Prolonged Oxygen Therapy Research Articles

Letters to the Editor

As Dr Sweet states "knowledge of the etiology and pathogenesis of retrolental fibroplasia (RLF) is far from complete." While recent studies have shown that prolonged oxygen therapy with the associated difficulties in monitoring Pao2 may be more important than short-term hyperoxia in placing an infant at risk of developing RLF, the conclusion of authors of the cooperative study1 quoted by Dr Sweet was that the occurrence of RLF was unrelated to Pao2, "as determined by the limited information available from intermittent sampling" and that conservative administration of oxygen may have been responsible for failure to demonstrate quantitative association between Pao2 levels and disease.

The lung and oxygen toxicity

Within just a short time after the discovery of oxygen 200 years ago, Joseph Priestley, one of its codiscoverers, was already cautioning that oxygen "might burn the candle of life too quickly, and too soon exhaust the animal powers within."¹Priestley's prescient speculations about the toxic nature of excess O₂. have been confirmed by a host of succeeding investigators. Today, most clinicians are well aware of the toxic consequences to the lung of prolonged exposure to high tensions of O₂, yet physicians involved in intensive care are frequently confronted by situations in which prolonged hyperoxic therapy is a necessary part of the management of neonatal and adult patients with severe respiratory distress. Unfortunately, no pharmacological agent is available to help circumvent the development of pulmonary toxicity associated with prolonged high oxygen therapy. The spectrum of O₂-induced lung injury, including pulmonary edema, atelectasis, consolidation, congestion, hemorrhage,

The Lung and Oxygen Toxicity

Within just a short time after the discovery of oxygen 200 years ago, Joseph Priestley, one of its codiscoverers, was already cautioning that oxygen "might burn the candle of life too quickly, and too soon exhaust the animal powers within."¹Priestley's prescient speculations about the toxic nature of excess O₂. have been confirmed by a host of succeeding investigators. Today, most clinicians are well aware of the toxic consequences to the lung of prolonged exposure to high tensions of O₂, yet physicians involved in intensive care are frequently confronted by situations in which prolonged hyperoxic therapy is a necessary part of the management of neonatal and adult patients with severe respiratory distress. Unfortunately, no pharmacological agent is available to help circumvent the development of pulmonary toxicity associated with prolonged high oxygen therapy. The spectrum of O₂-induced lung injury, including pulmonary edema, atelectasis, consolidation, congestion, hemorrhage,

Postoperative arterial hypoxaemia.

Postoperative arterial oxygen tension was measured in a group of patients. Unacceptably low levels were found in 32% of the patients and this hypoxaemia persisted in some cases for three days. The results enforce the principle that some patients whould be given prolonged oxygen therapy and this should cease only when blood gas analysis demonstrate the patients ability to maintain a safe PaO2 breathing air.

Microbial Flora of the Larynx, Trachea, and Large Intestine of the Rat after Long-term Inhalation of 100 Per Cent Oxygen

Effects of long-term inhalation of 100 per cent oxygen on the microbial flora of the rat larynx, trachea, and large intestine were studies. Rats were kept 14 days in an atmosphere of 100 per cent oxygen after being conditioned to high oxygen concentrations by exposure to three cycles of 100 per cent oxygen (two days) alternating with 40 percent oxygen (two days). Controls were kept under similar conditions in normal atmosphere. Rats were sacrificed, and at necropsy laryngotracheal swabs and fecal material from the large intestine were obtained and cultured for bacteria and fungi. Streptobacillus moniliformis, the predominant microorganism in the upper tracheas of controls, was not isolated from the oxygen-treated rats. Alpha-hemolytic streptococcus and Staphylococcus albus were present in control rats, but were found less frequently in rats exposed to oxygen. Pseudomonas and Proteus, infrequently isolated from controls, were predominant and sometimes the only microorganisms isolated from oxygen-treated rats. The data indicate that prolonged exposure of the rat to 100 per cent oxygen shifts the microbial flora in the upper respiratory tract from mainly gram-positive to mainly gram-negative bacteria. In contrast, there was no significant difference between the microbial flora in large intestines of control and oxygen-treated rats. The possibility that similar changes may occur in man should be considered when prolonged oxygen therapy is contemplated.

Ideas and anomalies in the evolution of modern oxygen therapy.

Ideas and anomalies in the evolution of modern oxygen therapy.

Progressive Impairment of Pulmonary Antibacterial Defense Mechanisms Associated with Prolonged Oxygen Administration.

Meeting Abstracts1 May 1970Progressive Impairment of Pulmonary Antibacterial Defense Mechanisms Associated with Prolonged Oxygen Administration.Gary L. Huber, M.D., F. Marc LaForce, M.D.Gary L. Huber, M.D.Search for more papers by this author, F. Marc LaForce, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-72-5-808_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe lung is the primary target organ for normobaric oxygen toxicity. In addition, pulmonary bacterial infection is a frequent complication of prolonged oxygen therapy. A progressive, dose-related deterioration in pulmonary antibacterial defense mechanisms was induced in 215 laboratory mice by exposure to oxygen tensions of 650 mm Hg for 12, 24, 48, 72 and 96 hr. An additional 65 mice, maintained in atmospheric air (oxygen tension: 140 mm Hg), were used as controls. An aerosol inoculum of radiotracer tagged (32P)Staphylococcus aureus(FDA 209P, type 42D) was delivered to oxygen treated and control animals for 30 min. The animals were... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Boston, Mass. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPulmonary Oxygen ToxicityConcanavalin A distribution in polymorphonuclear leukocytes and alveolar macrophages during hyperoxiaFunctional activities of alveolar macrophages in rat exposed to hyperoxia (normobaric O2)Pulmonary Oxygen ToxicityBlood loss and factors affecting pulmonary antibacterial defensesDehydration and factors affecting pulmonary antibacterial defenses 1 May 1970Volume 72, Issue 5Page: 808-808KeywordsFood and Drug AdministrationLungsOxygenPulmonary diseasesResearch laboratoriesStaphylococcus aureusToxicity Issue Published: 1 May 1970 PDF downloadLoading ...

