SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Seven episodes of adult respiratory distress syndrome, occurring in leukemic patients with longstanding (average 11 days) and severe neutropenia (less than 0.1 x 10(9)/1) are described. Pathological and clinical data give further support to the view that the complement-neutrophil pathway is not the only mechanism in generating clinical ARDS in leukemia patients.
An animal model of respiratory distress syndrome (RDS) was made with homologous bone marrow extraction in dogs, which had a similar alter to clinic ARDS patients in blood gases, chest X-ray films and pulmonary pathologic findings. Its pathogenetic key point was extensive pulmonary fat emboli, while active oxygen and neutrophil elastase also play an important role in it. Our results indicate that this model is a rather better one, and anisodamine has some therapeutic effects on the experimental RDS model.
Despite extensive investigation, the pathogenesis of the adult respiratory distress syndrome (ARDS) remains uncertain. As yet, there is no clear explanation of why some patients at risk for ARDS develop the syndrome, whereas others do not. Neutrophils and complement fragments have been implicated in the acute lung injury, but it is clear from published data that evidence of complement activation alone predicts neither the development nor the severity of ARDS. We investigated whether the combination of endotoxin, a leukocyte-priming agent, and complement fragments, leukocyte-stimulating agents, was associated with the development of ARDS. Ninety-eight patients were identified as being either at risk for the development of ARDS or having ARDS, and serial blood samples were obtained. There was no correlation between C5 fragments and the development of ARDS. C3 fragment levels were increased in 89% of the patients with ARDS, but they were also increased in 62% of patients at risk. Endotoxin was detected in 74% of the plasma samples obtained from patients at risk who subsequent developed ARDS and in 64% of the plasma samples obtained from the patients with ARDS. In contrast, only 22% of the plasma samples obtained from the patients at risk who did not develop ARDS had measurable endotoxin. We suggest that the combination of endotoxin and complement fragments may be one mechanism involved in the development of ARDS.
In three cases of pulmonary tuberculosis associated with the adult respiratory distress syndrome the clinical features, which were similar to those of patients with miliary tuberculosis and adult respiratory distress syndrome, included a history of cough, fever, and dyspnoea on effort, and the physical signs of fever, tachypnoea, pulmonary adventitious sounds, tachycardia, and hepatomegaly. In these cases the radiological features, though suggestive of diffuse pulmonary oedema, were more prominent on the side in which the cavitatory lesion appeared. The diagnosis of tuberculosis was made easily from direct examination of sputum. Despite early ventilatory support and antituberculous therapy, two of the three patients died. Postmortem examination of the lungs in these cases showed evidence of acute alveolar damage (loss of type 1 pneumocytes and the presence of hyaline membranes within alveolar ducts) and of chronic alveolar damage (interstitial and alveolar fibrosis).
A case of gonococcal septicemia with monoarticular arthritis and adult respiratory distress syndrome is presented. Prompt treatment of the infection and early treatment for the adult respiratory distress syndrome prior to the full development of the syndrome appeared to ameliorate the course of illness to the extent that intubation and mechanical ventilation were not required. The patient was successfully traeted in a community hospital with a relatively short course of therapy and full recovery.
Lambs suffering from Acute Respiratory Distress Syndrome (ARDS) showed elevated PCV, neutrophilia, a tendency towards lymphopenia, eosinopenia, hyperphosphatemia, hypoglycemia and extremely low serum Ca values during the first couple of days after the outbreak of symptoms. During the very early phase, plasma potassium values were mostly lowered (Figs. 1-3, Table I). The possible involvement of histamine is shortly discussed: either 1) through an atopic reaction, 2) because of acute ruminal acidosis and sudden histamine formation, or 3) involvement of endotoxins.
