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The authors report two cases of round atelectasis that showed increased accumulation of technetium (Tc) 99m depreotide on planar and single photon emission computed tomographic scintigraphy. It should be considered that round atelectasis is a potential nonmalignant cause for positive 99mTc depreotide scintigraphy.
Forty-two patients undergoing major colonic surgery were assigned at random to receive isoflurane-fentanyl anaesthesia with nitrous oxide in oxygen, propofol-fentanyl anaesthesia with air in oxygen or propofol-fentanyl anaesthesia with nitrous oxide in oxygen. The groups were comparable in demographic data. Atelectases were identified, and the area measured by computerised tomography of the chest 203 +/- 69 min after extubation, and oxygenation was determined by arterial blood gas samples taken during operation at 30, 60, 90 and 120 min after extubation and on postoperative days 1, 2 and 3. Atelectases were seen in all three groups with no differences in the mean area between groups. After operation, the effect of 4 l.min-1 of oxygen by nasal catheter on PaO2 was similar in all groups. A significant decrease in PaO2 was found during the first 3 days after surgery, and was also the same in all groups. There was no correlation between area of atelectasis and postoperative PaO2. We conclude there is no difference in the incidence of postoperative atelectasis or oxygenation when using propofol, with or without nitrous oxide or isoflurane.
Collapse of the left lower lobe is sometimes accompanied by linear atelectasis in the lingula. The lingular atelectasis may be more readily apparent than conventional signs of left lower collapse. The mechanism of this association as first described by Nordenström is discussed and its value as a diagnostic sign emphasised.
The anatomical basis of gas exchange impairment in the anaesthetised horse was studied by computerised tomography (CT; three shetland ponies) and morphological analysis (one pony and three horses). By means of CT, densities were seen in dependent lung regions early during anaesthesia, both with spontaneous breathing and with mechanical ventilation. The densities remained for some time where they had initially been created when the animal was turned from dorsal to sternal recumbency. Deep insufflation of the lungs reduced the dense area. Gas exchange was impaired roughly in proportion to the dense area. On histological analysis, the densities were atelectatic and congested with blood. Gravimetry showed no more extravascular water per unit lung tissue in the atelectatic than in the 'normal' regions, and the blood content was increased only slightly. It is concluded that the horse develops atelectasis in dependent lung regions early during anaesthesia in dorsal recumbency, and that atelectasis is the most likely explanation for the large shunt and impaired arterial oxygenation regularly seen during anaesthesia.
Of 181 patients undergoing major abdominal surgery 116 developed chest complications associated with a metabolic acidosis, low Pco2, depressed tidal volume, increased respiratory rate, but no increase in minute volume. In a matched group of 116 patients given intravenous bicarbonate postoperatively only 15 developed chest complications. This suggests that respiratory physiological dead space decreases in patients with pulmonary collapse and atelectasis following surgery. Acidotic respiration proved inefficient in the postoperative period, and intravenous bicarbonate had a very pronounced effect on the tidal and minute volumes of acidotic patients with pulmonary collapse and atelectasis.
During a 10-year period 28 patients with shrinking pleuritis with atelectasis (SPA) were observed and operated upon. This lesion has been given different names in the literature, for instance rounded atelectasis, pleuroma, pulmonary pseudotumour, and lung folding. All patients except two were operated upon because of a diagnosis of pulmonary tumour. However, at operation no tumour was found. The aetiology and pathogenesis of SPA are discussed on the basis of X-ray, operative, and histopathological findings.
During 14 years 34 patients were operated on for shrinking pleuritis with atelectasis. They were followed up after one to 14 years (mean 6.0) by interview, chest radiography, and spirometry. Most were in good condition, but a reduction in vital capacity had occurred in eight and in FEV1 in 15 patients. Radiographs were normal in 28 patients except for small pleural or parenchymal fibrotic changes. One patient had a suspected recurrence of shrinking pleuritis with atelectasis after nine years, suggesting continuation of the disease process despite operation.