Pulmonary and Respiratory Function Changes in Survivors of Hyaline-Membrane Disease

With the possibility existing that survivors of the respiratory-distress syndrome of the newborn may have lung changes secondary to therapy, chest roentgenograms, PaO 2 and A-a oxygen gradients in 12 selected patients who survived hyaline-membrane disease were observed and measured. Three of four infant survivors had abnormal chest roentgenograms for as long as two years. Abnormally large A-a gradients present at birth became normal by nine months. Five of eight long-term survivors had abnormal chest roentgenograms. This group as a whole had an abnormally low PaO 2 and an increased A-a oxygen gradient. Eight of 14 children born prematurely and who developed retrolental fibroplasia secondary to prolonged oxygen therapy but who had no history of respiratory distress had abnormal chest roentgenograms similar to survivors of hyaline-membrane disease. These similarities suggest that abnormally high inspired oxygen tensions (> 280 mm Hg) cause the long-term changes seen by us in survivors of hyaline-membrane disease.

Clinical evaluation of prolonged ambulatory oxygen therapy in chronic airway obstruction

Abstract Twenty patients with chronic airway obstruction have received continuous portable oxygen therapy on a home basis for from six to twenty-five months; improvement in activity level has been observed in all. Secondary polycythemia has been reversed in those with an elevated hematocrit level. A gain in dry weight was observed in most patients. The data reported suggest that oxygen is safe when used in a controlled fashion by nasal prongs with sufficient flows to bring the arterial oxygen pressure (pO 2 ) to normal. The practicality and economics of continuous home oxygen therapy are discussed.

Radiographic features of pulmonary oxygen toxicity in the newborn: Bronchopulmonary dysplasia.

A new syndrome of pulmonary disease following prolonged oxygen and respirator therapy of the respiratory distress syndrome of the newborn has recently been reported (13). This disease entity has been called bronchopulmonary dysplasia to emphasize the involvement of all the tissues of the developing lung in the pathologic process. It is believed to represent the toxic manifestations of 80–100 per cent oxygen (high O2) on the developing lung superimposed upon the healing phase of respiratory distress syndrome. Based on clinical, radiologic, and pathologic findings, bronchopulmonary dysplasia has been divided into four stages: Stage I: Clinically and radiographically resembles ordinary respiratory distress syndrome except for excessive mucosal necrosis (one to three days of age). Stage II: Characterized by marked radiopacity of the lungs, inability to be weaned from high O2, and cycles of alveolar injury and repair (four to ten days of age). Stage III: Radiographic cystic appearance of the lungs with respiratory mucosal lesions, focal emphysema and persistence of hyaline membranes, and gradual weaning from high O2 (ten to twenty days of age). Stage IV: Symptomatic chronic lung disease predominant, with strands of pulmonary parenchymal density, increased thoracic volume, and cardiomegaly which may gradually clear or progress to cor pulmonale and death (beyond one month of age). This communication documents in greater detail the characteristic radiographic evolution of the pulmonary changes seen in this syndrome. Clinical Findings The 32 patients presented in the original report represented all the infants with severe respiratory distress syndrome, but without serious congenital abnormalities, who required twenty-four hours or more of continuous intermittent positive pressure respiration with high O2 as a lifesaving measure at the Stanford Premature Infant Research Center from September 1962 to November 1965. The patients selected for respirator therapy had failed to respond to more conservative therapy (antibiotics, control of body temperature, intravenous glucose and sodium bicarbonate to combat acidosis) and were cyanotic in 100 per cent oxygen, appeared moribund, and had undergone one or more prolonged apneic spells. The appearance of chronic lung disease—the late stage of bronchopulmonary dysplasia—was seen in only those infants who received more than six days (one hundred and fifty hours) of continuous high O2 therapy and lived longer than four weeks. Of the 13 infants treated with high O2 in excess of six days, 9 lived beyond four weeks of age. All 9 demonstrated prolonged pulmonary disease with cyanosis when crying or out of supplemental O2, and fine, diffuse râles were heard throughout the lungs or at the lung bases. Five of these infants died with cardiac enlargement and cor pulmonale between one and eleven months of age.

OXYGEN THERAPY IN THE NEWBORN

The only satisfactory method of managing oxygen therapy for respiratory-distress syndrome (R.D.S.) is to measure the PaO2. 370 babies have had serial arterial blood-gas tensions measured: 203 of them had R.D.S. The mortality for R.D.S. was 32.5% with a low incidence of cerebral palsy and only two significant cases of retrolental fibroplasia despite prolonged oxygen therapy at concentrations of greater than 40% in many survivors. The normal PaO2 increases from 69 mm. Hg six hours after birth to 90 mm. Hg at forty-eight hours. Umbilical arterial catheterisation provides a convenient technique for sampling arterial blood but because of the existence of significant net right-to-left ductus arteriosus shunts, preductal sampling may be advisable to prevent retinal PaO2 reaching the probable danger level of 160 mm. Hg. A simpler and probably acceptable alternative is to maintain the lower abdominal aorta Po2 between 60 and 90 mm. Hg.

Changes in lung volume, diffusing capacity, and blood gases in men breathing oxygen.

Changes in lung volume, diffusing capacity, and blood gases in men breathing oxygen.