To further understanding of the epidemiology of acute respiratory distress syndrome (ARDS), we prospectively identified 695 patients admitted to our intensive care units from 1983 through 1985 meeting criteria for seven clinical risks, and followed them for development of ARDS and eventual outcome. ARDS occurred in 179 of the 695 patients (26%). The highest incidence of ARDS occurred in patients with sepsis syndrome (75 of 176; 43%) and those with multiple emergency transfusions (> or = 15 units in 24 h) (46 of 115; 40%). Of patients with multiple trauma, 69 of 271 (25%) developed ARDS. If any two clinical risks for trauma were present, the incidence of ARDS was 23 of 57, or 40%. During the study period, we identified 48 patients with ARDS who did not have one of the defined clinical risks, yielding a sensitivity of 79% (179 of 227). Secondary factors associated with increased risk for ARDS in clinical risk subgroups include an elevated Acute Physiologic and Chronic Health Evaluation II (APACHE II) score in patients with sepsis and increased APACHE II and Injury Severity Scores (ISS) in trauma victims. Mortality was threefold higher when ARDS was present (62%) than among patients with clinical risks who did not develop ARDS (19%; p < 0.05). The difference in mortality if ARDS developed was particularly striking in patients with trauma (56% versus 13%), but less in those with sepsis (69% versus 49%). The mortality data should be interpreted with caution, since the fatality rate in ARDS patients appears to have decreased in our institution from the time that these data were collected.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: To evaluate the effects of surfactant replacement therapy on the pulmonary artery pressure in infants with respiratory distress syndrome. DESIGN: Nonrandomized, "before-after" trial. SETTING: Neonatal intensive care unit at a referral center. PARTICIPANTS: Ten preterm infants with respiratory distress syndrome. INTERVENTIONS: Administration of two or four doses of an exogenous synthetic surfactant at 12-hour intervals. MEASUREMENTS AND RESULTS: Systolic pulmonary artery pressure was estimated by measuring tricuspid regurgitant flow velocity with the Doppler method before and, on average, 45 minutes after administration of synthetic surfactant. Measurable recordings were technically obtainable on 18 of 23 occasions. Surfactant instillation decreased pulmonary artery pressure significantly on 17 of 18 occasions, but did not change the systemic blood pressure. Twelve hours after surfactant treatment, pulmonary artery pressure measured on nine occasions returned to the pretreatment level. No change in the velocity or magnitude of the ductal left-to-right shunting due to exogenous surfactant was found. CONCLUSIONS: Synthetic surfactant replacement therapy in infants with respiratory distress syndrome induces a significant, but transient decrease in systolic pulmonary artery pressure with no effect on the ductal shunt.
In several species prostaglandin E2 (PGE2) appears to be the most important prostanoid to regulate patency of the ductus arteriosus. We measured the arterial plasma concentration of PGE2 in 29 premature infants (17 with respiratory distress syndrome alone and 12 with respiratory distress syndrome and patent ductus arteriosus) to determine if there was an association between circulating PGE2 and patent ductus arteriosus. The PGE2 concentrations during the first two days after birth were higher than PGE2 concentrations after the third postnatal day (17.1 +/- 3.1 pg/ml, mean +/- SEM, n = 23, vs 6.12 +/- 0.63 pg/ml, n = 19, P < .005). By the third postnatal day, arterial concentrations were similar to adult venous values. There was no significant difference between the plasma PGE2 concentrations in the 12 infants with patent ductus arteriosus and the concentrations in the 17 infants who had no signs of patent ductus arteriosus. These findings do not support the hypothesis that an increased concentration of circulating PGE2 is the primary cause for the persistent patency of the ductus arteriosus in preterm infants with respiratory distress syndrome.
Aspirin has been reported to induce the adult respiratory distress syndrome (ARDS) in humans. The mechanism of injury appears to be similar to other forms of experimentally induced high-permeability edema in which leukocytes play an important role. In a patient who suffered two episodes of aspirin-related ARDS, bronchoalveolar lavage showed a significant influx of leukocytes. This represents the first reported bronchoalveolar lavage in aspirin-related ARDS, as well as the first documentation of the nonhydrostatic nature of the edema in a patient with recurrence of this entity.
Long-term follow-up of 9 survivors of the adult respiratory distress syndrome at 39 to 83 months demonstrated 2 patients with continued improvement of their restrictive pattern, 3 patients with stable mild obstructive disease, one patient who had had chronic obstructive pulmonary disease before the adult respiratory distress syndrome with continued pulmonary deterioration, and 4 patients without symptoms and with normal pulmonary function tests. Attention is drawn to bronchial reactivity as defined by a bronchodilator response of more than 60 per cent increase in maximal mid-expiratory flow, positive methacholine challenge, or development of bronchospasm after exercise in 3 patients having clinical symptoms of wheezing on recovery.
Prone position ventilation (PPV) became an effective method of management of ARDS since 1974. Its positive effects on arterial oxygenation have been amply described, but its impact on the results of treatment and hospital mortality remains a disputable point. We observed 2 groups of patients, 36 pts. each, with ARDS after cardiovascular surgery. The main causes of ARDS were shock syndrome, massive blood loss and transfusion, previous COPD, and postcardiopulmonary bypass ALI. Because of impaired lung function (PaO2/FiO2 < 200), all patients were supported by special methods of ventilation including PEEP, high FiO2, and PCV with inverse I:E ratio. In the main group, PPV was started on days 3.6 +/- 1.2 postoperation. Daily duration of PPV was 4-12 h, after which the patients were turned into a supine position. Controls were treated in a supine position. The groups were identical by age, sex, types of surgery, severity of ARF, and manifestations of MOSF. PPV improved lung function and arterial oxygenation. Clinical outcomes were better in the PPV group than in the controls: a lower frequency of threatening arrhythmia, better results of MOSF treatment, and lower mortality (69 and 33.4%, respectively). Prone position is an effective measure improving arterial oxygenation in patients with ARDS after cardiovascular surgery. The main results of PPV are decrease in complications induced by hypoxia and higher survival rate.
