Severe Atelectasis Research Articles

Flexible Bronchoscope-Directed Catheter Removal of Mucus Plugs in a Child With Plastic Bronchitis

Plastic bronchitis is a rare, serious, and sometimes fatal problem that can follow a Fontan palliative procedure. We report a child with post-Fontan plastic bronchitis. The child developed recurrent and severe atelectasis of multiple lobes. The tenacious mucus plugs were removed using a flexible bronchoscopy-directed catheter suctioning at the bedside. This obviated the need for rigid bronchoscopy, which is the standard practice of removing mucus plugs in plastic bronchitis. The procedure was tolerated well and resulted in instantaneous improvement in oxygenation.

Surfactant use for neonatal lung injury: beyond respiratory distress syndrome.

Surfactant has led to a significant reduction in neonatal mortality for premature infants with lung immaturity and respiratory distress. However, surfactant therapy has been shown to be effective in the treatment of a number of other neonatal respiratory disorders and the evidence for surfactant use in such circumstances is presented. Meconium aspiration is characterised by severe atelectasis, the influx of neutrophils, edema, and hyaline membranes, with decreased levels of SP-A and SP-B and the large aggregate fraction of lung surfactant, and altered surfactant surface morphology. Meconium contains cholesterol, free fatty acids and bilirubin all of which can interfere with surfactant function in a dose-dependent fashion. Providing larger amounts of surfactant can overcome some of this inhibition. Animal models of meconium aspiration treated with surfactant have improved histology, lung mechanics and gas exchange. Studies in human infants with meconium aspiration have found elevated concentrations of total protein, albumin, and membrane-derived phospholipid in lung lavage fluid, and haemorrhagic pulmonary edema. Clinical studies in such neonates have reported improved gas exchange and clinical outcomes following surfactant treatment. More recently surfactant lavage has been shown to be a potentially efficacious therapy for such infants. The inflammatory exudate containing plasma proteins and cytokines which accompanies neonatal pneumonia may inactivate surfactant. Surfactant treatment given to animals following the tracheal instillation of group B Streptococcal resulted in significantly less bacterial growth and improved lung function. Small clinical experiences have demonstrated the benefit of surfactant to infants with pneumonia/sepsis. Pulmonary haemorrhage, which some consider a complication of surfactant therapy, has also been effectively managed using surfactant instillation. The hemoglobin and red blood cell lipids may act to inhibit natural surfactant and treatment with surfactant has been shown to improve outcome for infants with pulmonary haemorrhage. Animal models of congenital diaphragmatic hernia (CDH) have hypoplastic lungs with evidence of decreased lamellar bodies in their type II pneumocytes and resultant surfactant deficiency, and respond to surfactant replacement with improved gas exchange and lung mechanics. The lungs of human infants with CDH contain less phospholipids and phosphatidylcholine per milligram of DNA than control infants. Case reports have reported a benefit of surfactant for infants with CDH. In the near-term infants with severe respiratory distress, surfactant is one of the therapies along with inhaled nitric oxide and high frequency ventilations, that have resulted in improved outcomes. Surfactant treatment may be of significant benefit in newborn infants with respiratory compromise secondary to a number of insults, and further prospective evidence of its efficacy in such disorders is needed.

Successful ventilatory management of post‐anesthetic airway collapse and hypoxemia in a dog

Abstract Objective: To report a life‐threatening complication (airway collapse) associated with a common procedure (anesthesia) and to describe its successful management.Case Summary: A dog without pre‐existing signs of respiratory disease developed hypoxemia and severe atelectasis in the post‐anesthetic recovery period and was demonstrated, by bronchoscopic examination, to have severe airway collapse. Mechanical ventilation was used to re‐expand collapsed lung units and to prevent re‐collapse. A ventilation strategy designed to minimize airway and alveolar trauma was used. The dog was successfully weaned from the ventilator and made a full recovery.Unique Information Provided: Acute, severe hypoxemia due to airway collapse occurred in the post‐operative period in a dog with no signs of pre‐existing respiratory disease. The dog was successfully managed with short‐term mechanical ventilation. High frequency jet ventilation was used for a diagnostic bronchoscopy.

The protective effect of hepatocyte growth-promoting factor (pHGF) against hydrogen peroxide-induced acute lung injury in rats.

