.

Carcinoma, Squamous Cell↗

PubMed2003

Ventilator-associated pneumonia and atelectasis: evaluation through bronchoalveolar lavage fluid analysis.

OBJECTIVE: Surfactant offers protection against alveolar collapse and contributes to the local defense mechanism, but it is unclear if surfactant alterations have a role in the development of atelectasis or ventilator-associated pneumonia (VAP). The present study was undertaken to monitor surfactant, as well as biochemical BAL fluid alterations, during the course of VAP and atelectasis in mechanically ventilated patients without primary cardiopulmonary disease, to elucidate the pathogenesis and to differentiate these two entities. DESIGN. Prospective controlled study. SETTING: 14-bed general ICU of a 750-bed University Hospital. PATIENTS: Sixty-one ventilated patients, without primary cardiopulmonary disease-normal initial chest X-ray, satisfactory oxygenation (PaO(2)/FiO(2)>300 mmHg), and expected time of ventilation exceeding 2 weeks-were initially enrolled. Twelve of them developed VAP and eight lobar or segmental atelectasis during the 2-week study period. INTERVENTIONS: An initial BAL was performed in all patients within 48 h from admission. Patients who developed VAP or atelectasis were subjected to a second and third BAL during and after the resolution of VAP or atelectasis, respectively. MEASUREMENTS AND RESULTS: VAP and atelectasis resulted in a significant increase of total protein and markers of inflammation, such as PAF and neutrophils, which partially remitted after their resolution. Large surfactant aggregates, which contribute to surface tension decrease, were significantly reduced during both entities and remained low even after their resolution. CONCLUSIONS: BAL alterations during VAP and atelectasis suggest increased alveolar-capillary permeability, severe surfactant abnormalities, and signs of local inflammatory reaction. These alterations are associated with the observed deteriorated gas exchange and lung mechanics and could predispose to further lung injury in ventilated patients.

Analysis of Variance↗

PubMed1995

Prevention of atelectasis during general anaesthesia.

Atelectasis is an important cause of impaired gas exchange during general anaesthesia; it causes pulmonary shunting. We studied the effects of gas composition on the formation of atelectasis and on gas exchange during the induction of general anaesthesia. In 12 adult patients, the lungs were ventilated with 30% oxygen in nitrogen during anaesthesia induction, and in another 12, a conventional technique was used (100% oxygen during induction and 40% oxygen in nitrogen thereafter). Extent of atelectasis was estimated by computed tomography and the ventilation-perfusion relation (VA/Q) by the multiple inert gas elimination technique. After anaesthesia induction, there was little atelectasis in the 30% oxygen group (mean 0.2 [SD 0.4] cm2) and a significantly greater amount (4.2 [5-6] cm2; p < 0.001) in the 100% oxygen group. Patients in the 30% oxygen group were observed for another 40 min. 6 continued to receive 30% oxygen (subgroup A) and 6 were ventilated with 100% oxygen (subgroup B). During this time, the amount of atelectasis increased to 1.6 (1.6) cm2 in subgroup A and to 4.7 (4.5) cm2 in subgroup B (p = 0.047 for difference between groups). In subgroup A, the shunt (VA/Q < 0.005) increased from 1.6 (2.0)% of cardiac output to 3.2 (2.7)%, but the arterial oxygen tension did not change. In subgroup B, the shunt increased from 2.6 (5.2)% to 9.8 (5.7)% of cardiac output. These results suggest that the composition of inspired gas is important in atelectasis formation during general anaesthesia. Use of a lower oxygen concentration than is now standard practice might prevent the early formation of atelectasis.

Adult↗