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Fibronectin (FN) has been postulated to prevent gram-negative bacillary (GNB) colonization of the oropharynx by covering epithelial cell GNB receptors. We investigated the distribution of FN along the luminal surface of oropharyngeal epithelium in animals and humans. Examination of buccal epithelial biopsies obtained from normal rats revealed no luminal surface FN by either immunofluorescent or immunoperoxidase staining. Extraction of epithelial surface proteins and quantitation of FN by rocket immunoelectrophoresis and electrophoretic transfer to nitrocellulose followed by immunologic detection also detected no FN from normal animals' oropharyngeal biopsies. Buccal epithelial biopsies from three normal humans were examined for FN using electrophoretic transfer to nitrocellulose followed by immunologic detection, and no FN was demonstrable. Our results suggest that FN is not present on the oral epithelial surface of healthy rodents or humans, and that FN may not be involved in the pathogenesis of bacillary colonization.

Intrapulmonary deposition of the proteolytic enzyme papain produces a lesion resembling emphysema in experimental animals. The natural history of this lesion has not been well defined. The present study was performed to evaluate changes in lung structure and function with aging in normal rats and rats exposed to an aerosol of papain at 2 mo of age. Groups of control and papain-exposed animals were studied at 4, 8, and 18 mo of age. The parameters of lung function studied were specific airways' conductance (G(aw)/TGV), diffusing capacity per unit of alveolar volume (D(Lco)/V(A)), diffusing capacity (D(Lco)), and functional residual capacity (FRC). Morphometric parameters were the postfixation lung volume (V(L)) and mean chord length (L(M)); internal surface area (ISA) and ISA extrapolated to both the mean V(L) of the corresponding papain group and a V(L) of 10 ml (ISA(10)) were calculated. At 4 mo of age L(M) and FRC were significantly increased and ISA, D(Lco)/V(A), and D(Lco) were significantly reduced in the papain group. At 8 mo of age L(M) was significantly increased and ISA was significantly decreased in the papain group: physiologic studies were not performed in this group. At 18 mo of age L(M) was significantly increased and D(Lco)/V(A), D(Lco), and ISA were significantly decreased. Neither progression nor healing of the lesion was observed despite similar lung growth in both groups. This study demonstrates that a single proteolytic lung injury produces a fixed deficit of lung parenchyma. Progressive lung destruction may require repeated or continuous lung injury.

In seven of 30 consecutive patients with the adult respiratory distress syndrome, disseminated intravascular coagulation (DIC) developed. Increasing respiratory dysfunction characterized by decreased effective static compliance and increased hypoxemia coincided with the development of DIC. Patients in whom DIC developed were characterized by a high incidence of bleeding, gangrene of the extremities, renal dysfunction, mortality and autopsy evidence of fibrin microthrombi in the lungs, kidney and skin. In 12 of 23 patients who did not meet the criteria for DIC, the platelet count decreased by at least 50 per cent of the initial values at some time during their illness. Fibrin microthrombi were found in the lungs in the majority of the patients subjected to autopsy. These data support the concept that depostion of platelet on damaged pulmonary capillary endothelium may be more common in the adult respiratory distress syndrome than the DIC syndrome.

Patients with a history of chronic debilitating disease due to a variety of causes are known to be at risk for infection with coliform gram-negative bacilli when they present with community-acquired pneumonia. Empiric treatment with broad-spectrum parenteral antibiotics is often begun in such patients pending the result of blood and other cultures. The optimal duration of broad-spectrum empiric therapy in such patients when cultures fail to reveal a specific pathogen is unknown. Review was made of the charts of 131 patients with community-acquired pneumonia admitted to the hospital and treated with broad-spectrum parenteral antibiotics in whom a specific pathogen was never isolated. Overall, 89 percent of these patients were cured without complication or relapse. Patients receiving broad-spectrum therapy for four days or less due to rapid clinical improvement had a successful outcome in 95 percent of cases. It is concluded that broad-spectrum parenteral antibiotic therapy can safely be abbreviated provided response to therapy is prompt.

1. Patients should be divided preoperatively into low- or high-risk categories, depending on their probability of developing postoperative pulmonary complications. The evaluation should include spirometry as well as an assessment of the previously defined risk factors. 2. Patients in a low-risk category need only instruction in deep breathing pre- and postoperatively. Routine use of supplemented oxygen postoperatively is reasonable until it can be demonstrated whether such is necessary. 3. High-risk patients should be as free as possible of respiratory secretions at the time of surgery. A regimen for this purpose includes cessation of smoking, and administration of inhaled bronchodilators followed by chest percussion and postural drainage. 4. High-risk patients should be carefully instructed in deep breathing and coughing preoperatively. A mechanical device such as an incentive spirometer may be beneficial in this regard. If it is not possible to achieve spontaneous deep breathing, an attempt to accomplish this by IPPB may be undertaken. The tidal volume desired should be ordered. If IPPB does not result in large tidal volumes, it should be discontinued. 5. The deep breathing procedure found to be most successful preoperativelly should be continued postoperatively. 6. The patient should be as mobile as possible while in bed and ambulated as soon as is feasible. 7. Patients with preoperative expiratory flows of less than 20% of predicted values or with chronic hypercapnia should be carefully observed for postoperative ventilatory failure.