To examine the protective effect of hepatocyte growth-promoting factor (pHGF) in hydrogen peroxide (H(2)O(2))-induced acute lung injury in rats, we observed the pathological changes in lung tissue by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and by light and electron microscopy. We also measured the serum levels of lipid peroxide (LPO). At 6 to 24 h after H(2)O(2) injection, the level of LPO was significantly higher in the H(2)O(2) group than in the H(2)O(2) + pHGF-treated group. This finding indicated that pHGF protected against cell membrane damage in H2O2-induced acute lung injury. Positive TUNEL signals were found in capillary endothelial cells, alveolar epithelial cells, and inflammatory cells. In the H(2)O(2) + pHGF-treated group, TUNEL-positive signals were reduced compared with those in the H(2)O(2) group. This finding indicated that pHGF acts to suppress apoptosis. In the H(2)O(2) group, severe pulmonary edema was seen 3 h after H(2)O(2) injection, and at 24 h, severe atelectasis was seen. In the H(2)O(2) + pHGF-treated group, pulmonary edema was scarcely seen and severe atelectasis was not found. This finding indicated that pHGF acts to suppress both severe pulmonary edema and atelectasis. In the H(2)O(2) group, the formation of subendothelial blebs and disruption of endothelial cells was observed. Edema and disruption were seen in type I epithelial cells. In type II lung epithelial cells, mitochondria were swollen and microvilli had disappeared. In the H(2)O(2) + pHGF-treated group, the formation of subendothelial blebs was seen, but no severe subendothelial blebs were observed. Disruption of capillary endothelial cells and type I epithelial cells was not evident, nor was there damage to type II lung epithelial cells. These findings indicated that pHGF protects the progression of H(2)O(2)-induced acute lung injury, and showed that pHGF acts to stabilize the cell membrane in capillary endothelial cells and lung epithelial cells.

Canalplasty for chronic tympanic membrane atelectasis

Purpose: Canalplasty to prevent accumulation of squamous debris has been proposed as an alternative to tympanoplasty for the treatment of tympanic membrane atelectasis and early cholesteatoma. The goal of this article is to report our experience with canalplasty for the treatment of advanced middle ear atelectasis. Materials and Methods: A retrospective review was performed on all patients that underwent tympanoplasty or canalplasty at the University of Florida since 1992. Eight ears (seven patients) with severe atelectasis were found to have been treated with canalplasty (without middle ear reconstruction) to marsupialize the retraction pockets. Results: Follow-up was conducted at an average of 22 months. Four ears required repeat surgical intervention after an average of 12 months: three required canal wall down mastoidectomies for cholesteatoma, and a tympanoplasty was necessary in one case for persistent perforation. Four ears not requiring revision were without cholesteatoma or perforation at an average follow-up time of 26 months. Mean audiometric thresholds were stable or improved, irrespective of the need for revision surgery. Conclusions: Canalplasty may be an alternative for the treatment of atelectasis in selected patients; however, close follow-up after surgery is necessary because of the potential for progression to cholesteatoma.

Surgical Treatment of Endobronchial Tuberculosis

The incidence of tuberculosis remains fairly high in some developing countries. Endobronchial tuberculosis may cause bronchostenosis, with potentially severe respiratory symptoms, atelectasis and secondary pneumonitis. Thirty-two surgically treated cases of tuberculous bronchostenosis (33 operations) are presented. In 13 cases segmental resection or lobectomy was performed with bronchoplastic procedures. Anastomotic stenosis necessitated pneumonectomy 5 years later in one of the 13 and one patient had wound infection. Nineteen patients underwent pulmonary resection without bronchoplasty. Apart from the patient with anastomotic stenosis, all 32 were symptom-free in the follow-up period. Forced expiratory volume was significantly improved in the ten tested patients with bronchoplasty. The results suggest that surgical treatment is safe for endobronchial tuberculosis with poor response to specific chemotherapy. In addition to checking progression of the disease, bronchoplasty helps to preserve lung function. Appropriate chemotherapy should be given for 9–12 months perioperatively to prevent recurrence and restenosis.

Analysis of glucocorticoid and mineralocorticoid signalling by gene targeting.

