Indications for flexible versus rigid bronchoscopy in children with suspected foreign-body aspiration.
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Biomedical subjects
Publications and source records attributed to U B Prakash.
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OBJECTIVE: To analyze the clinical and pathologic features of biopsy-proven pulmonary hamartomas at a tertiary referral center. DESIGN: We retrospectively reviewed institutional data on pulmonary hamartomas for a 17-year study period. MATERIAL AND METHODS: The Mayo Clinic computerized medical records database was searched for patients who had biopsy, excision, or autopsy diagnosis of pulmonary hamartomas from 1976 through 1992. Medical records and all available histologic sections were reviewed. RESULTS: Of the 215 patients with histologically confirmed pulmonary hamartoma, 141 were men and 74 were women (approximately a 2:1 ratio). Two hundred eight patients were asymptomatic, 54 of whom were undergoing assessment for a comorbid disease process. Only four patients had new onset of respiratory symptoms. The peak incidence of occurrence was in the seventh decade of life. The mean size of the hamartomas were 1.5 cm (range, 0.2 to 6.0); no lobe was predominantly involved. Most hamartomas were resected by simple or wedge excision. Sixty-three patients (29.3%) had a concurrent neoplasm (most commonly, lung carcinoma). Follow-up ranged from 2 to 192 months (mean, 61). Eight postoperative deaths occurred. No recurrent pulmonary hamartomas developed. In one patient, lung carcinoma developed 33 months after excision of a hamartoma. In a second patient, sputum cytologic findings were abnormal 9 years later. A third patient had biopsy-proven adenocarcinoma metastatic to bone and an indeterminate lung nodule 2 years after resection of a pulmonary hamartoma. CONCLUSIONS: Pulmonary hamartomas are benign lung neoplasms that, in our referral population occurred most commonly in asymptomatic older men. A substantial number of our patients had concurrent neoplasms; however, many had been referred for cancer treatment. We found no evidence of either a malignant transformation or an unexplained association with other lung neoplasms.
Thoracic endoscopy encompasses bronchoscopy, esophagoscopy, laryngoscopy, mediastinoscopy, and thoracoscopy (pleuroscopy). In this article, the role of documentation as it applies to bronchoscopy is discussed. However, the discussion is generally applicable to other thoracic endoscopy procedures.
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This study was designed to characterize the clinical spectrum and course of tracheobronchial involvement in Wegener's granulomatosis (WG). Of the 51 patients with biopsy-proven WG who underwent bronchoscopy at least once at our institution between January 1982 and November 1993, 30 (59%) had endobronchial abnormalities due to WG. Initial findings included subglottic stenosis in five (17%), ulcerating tracheobronchitis with or without inflammatory pseudotumors in 18 (60%), tracheal or bronchial stenosis without inflammation in four (13%), and hemorrhage without identifiable source in two (4%) patients. Nine patients with ulcerating tracheobronchitis on initial study had subsequent bronchoscopies for continued symptoms, which in seven cases documented the progression from ulcerating tracheobronchitis to stenosis without inflammation. Bronchoscopic interventions included dilation by rigid bronchoscope in three, YAG-laser treatment in one, and placement of silastic airway stents in three patients. Only the stents provided persistent airway patency. Endobronchial biopsies were performed on 21 occasions in 17 patients. Half of the specimens were helpful in establishing the diagnosis and in all but three in assessing disease activity. While antineutrophil cytoplasmic antibody titers reflect overall disease activity, no correlation with endobronchial inflammatory activity was apparent.
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The pathogenesis of ruptured intracranial aneurysms and cervical artery dissections is poorly understood but may be similar in these two disorders. We report four patients with alpha 1-antitrypsin deficiency who developed a ruptured intracranial aneurysm or spontaneous dissection of the cervical internal carotid artery. Three patients were heterozygous for the deficient allele (PiMZ or PiGZ) and one was homozygous (PiZZ). A deficiency of alpha 1-antitrypsin or one of the other protease inhibitors could result in degradation of the arterial wall through an imbalance between proteolytic enzymes and their inhibitors, thereby predisposing the arterial wall to dissection or aneurysm formation.
OBJECTIVE: To elucidate the putative arteriopathy associated with alpha 1-antitrypsin (alpha 1-AT) deficiency. DESIGN: We retrospectively studied the frequency of occurrence of fibromuscular dysplasia (FMD) in patients with alpha 1-AT deficiency in whom a postmortem examination had been done during a 10-year period at the Mayo Clinic. MATERIAL AND METHODS: The medical records of all patients in whom an autopsy was done at the Mayo Clinic between 1983 and 1992 were reviewed to identify all those with a diagnosis of alpha 1-AT deficiency or FMD. RESULTS: Arterial FMD was found in 2 of 6 patients with alpha 1-AT deficiency (33.3%; 95% confidence interval, 4.3 to 77.7%) in comparison with 23 of 6,690 patients without alpha 1-AT deficiency (0.3%; 95% confidence interval, 0.2 to 0.5%). In both patients with alpha 1-AT deficiency and FMD, the arterial media was thickened and composed of irregular arrays of muscular and connective tissue fibers in a background of mucoid ground substance. CONCLUSION: These findings provide further evidence for an underlying arteriopathy in patients with alpha 1-AT deficiency and suggest that FMD may be a non-specific disorder.