Retrospective and prospective analyses of chest radiographs of patients following coronary artery bypass surgery were undertaken. Left lower lobe pulmonary infiltrate and/or atelectasis developed in 13 of 40 (32.5%) patients who were operated upon without topical cooling of the heart with ice, and in 77 of 122 (63.1%) patients in one group and 34 of 40 (85.0%) patients in another group who were operated upon with topical cooling of the heart with ice. This difference was highly significant (p less than 0.001). Of the patients in one group in whom left lower lobe abnormality developed, 69.2% had paralysis or paresis of the left hemidiaphragm. It is evident that application of ice to the phrenic nerve can lead to temporary paralysis of the left of the diaphragm, with subsequent development of left lower lobe pulmonary infiltrate and/or atelectasis.
The effects of hyperinflation and of atelectasis on accumulation of fluid in the lung was studied in 12 anesthetized spontaneously breathing puppies. Vascular pressures were raised and the plasma colloid osmotic pressure was reduced by the infusion of 0.9% saline thus promoting the formation of pulmonary edema. A tracheostomy was performed and the left lower lobe catheterized in all puppies. In five puppies hyperinflation of the left lower lobe was achieved by applying a continuous positive airway pressure (CPAP) of 10 Torr. In seven other puppies the left lobe was made atelectatic by occluding its bronchus after ventilating the lungs with 100% oxygen. The right lung was ventilated to ambient pressure in all puppies. The extravascular lung water content was determined by the difference in wet and dry lung weights corrected for residual blood. We found that hyperinflation produced by CPAP enhanced and atelectasis opposed fluid accumulation in the puppy lung.
We investigated the degree to which strength of pulmonary hypoxic vasoconstriction affects perfusion of pulmonary shunt pathways in acute atelectasis. In 17 intact supine dogs (anesthetized, paralyzed, and ventilated) we produced left lower lobe atelectasis by occluding the lobar bronchus during oxygen inhalation. Subsequently, shunt fraction (reflecting perfusion of that lobe) was measured using an SF6 infusion while the dogs breathed room air; the mean was 26% (range 14-40%). Pulmonary pressor response to hypoxia was assessed in 13 dogs using the increase in pulmonary end-diastolic gradient (PDG) produced by inhalation of 10% oxygen. Those animals with the largest increase in pulmonary diastolic gradient had the smallest shunt fraction while breathing room air, whereas those with the smallest response had the largest shunt fraction. The contribution of local hypoxia to vasoconstriction in the shunt pathway was assessed in 13 dogs breathing room air by measuring the increase in shunt fraction produced by infusing prostaglandin E1 (PGE1). Those with the largest increase in shunt fraction had the smallest pre-PGE1 shunt fraction. Thus the strength of pulmonary vascular reactivity to hypoxia markedly influences the degree of vasoconstriction in shunt pathways and is a major determinant of shunt pathway perfusion.
The extravascular volume of distribution for heat in the lung has been advocated for the measurement of lung water. The purpose of these experiments was to investigate how extremes of ventilation-perfusion mismatch influence this measurement. Twenty-six dogs were studied with right and left atrium-to-aorta thermal and dye-dilution curves before and 60 min after total right main-stem bronchial obstruction or microembolization of the pulmonary circulation with 0.275-mm glass beads. Whereas atelectasis had no influence on our measurements, embolization with 0.32 g/kg of beads decreased the detected pulmonary blood volume from 10.63 to 8.55 ml/kg and increased the extravascular thermal volume (ETV) from 9.89 to 10.99 ml/kg. Embolization with 0.65 g/kg decreased the detected ETV from 9.29 to 8.38 ml/kg, while the extravascular wet-to-dry weight ratio was increased, and the regression of postmortem extravascular mass on ETV differed from control. We conclude that microembolization but not atelectasis causes errors in the measurement of lung fluid when the thermodye technique is used. The errors are variable and depend on the degree of embolization.