To get a better understanding of the role of glucocorticoid and mineralocorticoid signalling during development and in whole animal physiology, we have disrupted the mouse glucocorticoid and mineralocorticoid receptor gene by gene targeting. Most of the mice with a disrupted glucocorticoid receptor gene die within the first hours after birth due to severe lung atelectasis. Perinatal induction of gluconeogenic enzymes in the liver is impaired. Feed back control of the glucocorticoid synthesis via the hypothalamic-pituitary-adrenal axis is perturbed leading to increased plasma levels of corticosterone and adrenocorticotrophic hormone. Increased activity of the hypothalamic-pituitary-adrenal axis results in extensive hypertrophy and hyperplasia of the cortical zones of the adrenal and induction of genes involved in steroid biosynthesis. The adrenal medulla is disorganized and severely reduced in size; cells capable of adrenaline synthesis are missing. Mineralocorticoid receptor deficient mice die around day 10 after birth. Weight loss precedes death of homozygous mutant mice and is correlated with an increase in the haematocrit. As a consequence of this mutation plasma levels of renin, angiotensin II, and aldosterone are highly elevated.

Postoperative pulmonary function after laparoscopic and open cholecystectomy

In this prospective, randomized study, we compared 42 patients undergoing laparoscopic cholecystectomy and 40 undergoing open cholecystectomy to determine if laparoscopic cholecystectomy results in less respiratory impairment and fewer respiratory complications. Pulmonary function tests, arterial blood-gas analysis and chest radiographs were obtained in both groups before operation and on the second day after operation. Postoperative pain scores and analgesic requirements were also recorded. After operation, a significant reduction in total lung capacity, functional residual capacity (FRC), forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and mid-expiratory flow (FEF25-75%) occurred after both laparoscopic and open cholecystectomy. The reductions in FRC, FEV1, FVC and FEF25-75% were smaller after laparoscopic (7%, 22%, 19% and 23%, respectively) than after open (21%, 38%, 32% and 34%, respectively) cholecystectomy. Laparoscopic cholecystectomy was also associated with a significantly lower incidence (28.6% vs 62.5%) and less severe atelectasis, better oxygenation and reduced postoperative pain and analgesia use compared with open cholecystectomy. We conclude that postoperative pulmonary function was impaired less after laparoscopic than after open cholecystectomy.

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.

Aerosolized deferoxamine prevents lung and systemic injury caused by smoke inhalation

We assessed the role of oxidant release at the airway mucosal surface on airway injury and systemic response to a severe smoke insult. Adult sheep (n = 20) were insufflated with well-characterized smoke from burning cotton toweling. A standardized dose of 12 breaths of smoke with a tidal volume of 20 ml/kg was given under anesthesia. Sheep were awakened, monitored for 24 h, and killed; data were compared with control sheep. Sheep were given 1) humidified oxygen, 2) continuous aerosol of 10% deferoxamine (DFO)-pentastarch solution beginning after smoke, 3) DFO-alone aerosol, or 4) pentastarch-alone aerosol. DFO has antioxidant properties directly and chelates iron. Severe respiratory failure occurred in all but DFO-pentastarch group. Shunt fraction increased from a control of 4%. Histological assessment revealed severe airway mucosal edema, ulceration, bronchorrhea, and severe atelectasis but only moderate alveolar edema. Increased lipid peroxides were also noted in free airway fluid and in bronchoalveolar lavage fluid. In addition, oxygen consumption increased by 75%, fluid requirements increased threefold, and protein-rich systemic soft tissue lymph flow doubled, all significant increases compared with control sheep. No significant physiological or histological changes were noted in DFO-pentastarch aerosol group. We conclude that 1) oxidants possibly initiated through free iron release are involved in severe smoke-induced airway injury and resulting systemic inflammatory response, probably through an amplified oxidant injury and 2) an aerosol of a DFO-pentastarch complex prevents the injury process, whereas DFO alone is not effective as an aerosol.