This study correlated levels of activated fibrinolysis with the presence, extent, and rate of resolution of angiographically documented pulmonary emboli. Pulmonary emboli demonstrable by angiography were associated with detectable fibrin split products in the serum of 24 of 25 patients. In the absence of increased fibrin split products, pulmonary emboli large enough to be demonstrated by angiography were found in only 2 of 25 positive pulmonary angiograms. Spontaneous resolution of pulmonary emboli could not be correlated with the the concentration or persistence of fibrin split products but did correlate well with the presence of a reversible precipitating cause. Thrombophlebitis in the absence of clinical evidence of pulmonary embolism was not associated with increased concentrations of fibrin split products in eight of nine patients. The one patient with increased fibrin split product concentration had evidence on lung scan of silent pulmonary embolism.

The prevalence of respiratory symptoms and chest radiographic and spirometric abnormalities was assessed among 397 employees of an activated carbon plant. Definite radiographic findings of pneumoconiosis, consisting of p-type, rounded opacities in the lower lung fields without firbosis or coalescence, were present in 9.6% of men and were related to cumulative dust exposure. Lesser degrees of radiographic abnormality suggesting pneumoconiosis were present in 11% of men and 2% of women. Spirometric values were substantially lower in blacks than in whites. However, cumulative dust exposure was not an important determinant of pulmonary function in either race. Review of lung biopsy speciments that had been obtained previously in two employees revealed extensive carbon depositiion but minimal associated fibrosis. Prolonged inhalation of activated carbon dust leads to pulmonary deposition of carbon and raciographic signs of pneumoconiosis; such deposition has little, if any, effect on respiratory symptoms or pulmonary function.

A sensitive technic using indium111 chloride was devised to investigate the occurrence of pharyngeal aspiration. Twenty normal subjects and 10 patients with depressed consciousness were studied. Forty-five per cent of the normal subjects aspirated during deep sleep. Normal subjects who did not aspirate were noted to sleep poorly. Seventy per cent of the patients with depressed consciousness aspirated. Aspiration of pharyngeal secretions occurs frequently in patients with depressed sensorium and also in normal adults during deep sleep. Bacterial pneumonia may result when aspirated bacteria are not effectively cleared. This may result when clearance mechanisms are impaired or when they are overwhelmed by large volumes of aspirated secretions.

The prevalence of gram-negative bacilli among the oropharyngeal bacterial flora was low in physiologically normal subjects despite hospital exposure but rose markedly in patients with illnesses of varying severity. This increased prevalence was not correlated with antibiotic administration or inhalation therapy, was not dependent on duration of hospitalization and correlated best with the clinical severity of illness. Increased exposure to these organisms alone does not adequately explain these findings, suggesting that pharyngeal clearance mechanisms are impaired in these patients. Since most bacterial pneumonias begin with the aspiration into the lung of bacteria present in the upper respiratory tract, this alteration in the pharyngeal flora of ill patients may represent an important initial step in the pathogenesis of pneumonia due to gram-negative bacilli.

The stress imposed by exercise is usually considered deleterious to patients with cardiopulmonary disorders. For this reason limitation of activity is often recommended for patients with chronic obstructive pulmonary disease. However, Barach and associates 1,2 have repeatedly reported a clinical observation similar to ours, that patients with chronic obstructive pulmonary disease who continue to be active remain in relatively better health for a longer period of time than their more sedentary counterparts. Such observations prompted the present study to assess the physiological responses to progressive exercise training. Methods Patients with severe obstructive pulmonary disease and evidence of generalized physical disability were selected for the study. Patients with manifestations of left ventricular disease were excluded. In addition, patients who developed either multiple premature ventricular contractions or marked cyanosis during exercise were not included in the study. These latter excluded patients, subsequently trained while breathing supplemental oxygen, will form the basis of

