Infants pulmonary

In 1959, surfactant deficiency was identified as the major pathogenic factor in respiratory distress syndrome in infants. Pulmonary surfactant is a complex mixture of phospholipids, neutral lipids, and specific proteins which spread as a monolayer at the air-liquid... 

Inhaled NO has been used for treatment of persistent pulmonary hypertension of newborn infants, critical respiratory failure of preterm infants, and acute hypertension of adult cardiac surgery patients. PDE-5 inhibitors such as sildenafil are also effective for treatment of pulmonary hypertension. The combination of PDE-5 and NO inhalation yields additive beneficial effects on pulmonary hemodynamics. On the other hand, measurement of exhaled NO is a noninvasive and reproducible test that is a surrogate measure of airway inflammation in patients with bronchial asthma. 

Infant respiratory distress syndrome (IRDS), also known as hyaline membrane disease, is one of the most common causes of respiratory disease in premature infants. In fact, it occurs in 30,000 to 50,000 newborns per year in the U.S. — most commonly in neonates bom before week 25 of gestation. IRDS is characterized by areas of atelectasis, hemorrhagic edema, and the formation of hyaline membranes within the alveoli. IRDS is caused by a deficiency of pulmonary surfactant. Alveolar type II cells, which produce surfactant, do not begin to mature until weeks 25 to 28 of... 

Antioxidant therapy might be promising medication for the treatment of some lung disorders. For example, lecithinized phosphatidylcholine-CuZnSOD suppressed the development of bleomycin-induced pulmonary fibrosis in mice [284] these findings could be of relevance for the treatment of bleomycin-stimulated pulmonary fibrosis in humans. Davis et al. [285] recently demonstrated that the treatment of premature infants with recombinant human CuZnSOD may reduce early pulmonary injury. 

Infantile, generalized cardiomegalic AMD, or Pompe s disease, usually becomes manifest in the first weeks or months of life, with failure to thrive, poor suck, generalized hypotonia and weakness, also termed floppy infant syndrome. Macroglossia is common, as is hepatomegaly, which, however, is rarely severe. There is massive cardio-megaly, with congestive heart failure. Weak respiratory muscles make these infants susceptible to pulmonary infection death usually occurs before the age of 1 year and invariably before the age of 2 years [6]. 

No major teratogenic effects have been identified with the SSRIs or TCAs. However, evaluations to date suggest a possible association of fluoxetine with low birth weight and respiratory distress. Another study reported a sixfold greater likelihood of the occurrence of persistent pulmonary hypertension of newborn infants exposed to an SSRI after the twentieth week of gestation. 

Local administration of NO to the lungs has been shown to reverse pulmonary hypertension in animal models [103], importantly with no systemic side effects. This is likely to be as a result of surplus NO being removed as nitrosyl-hemoglobin [104]. Such advantages of gaseous NO were first reported in 1991 [105, 106]. In 1999 and 2001 NO gas was approved as a drug in the USA and European Union, for treating hypoxemic respiratory failure in infants [107]. 

Cystic fibrosis (CF) is a hereditary disease of abnormal fluid secretion. It affects cells of the exocrine glands, such as intestine, sweat glands, pancreas, reproductive tract, and especially the respiratory tract. The disease affects about 1 in 2500 infants of the Caucasian population to varying degrees of seriousness. Patients produce thickened mucus that is difficult to get out of the airway. This leads to chronic lung infection, which progressively destroys pulmonary function. 

A liposomal formulation containing a surfactant, which usually coats the mucosa of the bronehi and prevents a collapse of the alveolar vesieles of the lung, has been developed for patients who suffer from infant respiratory distress syndrome (IRDS) or adult-aequired respiratory distress syndrome (ARDS). Premature babies often suffer IRDS before the development of a funetional lung surfaetant and pulmonary gas exehange. ARDS is also a life-threatening failure and loss of the lung function and is usually acquired by illness or accident. Clinieal trials with liposomal surfactant have proved to be effective in prophylaetie treatment of IRDS and ARDS. 

Cardiovascular - Benign intracranial hypertension (pseudotumor cerebri) has been reported rarely. Bulging fontanels, as a sign of benign intracranial hypertension in infants, have been reported rarely. Changes in electrocardiogram (eg, nonspecific ST/T wave changes, bundle branch block) have been reported in association with pulmonary reactions. 

Aerosol - Several serious adverse events occurred in severely ill infants with life-threatening underlying diseases, many of whom required assisted ventilation. Additional reports of worsening of respiratory status, bronchospasm, pulmonary edema, hypoventilation, cyanosis, dyspnea, bacterial pneumonia, pneumothorax, apnea, atelectasis, and ventilator dependence have occurred. Sudden deterioration of respiratory function has been associated with initiation of aerosolized ribavirin use in infants. If ribavirin aerosol treatment produces sudden deterioration of respiratory function, stop treatment and reinstitute only with extreme caution, continuous monitoring, and consideration of coadministration of bronchodilators. 