Tympanic membrane atrophy, scarring, atelectasis and attic retraction in persistent, untreated otitis media with effusion and following ventilation tube insertion

Two hundred and twenty two children with persistent bilateral otitis media with effusion (OME) were treated with unilateral ventilation tube insertion and no treatment to the contralateral ear. The tympanic membrane changes in the operated and unoperated ears were compared during a 12 year follow-up. Segmental atrophy resulted from tube insertion whereas minor scarring and thickening of the pars tensa was related to the middle ear condition. Eighty three percent of untreated ears and 85% of those treated with tubes did not develop atelectasis. Sixty percent of untreated ears and 64% of treated ears did not develop attic retraction. Very few cases (1.5 and 2%) in untreated and treated ears, respectively developed severe atelectasis. The overall duration of OME was assessed from the pre-operative history of hearing loss, the 3 month period of pre-operative observation and the post-operative time with effusion. There is a relationship between duration of the disease and development of both atelectasis and attic retraction.

Effect of increasing the tidal volume of smoke breaths on smoke-induced lung dysfunction

We determined the effect of a graded increase in lung exposure to a toxic smoke by increasing smoke tidal volume (VT) or the number of smoke breaths. Sheep were anesthetized and then insufflated with cooled cotton toweling smoke; VT was 5, 10, or 20 ml/kg, and smoke breaths were varied from 12 to 48. The smoke had a uniform particle size (3 +/- 0.4 microns diam). Peak carboxyhemoglobin levels varied from 8 +/- 2 to 45 +/- 4% in the lowest to highest exposure groups, respectively. Animals were monitored unanesthetized for 24 h, and then they were killed. Oxygenation (ratio of arterial PO2 to fraction of inspire O2) decreased from 480 +/- 21 to 200 Torr, and compliance decreased by approximately 50% in the highest smoke exposure groups, whereas only a modest decrease in oxygenation and no compliance changes were seen with lesser exposures. A moderate tracheobronchitis, some atelectasis, and no alveolar edema were noted in the lower smoke exposure groups, whereas severe tracheobronchitis, airway edema, and alveolar atelectasis were observed in the highest exposure group. Only modest alveolar flooding was noted. Impaired oxygenation and anatomic injury correlated best with the total smoke delivered (r = 0.59). Increasing VT from 5 to 20 ml/kg did not increase airway or alveolar injury if the total smoke mass delivered was maintained constant. The degree of impaired oxygenation did not correlate with measured lung water (r = 0.27) or lung lymph flow (r = 0.31).

Differential effects of oxygen and barotrauma on lung injury in the neonatal piglet

In order to differentiate the effects of hyperoxia and barotrauma in the pathogenesis of acute neonatal lung injury, piglets were either hyperventilated (Paco2, 15-20 torr) for 48 hours with 100% oxygen (Group I), hyperventilated with 21% oxygen (Group II), normally ventilated (Paco2, 40-45 torr) with 100% oxygen (Group III), or normally ventilated with 21% O2 (Group IV) and compared to unventilated controls. Pulmonary function was tested, and biochemical indicators of lung injury were analyzed in tracheo-bronchial aspirates at 0, 24, and 48 hours. Bronchoalveolar lavage fluid was analyzed for surfactant composition and activity at the end of the study. At 48 hours, hyperoxic, hyperventilated piglets had significantly decreased dynamic lung compliance (30%) and increased pulmonary resistance (16%), aspirate cell count (190%), elastase activity (88%), albumin (214%), and total protein (150%) concentration. Qualitative light microscopy showed moderate to severe atelectasis, fibrinous exudate, edema, and inflammation. Normoxic, hyperventilated animals had comparable changes in pulmonary mechanics, but significantly milder cellular, biochemical, and morphologic changes. In hyperoxic, normocarbic animals pulmonary physiologic, cellular, and biochemical variables changed comparably to hyperoxic, hyperventilated animals; the pathologic changes were intermediate between hyperoxic, hyperventilated and normoxic, hyperventilated piglets. Normoxic, normocarbic animals had no significant changes in most variables over 48 hours; on morphologic examination their lungs were similar to unventilated controls and showed only mild edema. Surfactant had normal biophysical activity in all animals. Our results demonstrate that hyperoxia causes more significant physiologic, inflammatory, and histologic changes than barotrauma alone. Future attempts to prevent lung injury in neonates should be directed primarily at oxygen toxicity.

