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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Environmental lung injury may take the form of acute tracheobronchitis, asthma, pulmonary edema, chronic bronchitis, emphysema, allergic pneumonitis, fibrosing alveolitis, pleurisy, and neoplastic disease. Environmental factors eliciting these responses include irritant gases and fumes, oxidants, organic allergens, inorganic dust, bacterial enzymes, and high partial pressures of oxygen. The basic pulmonary reactions to these toxic agents--bronchoconstriction, vasoconstriction, increased vascular permeability, inflammation, carcinogenesis--may be mediated, aggravated, or modulated by biologically active substances. These humoral agents include biogenic amines (e.g. histamine): peptides (e.g., bradykinin, vasoactive intestinal peptide, and spasmogenic lung peptide); enzymes (e.g., proteases, superoxide dismutase, and mixed function oxidases); and acidic lipids (e.g., prostaglandins, prostaglandin endoperoxides, and thromboxanes).
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PMID:Environmental injury of the lung: role of humoral mediators. 35 83

Progressive pulmonary insufficiency appears to be a universal response to the lung to a variety of injuries which damage the pulmonary-capillary emdothelium. Persistent hyperventilation, unresponsive to the administration of oxygen, is the earliest clinical sign of this complication of trauma and should prompt close monitoring of pulmonary function (measurement of arterial blood gas and pH levels, Vd/Vt A-aDo2, minute ventilation, vital capacity and inspiratory force) to assess the severity of the disease, the need for mechanical ventilatory support and the effectiveness of treatment. Other pulmonary complications of burn injury range from carbon monoxide poisoning and narcotics overdosage in the immediate postburn period through marked hyperventilation directly related to burn size occurring in the absence of significant parenchymal change to later occurring hematogenous and airborne pneumonia. Inhalation injury, a chemical tracheobronchitis which significantly increases the mortality of a given-sized burn, may be present immediately postburn but clinically inapparent for 48-72 hours. 133Xenon lung scans permit early diagnosis of this pulmonary injury and the timely institution of a graduated therapeutic response keyed to the severity of pulmonary disability. Knowledge of the pathogenesis of each of these complications is requisite for the physician caring for burn patients and permits the employment of rational preventive and therapeutic measures.
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PMID:Progressive pulmonary insufficiency and other pulmonary complications of thermal injury. 109 77

Graded concentrations of oxygen were used to establish dose-duration relations for the effect of oxygen on tracheal mucous velocity and tracheobronchial histologic findings in the anesthetized dog. Observations of tracheal mucous velocity were made during 30-hour periods of breathing air (100-percent humidified and warmed to 38 degrees C) and oxygen mixtures (also 100-percent humidified and warmed to 38 degrees C). In animals breathing oxygen mixtures, the baseline tracheal mucous velocity was taken as the value while breathing room air at the experiment's start. No statistically significant differences in tracheal mucous velocity occurred during air breathing. Tracheal mucous velocity fell 45 percent from the baseline value after breathing 100-percent oxygen for two hours (P less than 0.01), fell 42 percent after 75-percent oxygen for nine hours (P less than 0.01) and fell 51 percent after 50-percent oxygen for 30 hours (P less than 0.001). Histologic examination of the trachea and major bronchi after six hours of 100-percent oxygen and 12 hours of 75-percent oxygen revealed signs of acute tracheobronchitis. Minor histologic alterations in the tracheobronchial tree occurred both in animals breathing air and 50-percent oxygen for 30 hours; therefore, histologic evidence of oxygen toxicity could not be established at 30 hours. These findings indicate that in the anesthetized dog, oxygen depresses mucous transport as a function of inspired oxygen concentration (FIO2) and that even FIO2 as low as 0.05 might be deleterious.
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PMID:Effect of oxygen in graded concentrations upon tracheal mucous velocity. A study in anesthetized dogs. 124 69