Both ventilator pattern and neutrophil activation influence lung injury in adult respiratory distress syndrome (ARDS). We therefore questioned whether ventilator pattern independently affects neutrophil accumulation and function in early ARDS. Thirty-five New Zealand White rabbits were anesthetized, paralyzed, and prepared using sterile techniques. Fifteen surfactant-depleted animals were randomized and ventilated for 4 h using high-frequency oscillatory ventilation (HFO) at 15 Hz with an inspired O2 fraction = 1.0 and arterial PO2 (PaO2) > 400 Torr (a pattern known to reverse atelectasis) or conventional mechanical ventilation (CMV) with PaO2 = 80-100 Torr (a pattern with some atelectasis despite positive end-expiratory pressure). Eight normal animals on CMV with PaO2 > 400 Torr served as a reference group (NorCMV). NorCMV animals progressively increased circulating polymorphonuclear neutrophil (PMN) numbers and had minor pressure-volume curve alterations but no other significant changes. Lavaged CMV animals developed the characteristic gas exchange and marked pressure-volume curve abnormalities of ARDS. Circulating PMNs remained constant but developed decreased chemotactic activity, whereas lung neutrophil numbers increased significantly (P = 0.0002) and had substantially enhanced chemiluminescence (P = 0.0003 vs. NorCMV animals). Although lavaged HFO animals accumulated an intermediate number of lung neutrophils (lung myeloperoxidase > NorCMV animals; P = 0.003), the chemiluminescence and chemotaxis of these PMNs were the same as in cells from NorCMV animals. We concluded that both the degree of neutrophil activation and lung injury can be minimized by preventing cyclic alveolar/airway expansion and collapse in the surfactant-deficient lung by use of appropriate ventilator patterns.
Recent computed tomography studies show that inspired gas composition affects the development of anesthesia-related atelectasis. This suggests that gas absorption plays an important role in the genesis of the atelectasis. A mathematical model was developed that combined models of gas exchange from an ideal lung compartment, peripheral gas exchange, and gas uptake from a closed collapsible cavity. It was assumed that, initially, the lung functioned as an ideal lung compartment but that, with induction of anesthesia, the airways to dependent areas of lung closed and these areas of lung behaved as a closed collapsible cavity. The main parameter of interest was the time the unventilated area of lung took to collapse; the effects of preoxygenation and of different inspired gas mixtures during anesthesia were examined. Preoxygenation increased the rate of gas uptake from the unventilated area of lung and was the most important determinant of the time to collapse. Increasing the inspired O2 fraction during anesthesia reduced the time to collapse. Which inert gas (N2 or N2O) was breathed during anesthesia had minimal effect on the time to collapse.
We present 4 patients undergoing hemodialysis in whom thoracic computed tomography (CT) suggested a diagnosis of rounded atelectasis (RA) with pleural effusion. The clinical setting and follow-up CT of all 4 patients confirmed this diagnosis. The pleural fluid of each appeared serosanguineous or hemorrhagic and predominantly consisted of lymphocytes. Biochemical analysis of this fluid revealed high levels of total protein, lactate dehydrogenase and glucose. Bacterial culture and polymerase chain reaction for Mycobacterium tuberculosis DNA was negative. Pleural biopsy specimens from 2 of the 4 patients showed evidence of fibrinous change and mesothelial cell hyperplasia. Pleural effusion from all 4 patients did not respond to either fluid restriction or aggressive hemodialysis-induced dehydration. The subsequent clinical course and thoracentesis were repeated, and in 1 patient, this was followed by tetracycline pleurodesis. However, 2 patients died during pre-pleurodesis and 1 died during post-pleurodesis, all due to respiratory failure. We propose that the clinical setting and follow-up thoracic CT and thoracentesis of patients receiving long-term hemodialysis confirmed a diagnosis of rounded atelectasis with uremic pleural effusion. We also propose that the prognosis of patients with refractory pleural effusion receiving long-term hemodialysis would be improved by early pleurodesis.