Gravity-Dependent Atelectasis

The authors identify the radiologic features of progressive atelectasis induced under conditions of reduced lung volume. Control (n = 5) and experimental (n = 7) animals were placed on high-frequency oscillation (HFO) ventilation (mean airway pressure: 3 cm H2O) for 6 hours. In the experimental animals, lung volume was artificially reduced by pneumoperitoneum during HFO ventilation. Computed tomography scans and chest radiographs were obtained every hour, and arterial blood gases analyzed. No changes were detected in the control animals. In the experimental animals, in which hypoxemia developed, homogeneous opacity in the dependent lung was found on CT images, and chest radiographs showed a diffuse homogenous shadow with loss of lung volume. Study of pathologic sections from the lung showed that the roentgenographic findings represented atelectasis. The lung was divided into three zones, from dependent to nondependent regions: severe atelectasis, mild atelectasis, and normal lung. Hyperinflations eliminated atelectasis seen on the CT images and alleviated hypoxemia; however an undesirable effect that causes barotrauma also was observed.

Phrenic Nerve Function and Its Relationship to Atelectasis After Coronary Artery Bypass Surgery

Atelectasis following coronary artery bypass surgery (CAB) occurs in the majority of patients. To determine the importance of operative variables in the development of postoperative atelectasis and the incidence of phrenic nerve injury caused by topical cold cardioplegic solution, we studied 57 patients (53 male, four female) undergoing CAB. Their mean age, +/- SD, was 58 +/- 13 years. Transcutaneous stimulation was used to evaluate phrenic nerve function preoperatively and postoperatively in 52 patients. An unequivocal paresis of the phrenic nerve was documented in five patients. In an additional 27 patients, the amplitude of the compound diaphragm action potential was reduced postoperatively. However, methodologic limitations did not allow the conclusion that this was secondary to a phrenic axonal degeneration. Discriminant analysis of intraoperative variables showed more severe atelectasis with a larger number of grafts, with a longer operative and bypass time, when the pleural space was entered, when a right atrial drain and a cardiac insulating pad were not used, and with a lower body temperature. It is concluded that phrenic paresis may occur after CAB and topical cold cardioplegia, but that other factors must explain the atelectasis found in the majority of patients.

Untreated persistent middle ear effusion.

Seventy-nine children have been followed with persistent middle ear effusion (MEE). They were scheduled for myringotomy and insertion of ventilating tubes (VT). Several factors delayed elective surgery for two-and-a-half years in a closed population. After that period, the children were again examined otomicroscopically and hearing tests were performed. MEE persisted in 69 per cent of the ears, but was absent in 31 per cent. Atelectasis appeared in 26 per cent of the ears; in only a very few cases did severe atelectasis develop. Complications following delay of myringotomy and introduction of VT are minor.

Atelectasis, retraction pockets and cholesteatoma.

This is a quantitative study of tympanic membrane atelectasis and retraction pocket dynamics. 308 ears. affected by various types of atelectasis were followed up for 9 years (average 3 years). 74 of these evidenced retraction pockets of the pars tensa and 127 retraction of the pars flaccida. The phenomenon of tympanic membrane atelectasis and retraction was found to be unstable. The condition of most ears improved or became stabilized, while in others (the minority, 10–20%) it deteriorated. This middle ear dynamics was observed irrespective of whether the ears were treated or not. The deterioration trend (of 10–20% of the ears) showed a progression from mild atelectasis all the way to deep retraction pockets. One retraction pocket of the membrana tensa (2%) and two of Shrapnell's membrane (2%) progressed and became small attic cholesteatomas. A steady linear increase in average age was observed, as one proceeds from a milder to a more severe degree of atelectasis. However, on reaching severe atelectasis or large retraction pockets, the mean age was found to be the same as that of a large control group of attic cholesteatomas. This latter finding suggests that while this study shows that retraction pockets to originate in atelectatic conditions and retraction pocket cholesteatomas may originate from retraction pockets, it is still doubtful whether this mechanism can account for all the middle ear cholesteatomas and epidermoid cholesteatomas we encounter. Other additional etiological processes should also be taken into consideration. The treatment of most atelectatic ears and mild retractions can be conservative. Follow-up of these ears is important. however. Once hearing has deteriorated or a non-cleansing pocket formed. ossiculoplasty. as well as replacement of the drum. is often indicated—and gratifying.