This hypothesis for the aetiology of the idiopathic respiratory distress syndrome of the newborn (IRDS) proposes that, although the aetiology is multifactorial, the factor of prime importance is the mobilization of substrate for surfactant synthesis. All factors known to influence the incidence, treatment, and prognosis of the IRDS can be shown to be associated with the mobilization of substrate and thereafter its continued availability for the synthesis of adequate surfactant. Thus factors which promote an antenatal increase in the breakdown of energy stores will be associated with a reduced incidence of the IRDS. On the other hand, despite adequate mobilization, factors associated with a lack of substrate secondary to poor transport of substrate, a reduction in pulmonary circulation or an alteration in fetal or neonatal metabolism which involves an increased utilization of substrate to provide energy, will be associated with an increased incidence of the IRDS.
Eleven patients with suspected adult respiratory distress syndrome (ARDS) and five control patients were studied using a computerized gamma imaging and analysis technique and 99mTc-labeled human serum albumin. The heart and right lung were imaged, lung:heart ratio was plotted vs. time, and a linear regression was fitted to the data points displayed. The slope of this fit was termed the "slope index." An index value of 2 standard deviations greater than the control mean was considered positive. Radiographs from the six positive studies revealed typical diffuse air-space disease. Radiographs from two of the five negative studies demonstrated air-space consolidation. Both of these patients had elevated pulmonary capillary wedge pressure, cardiomegaly, and clinical course consistent with cardiogenic pulmonary edema. These preliminary data demonstrated a good correlation between positive slope index and clinical ARDS.
Surfactant replacement for respiratory distress syndrome (RDS) following very prolonged rupture of the membranes (PROM) is of uncertain value. Seven preterm babies born after PROM (median 48 days, range 22-61 days) were compared with 14 babies without PROM. All had clinical and radiological evidence of severe RDS, requiring mechanical ventilation with inspired oxygen concentrations greater than or equal to 60%. Indices of oxygenation and "compliance" were compared before and serially up to 4 h after surfactant treatment. Before treatment the PROM babies had more severe lung disease, based upon higher inspired oxygen concentration and mean airway pressure, and lower arterial/alveolar oxygen tension ratio and ventilator efficiency index. These indices were significantly worse in the PROM group than the comparison group at all times after treatment. The poor response of the PROM group, perhaps because of pulmonary hypoplasia, suggests that surfactant replacement may not be beneficial for RDS in these babies.
Acute respiratory distress syndrome (ARDS) remains a significant cause of morbidity and mortality in surgical intensive care unit patients. A relatively predictable sequence of pathophysiologic events occur in the lung, which involve inflammatory mediators and neutrophils. The characteristic radiographic findings of ARDS may mimic ventilator-associated pneumonia (VAP), making the diagnosis of VAP difficult. The standard clinical criteria of fever, leukocytosis, purulent sputum, and infiltrate on chest radiograph are not specific for pneumonia in the surgical patient. The use of bronchoscopy with bronchoalveolar lavage and quantitative cultures can differentiate local and systemic inflammatory response to injury or blood loss from invasive bacterial pneumonia. Basing antibiotic therapy solely on the results of quantitative cultures is safe, because quantitative cultures identify VAP in less than half the patients with clinical evidence of pneumonia. Empiric therapy should be based on the microbiology of the intensive care unit rather than the results of the Gram stain.
Reports on thyroid function in newborns with respiratory distress syndrome (RDS) are controversial, the significance of obtained results is not clear. Therefore we conducted a longitudinal study of thyroid function in 35 infants with RDS (gestational age 24-36 weeks, birth weights 650-2770 g). 43 well prematures, matched for gestational age, served as controls. No significant differences were observed in cord blood TSH, T3, T4, TBG values and T4:TBG ratios between infants with and without RDS. Prematures with RDS showed lower levels of T3, T4, TBG and T4:TBG at 24 hours of age and increases of TSH values at 72 hours. Subsequently these prematures exhibited a spontaneous rise in thyroid hormone levels. Even non-surviving RDS-infants had initial T3, T4, T4:TBG and TSH values within the normal range. Thyroid hormone concentrations correlated significantly with the severity of pulmonary disease. Depressed thyroid hormone levels were found to be the result and not the cause of RDS. T4 or T3 therapy is not warranted in this condition.
Acute respiratory distress syndrome (ARDS) is a condition characterized by a high permeability oedema due to loss of the integrity of the alveolo-capillary barrier with impairment of normal surfactant function, resulting in an increased collapse tendency of the alveoli. Mechanical ventilation on such alveoli with repeated alveolar collapse and subsequent reexpansion results in severe lung parenchymal injury and may induce further surfactant impairment. This cam be prevented by maintaining alveolar volume at end-expiration by means of sufficient levels of positive end-expiratory pressure (PEEP). Recent evidence from experimental studies has shown that ventilator modes which allow end-expiratory collapse can induce bacterial translocation from the lung into the bloodstream and trigger the release of inflammatory mediators, which can also be presented by maintaining end-expiratory alveolar volume. These data suggest that the interaction between surfactant changes and mechanical ventilation may play a role in the transition of ARDS into the systematic inflammatory disease process of multiple system organ failure (MSOF).