Sahn and Scoggin 1 Sahn SA Scoggin C Fiberoptic bronchoscopy in bronchial asthma: A word of caution. Chest. 1976; 69: 39-42 Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar pointed out a problem which we have been aware of for many years, and that is bronchoscopically induced bronchospasm. We have learned the lesson the hard way also. I would like to point out two features of the problem that these investigators didn't discuss.

Safety, simplicity, and successful results are paramount requirements of any biopsy procedure. This is true especially of patients who are desperately ill, as are many afflicted with pneumonia due to Pneumocystis carinii. Use of very small flexible forceps through a fiberoptic bronchoscope as reported by Scheinhorn, Joyner, and Whitcomb (see page 294) seems to be just such a procedure.This protozoan organism needs to be morphologically identified by staining techniques and cannot be grown on culture medium. Examination of sputum, tracheal and bronchial secretions, and even peripheral bronchial brushings has not been reliable. Examination of pulmonary tissue or touch preparations from tissue has been necessary for dependable results. The quest has been, therefore, to find the safest and simplest method of obtaining pulmonary tissue.Transbronchoscopic lung biopsy using a rigid bronchoscope and a flexible forceps with a cup of approximately 2 by 4 mm dimensions is also a safe and simple procedure. This seems to be a reasonable compromise between the pathologist's insatiable appetite for more tissue (such as the entire lung!) and his frustration with tiny flecks of material. If the small cup on the forceps with a fiberoptic bronchoscope can provide sufficient material, however, this is a very satisfactory method. Complications from either forceps will be less than with any transthoracic method.A word of caution may be in order. Many patients with pneumonia due to Pneumocystis carinii are critically ill and hypoxic prior to bronchoscopy. Use of a fiberoptic bronchoscope transnasally compromises the airway and may produce deepening hypoxia. In such a patient, an intratracheal tube should be used for concomitant administration of oxygen. Use of the rigid bronchoscope also allows for supplemental oxygenation. Although Scheinhorn et al have not encountered the complication of bleeding as yet, this should be an anticipated hazard, which also can be handled very satisfactorily through a rigid bronchoscope. If the endoscopist elects to use the flexible instrument for biopsy, he should have the rigid bronchoscope handy and should be capable of using it for aspiration of blood and for packing the appropriate segmental bronchus with narrow gauze tape should bleeding ensue. Observance of these precautions (supplemental oxygenation and availability of a rigid bronchoscope) makes the “bedside” performance of this type of biopsy inadvisable.The simplicity of the procedure described by Scheinhorn et al appeals to me. I hope that my pathologists will not scream when I send them even smaller bits of tissue than previously. Safety, simplicity, and successful results are paramount requirements of any biopsy procedure. This is true especially of patients who are desperately ill, as are many afflicted with pneumonia due to Pneumocystis carinii. Use of very small flexible forceps through a fiberoptic bronchoscope as reported by Scheinhorn, Joyner, and Whitcomb (see page 294) seems to be just such a procedure. This protozoan organism needs to be morphologically identified by staining techniques and cannot be grown on culture medium. Examination of sputum, tracheal and bronchial secretions, and even peripheral bronchial brushings has not been reliable. Examination of pulmonary tissue or touch preparations from tissue has been necessary for dependable results. The quest has been, therefore, to find the safest and simplest method of obtaining pulmonary tissue. Transbronchoscopic lung biopsy using a rigid bronchoscope and a flexible forceps with a cup of approximately 2 by 4 mm dimensions is also a safe and simple procedure. This seems to be a reasonable compromise between the pathologist's insatiable appetite for more tissue (such as the entire lung!) and his frustration with tiny flecks of material. If the small cup on the forceps with a fiberoptic bronchoscope can provide sufficient material, however, this is a very satisfactory method. Complications from either forceps will be less than with any transthoracic method. A word of caution may be in order. Many patients with pneumonia due to Pneumocystis carinii are critically ill and hypoxic prior to bronchoscopy. Use of a fiberoptic bronchoscope transnasally compromises the airway and may produce deepening hypoxia. In such a patient, an intratracheal tube should be used for concomitant administration of oxygen. Use of the rigid bronchoscope also allows for supplemental oxygenation. Although Scheinhorn et al have not encountered the complication of bleeding as yet, this should be an anticipated hazard, which also can be handled very satisfactorily through a rigid bronchoscope. If the endoscopist elects to use the flexible instrument for biopsy, he should have the rigid bronchoscope handy and should be capable of using it for aspiration of blood and for packing the appropriate segmental bronchus with narrow gauze tape should bleeding ensue. Observance of these precautions (supplemental oxygenation and availability of a rigid bronchoscope) makes the “bedside” performance of this type of biopsy inadvisable. The simplicity of the procedure described by Scheinhorn et al appeals to me. I hope that my pathologists will not scream when I send them even smaller bits of tissue than previously.

