Elective delivery and the neonatal respiratory distress syndrome.

A prospective study was carried out to determine how often moderate or severe respiratory distress syndrome in infants delivered electively after 32 weeks'' gestation or more is avoidable. During a 9-month period 64 such newborns were evaluated. The disease was considered avoidable in 14 (22%) since the indication for elective delivery was questionable. The mean birth weight and gestational age of these 14 infants were 2550 +/- 430 g and 36.3 +/- 1.7 weeks, and the mortality was 14%. This study demonstrated that elective delivery can produce severe neonatal complications, that despite their availability diagnostic tests of fetal age and maturity of the fetal lungs are not being used universally, and that the indications for elective delivery in cases of premature rupture of the membranes must be re-evaluated.     

Prognosis for infants with idiopathic respiratory distress syndrome.

Infants with the idiopathic respiratory distress syndrome admitted to the intensive care unit during January 1972 to September 1974 were reviewed. The overall mortality rate for infants whose birth weight was 1000 g or more was under 10%, and for those who established spontaneous respiration after birth it was less than 5%. The hyperoxia test was not a useful guide to prognosis. It was possible on the basis of the infants'' ability to establish spontaneous ventilation after birth to divide them into two groups. In those who established adequate ventilation the mortality rate was 4-5%; in those who did not it was 57%. This test should be generally applied, since not only does it give an immediate guide to the severity of the disease, which is better than that provided by birth weight, gestational age, or the hyperoxia test, but it may be applied to infants born in and outside a hospital providing neonatal intensive care. Improvement in the outlook for infants with a bad prognosis will be achieved only by improvements in perinatal care designed to minimize severe intrapartum asphyxia in infants of low birth weight.     

Acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) can be associated with various disorders. Among these, coronavirus infection may cause life-threatening severe acute respiratory syndrome (SARS). In this review, we present animal models and techniques for the study of ARDS, and discuss the roles and possible mechanisms of various chemical factors, including nitric oxide (NO). Our early work revealed that cerebral compression elicits severe hemorrhagic pulmonary edema (PE), leading to central sympathetic activation that results in systemic vasoconstriction. The consequence of systemic vasoconstriction is volume and pressure loading in the pulmonary circulation. Vasodilators, but not oxidant radical scavengers, are effective in the prevention of centrogenic PE. In isolated perfused lung, exogenous and endogenous NO enhances lung injury following air embolism and ischemia/reperfusion. In contrast, NO synthase (NOS) inhibitors reverse such lung injury. Although NO is important in maintaining vasodilator tone, hypoxia-induced pulmonary vasoconstriction is accompanied by an increase instead of a decrease in NO release. In animal and isolated lung studies, endotoxin produces acute lung injury that is associated with increases in cytokines and inducible NOS mRNA expression, suggesting that NO is toxic to the lung in endotoxin shock. Recently, we reported several rare cases that indicate that ARDS in patients with Japanese B encephalitis, lymphangitis with breast cancer and fat embolism is caused by different mechanisms. Our early and recent studies on ARDS and PE may provide information for clinical practice and the understanding of the pathogenesis of SARS.     

Adult respiratory distress syndrome in Leptospira canicola infection.

A man was admitted to the Johannesburg Hospital with a history of fever, diarrhoea, and dry cough for four days. He began to produce bloodstained sputum and was found to have severe arterial hypoxaemia. Radiography showed widespread opacification over both lung fields, and the clinical and haemodynamic features were consistent with the adult respiratory distress syndrome. Serology for Leptospira canicola was positive. Despite antibiotics, supportive therapy, and ventilation the patient died. Necropsy excluded cardiac disease. This case shows that leptospirosis may cause the adult respiratory distress syndrome.     

Chemokines in acute respiratory distress syndrome

A characteristic feature of all inflammatory disorders is the excessive recruitment of leukocytes to the site of inflammation. The loss of control in trafficking these cells contributes to inflammatory diseases. Leukocyte recruitment is a well-orchestrated process that includes several protein families including the large cytokine subfamily of chemotactic cytokines, the chemokines. Chemokines and their receptors are involved in the pathogenesis of several diseases. Acute lung injury that clinically manifests as acute respiratory distress syndrome (ARDS) is caused by an uncontrolled systemic inflammatory response resulting from clinical events including major surgery, trauma, multiple transfusions, severe burns, pancreatitis, and sepsis. Systemic inflammatory response syndrome involves activation of alveolar macrophages and sequestered neutrophils in the lung. The clinical hallmarks of ARDS are severe hypoxemia, diffuse bilateral pulmonary infiltrates, and normal intracardiac filling pressures. The magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ARDS. Recent evidence shows that activated leukocytes and chemokines play a key role in the pathogenesis of ARDS. The expanding number of antagonists of chemokine receptors for inflammatory disorders may hold promise for new medicines to combat ARDS.