Etzel, R. A., Montana, E., Sorensen, W. G., Kullman, G. J., Allan, T. M., and Dearborn, D. G. (1998). Acute pulmonary hemorrhage in infants associated with exposure to Stachybotrys atra and other fungi. Arch. Pediutr. Adolesc. Med. 152, 757-762. 

Most adverse effects associated with aerosol ribavirin are local. Pulmonary function may decline if aerosol ribavirin is used in adults with chronic obstructive lung disease or asthma. Deterioration of pulmonary and cardiovascular function has also been seen in severely ill infants given this preparation. Rash, conjunctivitis, and rare cases of anemia have been reported. Health care workers exposed to aerosol ribavirin during its adminis-... 

The toxicity of di(2-ethylhexyl) phthalate was evaluated in 28 term infants with respiratory failure, 18 of whom received extracorporeal membrane oxygenation (ECMO) and were compared with 10 untreated infants. Various clinical parameters of liver, pulmonary and cardiac dysfunction were found to be unaffected in treated infants, even though the rate of administration ranged up to 2 mg/kg bw di(2-ethylhexyl) phthalate over 3-10 days (mean peak plasma concentration, 8 pg/mL). ECMO is considered to be the clinical intervention that results in the highest intravenous dose of di(2-ethylhexyl) phthalate (Karle et al., 1997). 

Nishizuka, Y., Nakakuki, K., and Sakakura, T. (1964). Induction of pulmonary tumors and leukemia by a single injection of 4-nitroquinoline 1-oxide to newborn and infant mice, Garm 55,495. 

Pulmonary diseases Aspiration pneumonia, bronchial asthma, prevention of infant respiratory distress syndrome, sarcoidosis... 

Mitochondrial P oxidation of fatty acids is the principal source of energy for the heart. Consequently, inherited defects of fatty acid oxidation or of carnitine-assisted transport often appear as serious heart disease (inherited cardiomyopathy). These may involve heart failure, pulmonary edema, or sudden infant death. 

Bizzarre M, Gross I, Bizzarre M. Inhaled nitric oxide for the postoperative management of pulmonary hypertension in infants and children with congenital heart disease. Cochrane Database Syst Rev. 2005 CD005055. 

Tolazoline is similar to phentolamine. Tolazoline has very limited clinical application in the treatment of pulmonary hypertension in newborn infants with respiratory distress syndrome. Its efficacy in this condition is doubtful, and the drug is rarely used. 

Hepatonephritis and pulmonary edema were reported as causes of fetal death. The presence of PCE in breast milk was the cited reason for obstructive jaundice in a 6-week old infant (ref. 35. P 303). A study by Schwetz et al. (ref. 68) indicates that PCE may be teratogenic. Delayed skull-bone ossification and split stembrae were observed in mice, as well as increased fetal resorption, decreased fetal body weight and fetal subcutaneous edema. 

It is known that 02 is potentially toxic as was evident in premature infants where it caused retrolental fibroplasia (2) or in artificial ventilation where it caused pulmonary lesions (3) because of the formation of ROS. 

Roth B, Herkenrath P, Lehmann H-J, et al. 1988. Di-(2-ethylhexyl)-phthalate as plasticizer in PVC respiratory tubing systems Indications of hazardous effects on pulmonary function in mechanically ventilated, preterm infants. Eur J Pediatr 147 41-46. 

Tang, J. R., Markham, N. E., Lin, Y. J., McMurtry, I. F., Maxey, A., et al. 2004. Inhaled nitric oxide attenuates pulmonary hypertension and improves lung growth in infant rats after neonatal treatment with a VEGF receptor inhibitor. Am. J. Physiol. Lung Cell Mol. Physiol. 287 L344— L351. 

Salanitre E Rackow H (1969) The pulmonary exchange of nitrous oxide and halothane in infants and children. Anesthesiology, 30(4) 388-394. 

The clinical concentration exceeds the actual intraalveolar concentration that might be expected during therapy, because the material is diluted in situ by the liquid in the air spaces and their surfaces [65]. Other information gives some indication of the surfactant concentration in the normal lungs. The concentration in normal foetal pulmonary liquid [66] and the concentration required to restore alveolar function to immature neonatal infants and lambs [67] change from about 0.5 to 1.8 mg PL cm 3. These concentrations are close but slightly higher than both C, and just above C,. 

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