A review of 650 cases of pulmonary fungal disease observed at the Mayo Clinic during a ten-year period revealed that the thoracic roentgenogram in pulmonary fungal disease was readily distinguishable from that in classic sarcoidosis. Nevertheless, in order to exclude a mycologic cause, appropriate microbiologic and serologic studies should be performed in every case in which sarcoidosis is suspected or even seems to be established. A review of 650 cases of pulmonary fungal disease observed at the Mayo Clinic during a ten-year period revealed that the thoracic roentgenogram in pulmonary fungal disease was readily distinguishable from that in classic sarcoidosis. Nevertheless, in order to exclude a mycologic cause, appropriate microbiologic and serologic studies should be performed in every case in which sarcoidosis is suspected or even seems to be established.

The records of 81 patients with a roentgenologic pattern of diffuse reticulonodular pulmonary disease and a pathologic diagnosis of chronic interstitial pneumonitis and fibrosis were reviewed. All had restrictive patterns on pulmonary function testing with impairment of CO diffusing capacity. The most common features were characteristic dry rales, digital clubbing, and evidence of altered immune activity. Twenty patients manifested evidence of other disease thought to be of an autoimmune or hypersensitivity nature, with the pulmonary lesion dominating the clinical picture. The concept of "classic interstitial pneumonitis-fibrosis (CIP-F)" as a clinicopathologic syndrome has been proposed with the following categories: (1) definite-complete syndrome with rales, clubbing, and evidence of altered immune activity; (2) probable- rales and clubbing without evidence of altered immune activity; and (3) possible -histopathologic finding with or without evidence of altered immune activity but no rales or clubbing. Some patients progress from possible CIP-F to definite CIP-F; the latter category implies chronicity and commensurately worse prognosis.

Two patients are presented who had spontaneous disappearance of a calcified solitary pulmonary nodule. The mechanism of this uncommon event is unknown, but various theories are discussed. Two patients are presented who had spontaneous disappearance of a calcified solitary pulmonary nodule. The mechanism of this uncommon event is unknown, but various theories are discussed.

In this second segment of our article on pulmonary disease in the immunocompromised host (ICH), we review the infections associated with pulmonary infiltrates in the ICH and the diagnostic approaches for both infectious and noninfectious conditions. Although certain immunologic defects may predispose patients to specific infectious agents, virtually any infectious agent can cause pulmonary disease in any ICH. Physical findings and laboratory observations may give the clinician clues about probable causes of infection. Nevertheless, invasive diagnostic procedures—in particular, open-lung biopsy—are often necessary to diagnose pulmonary disease in the ICH. The relatively new technique of bronchoalveolar lavage is useful in diagnosing pulmonary disease in the patients with acquired immunodeficiency syndrome (AIDS). Further studies are necessary to confirm the reliability of this procedure as a diagnostic method in the ICH who does not have AIDS.

This study was made to determine the value of the esophageal motility test as a diagnostic procedure in cases of thoracic pain. A review was made of the records of 514 patients undergoing studies of esophageal motility at the Mayo Clinic from May, 1957, through April, 1959. From these varied clinical cases, 45 patients with a diagnostic problem of pain in the thorax were found in whom a definitive diagnosis had not been established by means other than the motility test. These 45 patients were found to form four main groups: (1) eight patients without objective evidence of either myocardial ischemia or esophageal motility abnormalities; (2) two patients with objective evidence of myocardial ischemia, but no abnormalities of esophageal motility records; (3) 17 with abnormalities of the esophageal motility records, but no objective evidence of ischemic myocardial disease, and (4) 18 patients with evidence of both abnormal esophageal motility and myocardial ischemia. The abnormal esophageal motility findings in these patients included, in order of frequency, the patterns for diffuse spasm, hiatal hernia, the hypertensive and the hyperreacting gastroesophageal sphincter. Various combinations of these motility disorders were often found in the same patient. The incidence of hypertensive gastroesophageal sphincter was exceedingly high. Clinical differentiation could not be made consistently between the pain of ischemic heart disease and that of esophageal motility disorders. It is recommended that when patients present a diagnostic problem related to pain in the thorax, ischemic heart disease should be excluded even though the presence of esophageal disorders is proved. The electrocardiogram after exercise may be helpful in the evaluation of such patients.

Acid-fast microorganisms with the cultural characteristics of avian tubercle bacilli were isolated from three specimens of sputum and a gastric washing from a patient with silicosis. These organisms were virulent for chickens and rabbits but failed to produce progressive disease in guinea pigs. The infected animals reacted slightly to old tuberculin but severely to avian tuberculin. Additional studies on one culture revealed it to be resistant in vitro to streptomycin, para-aminosalicylic acid and isoniazid, which is typical of avian tubercle bacilli. The patient died of cardiac failure. Sections of lung revealed extensive pneumonoconiosis and fibrosis. Birefringent crystals typical of silica were seen in sections examined with polarized light. It is believed that the avian tubercle bacilli played little part, if any, in the production of pulmonary fibrosis and that these microorganisms were able to proliferate because of the pre-existing silicotic lesions in a host for which avian tubercle bacilli are normally relatively avirulent.