Laryngotracheobronchial lesions were carefully documented in 26 neonatal autopsies and were classified into two main types. Type I lesions were focal desquamative or ulcerative, asynchronous, and variable in severity involving areas exposed to contact with endotracheal tube or suction catheter. These lesions are most likely due to trauma of artificial ventilation. Type II lesions were diffuse, necrotizing, more synchronous and uniform in severity involving tissues distal to the endotracheal tube and extending to second or third generation bronchi. The early or mild type II lesions consisted of coagulative necrosis of epithelial cells and mucosal oedema. The late or severe type II lesions showed features similar to those of necrotizing tracheobronchitis described by Metley et al. All the cases with type II lesions had been ventilated with 100 per cent oxygen continuously for at least 3 h during life. The use of pure oxygen may be an important factor leading to necrotizing tracheobronchitis.
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PMID:The histopathology of the upper airway in the neonate following mechanical ventilation. 320 50

This report describes a newly recognized iatrogenic lesion in newborns that we have termed necrotizing tracheobronchitis (NTB). Although it is related to assisted ventilation, it is different from previously described tracheal lesions in that it is most severe distal to the tip of the endotracheal tube and manifests a characteristic basophilic necrosis of the tracheal mucosa. Sloughing of tracheal mucosa, which occurs in the later stages, can cause respiratory obstruction. The lesion occurs over a wide range of gestational ages and birth weights as well as ventilatory rates, pressures, and supplemental oxygen concentrations. The severity of the lesion is related to the duration of ventilation. We believe NTB to be related to airflow through the endotracheal tube rather than to the effects of the tube itself because the lesion is worst beyond the end of the tube and extends into the major bronchi. A grading system is presented.
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PMID:Necrotizing tracheobronchitis in intubated newborns: a complication of assisted ventilation. 344 16

To compare high-frequency jet ventilation (HFJV) with pressure-limited time-cycled conventional ventilation (CV), we randomized 41 infants with clinical and radiographic evidence of respiratory distress syndrome during the first day of life to receive either HFJV or CV. Standardized ventilatory protocols were used for 48 hours, after which CV was administered to both groups. Despite comparable oxygenation (arterial/alveolar oxygen tension ratio), mean airway pressure was lower in the HFJV group (9 +/- 2 vs 13 +/- 2 cm H2O, P less than 0.001), and thus the arterial/alveolar oxygen tension ratio corrected for mean airway pressure was improved in the HFJV group (P less than 0.05). PaCO2 was lower during HFJV (37 +/- 3 vs 42 +/- 3 mm Hg, P less than 0.05) despite a comparable peak inspiratory pressure. The incidence of air leaks, progression of intraventricular hemorrhage, and mortality during the 48-hour period did not differ between the two groups. Bronchoscopies in eight infants given HFJV and five given CV revealed no microscopic evidence of necrotizing tracheobronchitis, but one infant given HFJV had evidence of necrotizing tracheitis at autopsy. We conclude that for 48 hours during the acute stage of respiratory distress syndrome, HFJV can maintain adequate gas exchange at lower mean airway pressure than during CV, without an increase in the incidence of side effects.
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PMID:Randomized trial of high-frequency jet ventilation versus conventional ventilation in respiratory distress syndrome. 354 78

The case report of a fatal result in an abortion requested because X-ray diagnostic studies of the gallbladder and intestine had been made during an undiagnosed early pregnancy is presented. A uterine vacuum aspirator had not been purchased by the hospital. A portable laboratory vacuum pump with an appropriate suction trap was used. The apparatus had been used previously in several abortion cases. After dilatation of the cervix and insertion of the aspirating cannula, the pump was turned on. A sudden massive effusion of bloody froth issued from around the cannula. The cannula was removed immediately. It was found that the tubing had been incorrectly connected. The aspirator tube was connected with the pressure outlet of the pump. The tubing was then correctly placed and the uterus emptied. The patient was given succinyl choline, intubated, placed in the Trendelenburg position, and monitored cardiographically. About 30 seconds after the uterine insufflation blood pressure became unobtainable. The pulse slowed to 50 beats/minute and respiration diminished. Cardiac ausculation revealed no sounds. Respiration was maintained using oxygen through an endoctracheal tube. The pulse was still palpable and the EKG showed abnormal QRS complexes. Cyanosis then became evident. Closed chest cardiac massage was used for 1 minute but the patient became pulseless and QRS complexes were bizarre. Then the chest was opened and each ventricle was needled. From each ventricle of the distended heart air hissed under pressure through the needle vent site. The ascending aorta was needled and air escaped under pressure. Cardiac color and action improved when aided by massage. Iv isoproterenol and intracardiac epinephrine were given. An electric defibrillator converted the cardiac rhythm to a sinus rhythm. Norepinephirne brought about hypertension. Blood and albumin were given iv. The patient never regained consciousness. Tracheostomy and a feeding gastrostomy were required. Urinary and respiratory infections followed and the patient died after 2 1/2 months. Autopsy revealed tracheobronchitis, bronchopneumonia, and pulmonary edema. The brain showed extensive cerebral cortical necrosis. The heart was normal. This maternal death was preventable.
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PMID:Air embolism and maternal death from therapeutic abortion. 502 50