Recurrent lobar atelectasis due to acquired bronchial stenosis in neonates

Bronchial obstruction by granulation tissue caused atelectasis in ten infants who required frequent suctioning and mechanical ventilation for more than 20 days. The endotracheal suctioning had been performed with a No. 6 or No. 8 French catheter with multiple end and side holes at the tip. Bronchoscopic examination revealed nodular and polypoid granulation at the level of the carina and bronchus, more often on the right side. In five infants, atelectasis was treated with gentle, less frequent suctioning and vigorous pulmonary toilet. Two of these infants died of severe atelectasis and chronic lung disease. Five infants underwent excision or cauterization of granulation tissue. Histopathologic examination of this tissue disclosed inflammation, fibrosis, and squamous metaplasia in each of the five specimens. Eight of the ten infants are alive without symptoms, the oldest being 27 months. Prevention may require critical analysis of suction techniques and the catheter tips employed. Whistle tip catheters should be avoided. Mild obstructive lesions can be managed by gentle and less frequent suctioning and aggressive pulmonary care, but severe obstruction, as determined by a compromise of the lumen of greater than 20%, may require excision or cauterization.

THE EFFECT OF IMMATURITY AND PRENATAL ASPHYXIA ON THE LUNGS AND PULMONARY FUNCTION OF NEWBORN LAMBS: THE EXPERIMENTAL PRODUCTION OF RESPIRATORY DISTRESS

1. The effect of immaturity on the lungs and pulmonary function of newborn lambs was assessed by delivering and observing 13 animals of varying gestational ages. In lambs of approximately 125-129 days gestation changes closely resembling those of human respiratory distress syndrome developed without asphyxia. These changes consisted of retraction of the chest wall, poor gas exchange, grossly liver-like lungs, reduced pulmonary surface activity, and, on histological examination, severe atelectasis, alveolar necrosis, and hyaline membranes. 2. Similar changes were found in 4 of 6 lambs subjected to severe prenatal asphyxia lasting for up to 4 hours which were between approximately 130-136 days gestation but not in three of four comparable control animals. 3. Prolonged prenatal asphyxia was followed by changes suggesting respiratory distress in only 1 of 6 lambs above 136 days gestation. One further lamb at 140 days gestation, acutely asphyxiated to the point of cardiac arrest, developed severe changes. 4. It is postulated that the experimental disease and the syndrome seen in the human infant are produced by similar mechanisms, and that the influence of prematurity is more important than that of asphyxia.

The Use of Enzymes and Wetting Agents in the Treatment of Pulmonary Atelectasis

1. Atelectasis is a common serious complication in both poliomyelitic patients and non-poliomyelitic patients, but is a much more complex problem in the former. 2. In patients who have atelectasis the secretions are thick, viscid and tenacious and in most instances purulent. They must be loosened and thinned to make removal more easy. This is best accomplished by the use of aerosol “tryptar” which is safe and easily administered by mask or through a tracheotomy tube. 3. A cough is absolutely essential in the treatment of atelectasis because an adequate means of moving the secretions once loosened is extremely important. Without adequate coughing, failures in treating atelectasis are inevitable. In non-poliomyelitic cases this coughing is best induced by tracheal catheterization. In poliomyelitic patients who have no cough this is done best by artificial means. 4. Aspiration of secretions during aerosol treatment and with coughing is essential in order to prevent flooding of the tracheobronchial tree by the liquefied secretions. 5. Tracheotomy is essential in most instances in patients who have little or no cough of their own or in those who are unconscious, because it is impossible to aspirate secretions adequately without a tracheotomy opening. 6. The so-called “reactions” to “tryptar” are actually due to inadequate removal of the secretions which have been liquefied by “tryptar” and thus flooding the tracheobronchial tree. 7. Atelectasis in non-poliomyelitic patients responds successfully to the use of “tryptar” within one to four days. Bronchoscopic aspiration is not necessary. In 30 cases treated with “tryptar” there was no failure. 8. In 88 cases of atelectasis in post-poliomyelitic cases “tryptar” was successful in clearing completely 87. In an additional 16 treated with “triton A-20,” seven cleared completely and the other nine were switched to “tryptar” with clearing. 9. In the post-poliomyelitic group of cases there were two deaths, one completely unrelated to atelectasis, the other because of a severe atelectasis with abscess formation in the involved lung.