To evaluate the usefulness of fiberoptic bronchoscopy for treatment of acute lobar atelectasis, 31 subjects were randomly allocated to fiberoptic bronchoscopy followed by respiratory therapy for 48 hours, or to respiratory therapy alone for the same period. No significant differences between groups with regard to restoration of volume loss were detected after the first treatment intervention, at 24 or at 48 hours (P greater than 0.20). Specifically, the mean percentage resolution of volume loss immediately after bronchoscopy (38 per cent) closely approximated that after the first respiratory therapy treatment in subjects who had not undergone bronchoscopy (37 per cent). An air bronchogram proved to be a predictor of delayed resolution for both groups. At 24 hours, 26 per cent of the air bronchograms demonstrated 83 per cent resolution (P less than 0.001). These results suggest that fiberoptic bronchoscopy does not add to respiratory therapy in the treatment of acute lobar atelectasis and that an air bronchogram predicts delayed resolution of collapse.
Chronic maxillary atelectasis is a descriptive term that refers to a persistent decrease in the sinus volume of the maxilla from inward bowing of the antral walls. Case reports with comparable clinical presentations have appeared sporadically in the literature; however, this disorder has remained poorly defined. The purpose of this study is to provide a formal definition of this condition by the establishment of diagnostic and staging criteria. A 10-year case analysis identified 22 adults, and a review of the literature revealed another 25. The average age at presentation in our study was 38.3 years. Most patients were symptomatic, and some presented with diplopia and hypoglobus. Inward bowing of the antral wall(s) and persistent opacification on computed tomography made the diagnosis. Chronic maxillary atelectasis was separated into three stages according to the degree of wall deformation. While most patients were symptomatic, a past history of absent or mild symptoms referable to the nose and sinuses was encountered more often in those patients with osseous wall deformation (p = .041). Mild or absent symptoms at the time of diagnosis should not be considered a negative risk factor for the development of facial deformity, especially if the sinus has features consistent with complete pneumatization. A middle meatal antrostomy appears to relatively safely correct the sinus problem, while orbital floor reconstruction for hypoglobus, found in stage III of the disease, can be accomplished effectively via a transconjunctival approach using a combination of bone allograft and porous polyethylene sheets.
Segmental and lobar pulmonary atelectasis is a common occurrence in mechanically ventilated patients. Standard therapy for atelectasis relies on positive pressure ventilation, positive and expiratory pressure (PEEP), tracheobronchial toilet and regular chest physiotherapy. Various adjuncts to physiotherapy such as bronchoscopic clearance of secretions have not proved to be of additional benefit. Bronchoscopic clearance of secretions followed by insufflation of room air at 30 cm H2O into the atelectatic segment was employed on ten occasions in mechanically ventilated patients. Rapid re-expansion of the collapsed segment or lobe occurred in seven out of the ten treatments.
Although treatment of refractory atelectasis has been improved by pulmonary insufflation through FOB with balloon cuff, low pulmonary compliance and high critical opening pressure of alveoli in the atelectatic areas require a more selective approach to prevent pressure dispersion to highly compliant zones. To achieve the highest insufflation selectivity and reduce patient discomfort, we have devised a small caliber balloon-tipped catheter to easily reach even the minor branches of the bronchial tree. This result was obtained by utilizing the performed curve of the catheter distal end after withdrawing the internal stylet. The catheter was introduced through the nostrils (16 patients) or through an endotracheal tube (two patients) and advanced under fluoroscopic guidance. Reexpansion of atelectatic areas was accomplished by repeated air injections through a 60-ml syringe. No complications were observed. Complete disappearance of x-ray film evidence of atelectasis was obtained in 15 patients and partial reexpansion in 3 patients.