Because of the complex composition of smoke generated during fires and the possible combination of inhalation injury with other pulmonary complications of burns, the clinical course of inhalation injury is variable. Because clinical manifestations may be delayed several hours and furthermore are not specific, fiberoptic bronchoscopy is most appropriate in diagnosing pulmonary injury at the time of admission. Dominating pathological feature is a membraneous tracheobronchitis. Acute airway occlusion with sloughed bronchial mucosa, oedema formation and pulmonary infection are the most common complications. Treatment includes administration of oxygen, use of bronchodilators, and, when necessary, mechanical ventilation. Supplemental oxygen delivered at high concentrations will increase CO elimination and should be administered to all patients until the blood level of carboxyhaemoglobin has been measured.
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PMID:[Inhalation injury of the lung]. 649 86

Four patients with cardiorespiratory failure caused by secondary kyphoscoliosis were studied. Polycythemia, cor pulmonale, restrictive lung pattern (functional residual capacity (FRC), 17 to 27% predicted; vital capacity (VC), 11 to 23% predicted), and abnormal arterial blood gases, primarily hypoventilation (PaO2, 31 to 44 mm Hg; PaCO2, 52 to 73 mm Hg), were seen in all. Supplementary oxygen, digoxin, diuretics, 15 min of intermittent positive-pressure breathing with inspired pressure (PI) 25 cm H2O 4 times daily, and tracheostomy failed to produce improvement. However, 12 h of nighttime ventilation (NTV) with PI 28 to 35 cm H2O through a permanent tracheostomy proved effective. Within 72 h, dyspnea at rest, restless sleep, and frequent waking resolved. Within 8 to 22 days, the PaO2 was approximately 58 mmHg and the PaCO2 was approximately 41 mm Hg while breathing 21% oxygen spontaneously during the day. The right heart failure resolved within 2 to 7 wk, and the hemoglobin count decreased to approximately 165 g/L within 2 to 6 months. There was a mean increase of 700 ml (72%) in functional residual capacity and 430 ml (49%) in vital capacity. The patients were discharged 2 days to 5 wk after NTV commenced. Daytime activity increased, approaching a normal life style. The improvement was sustained over a mean follow-up period of 3.4 yr. Problems included recurrent episodes of tracheobronchitis, mild self-limiting hemoptysis, and speech modification. Nighttime ventilation may be an effective alternative for long-term treatment of cardiorespiratory failure caused by secondary kyphoscoliosis.
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PMID:Nighttime ventilation improves respiratory failure in secondary kyphoscoliosis. 669 24

Smoke inhalation injury is a complex of disease processes best understood and treated when defined in terms of the time period after injury. The early phase (0 to 36 hrs) is characterized by diagnosis and treatment of carbon monoxide and cyanide toxicity and by management of early airways edema, bronchorrhea, and bronchoconstriction with aggressive pulmonary toilet. Between 1 and 5 days, the major characteristic is airways mucosal slough, tracheobronchitis, and increasing lung water and impaired gas exchange. Pulmonary toilet and infection control, as well as close management of fluid shifts, is the major treatment. With onset of the inflammation-infection phase, the risk of nosocomial pneumonia increases markedly, as does the impairment in lung function as a result of marked increase in oxygen consumption and CO2 production. Nutrition, stress modification, avoidance of muscle fatigue, and control of infection are the key treatment modalities.
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PMID:Smoke inhalation injury. 792 21


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