CHRONIC, obstructive pulmonary disease is the most frequent cause of physical disability associated with pulmonary disorders. The pathogenesis of disability arising from pulmonary disease can be summarized as follows: either pulmonary ventilatory or circulatory insufficiency may be responsible for exertional dyspnea which, in turn, causes fear and inactivity. Fear, itself, tends to promote further inactivity. Inactivity promotes diminished muscle tone, decreased muscle efficiency, easy fatigability, and progressive physical debility. All of these in turn lead again to more inactivity and exertional dyspnea. Thus a vicious cycle of events is established which eventually leads to even more serious difficulties, such as venostasis with the threat of phlebothrombosis and pulmonary embolization, increased bone resorption which may result in fractures and deformity, and decreased cardiac function. Having recognized the existence of debility, then the need for rehabilitation becomes apparent. The execution of a complete physiological treatment program,' prior to the active physical rehabilitation, must be considered as a prime requisite to a successful rehabilitation program. It is first necessary to improve ventilatory function to an optimum. The initial step consists of removal of all irritants, especially cigarette smoking and other pollutants. The existence of bronchial infection must be identified and treated with appropriate antibiotics. Bronchial edema and bronchospasm can be treated with oral and aerosol bronchodilator agents. When the cause of the obstruction is retained inflammatory exudate or secretions, as is so often the case, then bronchial hygiene becomes essential. The latter is probably the single most neglected aspect of treatment. The methods for achieving effective bronchial hygiene, which have been presented elsewhere,2-5 deserve much more comment than space will permit. Intensive use of saline or detergent aerosols (particularly heated aerosols), deep breathing, rotary postural drainage, with chest clapping or vibration and occasionally potassium iodide as an expectorant, will be necessary. Finally, in those situations where the inflammatory reaction is resistant to protracted and diligent therapy as outlined, the administration of steroids, either orally or by aerosol, may be indicated in order to improve bronchial integrity to an optimum. Patient edqgatiozm is one of the most important components of rehabilitation programs. The patient must be informed concerning the mechanical nature of his disease and the factors responsible for his breathing difficulty. In ventilatory obstructive disease, the work of breathing is done largely in overcoming the resistance to airflow.6 Thus it becomes essential that the patient maintain the slowest feasible respiratory pattern. In addition, because of the tendency for the airways to collapse during rapid ex

Inhalation-therapy equipment incorporating reservoir nebulization was sampled for bacterial contamination during a four-year period after the introduction of routine daily decontamination with 0.25 per cent acetic acid. The incidence of contamination was found to be less than 10 per cent during the last three study years, as compared to 84 per cent before the use of the acetic acid regimen. Residual contamination was related to personnel error or corrosion of nebulizer jets. During the "preacetic acid era" the prevalence of necrotizing pneumonia due to gram-negative bacilli at autopsy was 7.9 per cent, whereas in the last two years studied, the incidence was 2.2 and 2.1 per cent. This prevalence is similar to that found before the use of reservoir nebulizers. These data indicate that daily decontamination of reservoir nebulizer equipment with 0.25 per cent acetic acid is effective and practical in routine hospital use.

Hospital-acquired respiratory infections develop in approximately 5% of patients admitted to a general hospital [1, 2]. In a previous study [3] we analyzed factors predisposing to hospitalacquired necrotizing pneumonia. That study was based on the work of Fraenkel [4], which indicated that Pseudomonas aeruginosa produces a specific necrotizing hemorrhagic pneumonia recognizable by histologic appearance. Subsequently, other investigators have confirmed that such lesions occur in patients dying with gram-negative bacillary pneumonia [5, 6]. However, other histologic descriptions have been reported in pneumonias caused by gram-negative bacilli [7-10], and necrotizing pneumonia has been reported with infection caused by other types of bacteria [11]. The present study was undertaken to define the microbiologic spectrum of necrotizing pneumonia and to determine whether histopathologic criteria are sufficient to make a diagnosis of gramnegative bacillary pneumonia.

The following article on nebulization equipment calls attention to the fact that there is no single simple method of humidification which does not carry at least some risk of contamination. A study is made of several mechanical devices that are in common use and well known by their trade names. It is shown that techniques for decontamination are not equally effective in all cases. Strongly implied is the conclusion that all such pieces of mechanical equipment should in their distribution be accompanied by carefully specified instructions for effective decontamination.—Ed.

Endotracheal tubes have been used with increasing frequency to avoid the use of tracheostomies in patients with respiratory depression. Use of the tubes seems justified in decreasing patient morbidity when an episode of respiratory depression is transient or when episodes of respiratory failure are unlikely to recur. The use of endotracheal tubes, however, may be associated with certain complications with which the attending physician should be familiar.1-5This communication describes one such complication, namely, the tendency of some types of endotracheal tubes to collapse and thus obliterate the lumen when the cuff is excessively inflated. Report of a Case A 42-year-old woman was admitted to a local hospital with a one-week history of increasing cough, yellow sputum, and dyspnea, all of which were unresponsive to antibiotics. She had had a long-standing cough and exertional dyspnea despite a lower lobectomy on the right side in 1960 for bronchiectasis. On examination

Inhalation therapy equipment may potentially act as a vector of hospital-acquired pneumonia due to gram-negative bacilli. The major mechanism by which bacteria are disseminated is aerosolization of organisms in particle sizes that are sufficiently small to be deposited in terminal lung units. Ventilators and humidifiers are relatively innocuous in this regard, and small-volume Venturi nebulizers (medications nebulizers) are not frequently incriminated in nosocomial epidemics. Large-volume nebulizers of all designs (Venturi, spinning disk, or ultrasonic) are the primary source of aerosolized bacteria. The method of decontamination differs with nebulizer design, but any system of decontamination must be carried out at least once every 24 hours while the equipment is in use. No hospital can consider its procedure of decontamination satisfactory unless it has a continuing monitoring program to demonstrate that the degree of contamination does not exceed that of hospital air.