The ventriculoatrial shunt (VAS) was developed to control hydrocephalic syndromes effectively. Several complications, however, have been described after the procedure. One of the most serious consequences is the development of severe pulmonary hypertension attributed to multiple and recurrent pulmonary embolization caused by the catheter of the VAS; however, the frequency is exceedingly low. Herein we describe the experience with three patients in whom severe pulmonary hypertension developed after a VAS procedure. In two patients, refractory heart failure developed, an outcome that caused death within a brief period. The third patient underwent atrial thrombectomy and then pulmonary thromboendarterectomy; recovery was complete. Scientific evidence shows that initial embolization predisposes pulmonary vessels to develop further in situ thrombosis; thus, the vascular lung disease progresses despite removal of the embolic source. A review of the literature revealed that in patients with a VAS, pulmonary embolism and pulmonary hypertension were clinically diagnosed in only 0.4% and 0.3% of the cases, respectively, whereas postmortem diagnoses of pulmonary embolism and pulmonary hypertension were established in 59.7% and 6.3%, respectively. These discrepancies point out the difficulty of establishing the diagnosis of these serious pulmonary vascular complications while the patient is alive.
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The flexible and rigid bronchoscopes traverse the nasopharynx or oropharynx and carry with them the indigenous microbial flora to distal regions and may thus inoculate the tracheobronchial tree and possibly the pulmonary parenchyma. The three potential consequences of this event include: (1) onset of new infection in the tracheobronchial tree or lung parenchyma or, if the patient has preexisting infection, further spread of infection locally or to extrapulmonary sites; (2) spread of infection from one patient to another via the bronchoscope, if the methods of disinfection and sterilization are inadequate; and (3) pseudoinfection due to cross-contamination of the bronchoscope, resulting in isolation of organisms from the bronchoscopic specimens of a patient who is clinically not infected. Review of the literature indicates that the last-mentioned consequence is more commonly encountered in clinical practice. The occurrence of pseudoinfection inevitably leads to costly and time-consuming procedures to guarantee that the patients are not infected. Rigorous adherence to sterilization and disinfection procedures and a common sense approach to protecting the uninfected patients and bronchoscopy personnel from infected patients and instruments will prevent the risk of propagating infection through the bronchoscope. This can be accomplished by establishing a set of policies regarding disinfection, sterilization, and protection of uninfected patients, as well as the bronchoscopist and paramedical personnel involved in bronchoscopy.
Patients with mixed connective tissue disease (MCTD) exhibit clinical features of systemic lupus erythematosus (SLE), progressive systemic sclerosis or scleroderma (PSS), and polymyositis-dermatomyositis (PM-DM). In their sera is an unusually high titer of a circulating antinuclear antibody with specificity for a nuclear ribonucleoprotein antigen. Pleuropulmonary manifestations are common in MCTD and the incidence varies from 20% to 85%. The pleuropulmonary complications include pleural effusion, interstitial pulmonary processes, pulmonary arterial hypertension (PAH), pulmonary vasculitis, pulmonary thromboembolic phenomena, aspiration pneumonia, and hypoventilatory failure. Pulmonary vascular pathology with progressive PAH and cor pulmonale is the most serious complication of MCTD. The pleuropulmonary manifestations in MCTD are similar to the respiratory problems well recorded in SLE, PSS, and PM-DM. Even though the pleuropulmonary complications are common in MCTD, they may remain clinically inapparent until fatal complications ensue.
In 35 cases of pulmonary blastomycosis, the roentgenologic features were as follows: consolidation 26%, mass 31%, intermediate-sized nodules 6%, miliary pattern 11%, solitary cavity 9%, fibrotic and cavitary changes 6%, interstitial pattern 6%, diffuse alveolar involvement 3%, and mixed alveolar and interstitial infiltrate 3%. All symptomatic cases of consolidation were acute (symptoms for less than 1 month), and most were in young patients (mean age, 34 years). Consolidation constituted 58% of the acute cases in this series. Two of the nine cases of consolidation were asymptomatic epidemic cases detected by screening. A pulmonary mass was the most common initial manifestation in this series; it tended to occur in patients with chronic symptoms (more than 1 month). The mass was considered suggestive enough of bronchogenic carcinoma to necessitate resection in 55% of cases. The military form of pulmonary blastomycosis occurred in older patients with disseminated disease. Fibrotic and cavitary disease was chronic in nature. The presence of intermediate-sized nodules elsewhere in the lung proved to be a helpful diagnostic finding in several patients with consolidation, mass, or cavitary disease. Hilar adenopathy, postinfectious calcification, chest wall invasion, and pleural effusion occurred infrequently or not at all in this series.
Endoscopic esophageal variceal sclerotherapy (EVS) is often used in the treatment of upper gastrointestinal hemorrhage due to esophageal varices. We retrospectively reviewed the Mayo Clinic experience with EVS between 1980 and 1989 to determine the incidence of thoracic manifestations and chest roentgenographic abnormalities associated with this procedure. The study population consisted of 223 patients who underwent 390 EVS procedures. In all patients, chest roentgenography was done before and after EVS. Ethanolamine oleate or tetradecyl sulfate was used as the sclerosant. Fever, chest pain, and odynophagia were frequent findings after EVS and tended to be short-lived. Local complications at the site of injection, such as esophageal perforation (in 1% of EVS procedures) and abscess (in 0.3%), were infrequent but associated with substantial mortality. Esophageal stricture was noted as a late complication in less than 10% of patients, and clinically recognized aspiration pneumonitis was rare. Respiratory insufficiency developed after 14 EVS procedures. Chest roentgenographic abnormalities, which were commonly detected (after 85% of EVS procedures) but were rarely of clinical significance, included retrocardiac or mediastinal widening or densities (in 35%), pleural effusions (in 27%), atelectasis (in 12%), and pulmonary infiltrates (in 9%). Most thoracic manifestations after EVS are likely due to a local inflammatory response to the sclerosant.
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