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External respiration; Newborn; Infant; Congenital heart abnormalities; Congenital pulmonary abnormalities

Introduction

External breathing in infants usually indicates a serious medical condition. It is not uncommon in newborns. Improvements are usually seen over the next few days, and the baby becomes as saturated with room air as normal. Rarely, extrapulmonary respiration on day 1 or 2 may be associated with massive extrapulmonary aortic outflow with still high pulmonary vascular resistance [1]. For example, there are congenital anomalies such as large arteriovenous fistulas in the brain, so-called galenic fistulas, and sometimes in the liver. In some cases, newborns may develop heart failure due to ventricular or “pump failure” resulting from underlying cardiomyopathy or acute myocarditis. Persistent ductus arteriosus patency can delay the onset of external respiration in ductus arteriosus-dependent systemic circulation, such as stenosis in the absence of early ventricular decompensation and severe aortic stenosis [2]. If the ducts begin to close, the baby may experience external breathing due to obstructed ventricular dysfunction, and rapid closure of the ducts can even cause cardiogenic shock. In contrast, ambulatory-dependent pulmonary circuits, pulmonary atresia or severe Fallot syndrome tend to be associated with early cyanosis [3]. External respiration resulting from communication between the systemic and pulmonary circulation may take time to develop. High pulmonary vascular resistance in neonates limits left-to-right shunting, for example due to large ventricular septal defects or patent ductus arteriosus. As a result, tachypnea in such infants is usually delayed beyond the first 1-2 weeks of life [4].

Rarely, metabolic causes can cause acidosis, which can occur during the extrarespiratory period in neonates after acidosis begins with the onset of oral feeding. In some cases, acidosis can be due to renal failure, such as renal dysplasia. Aspiration of meconium, blood, or milk, severe pneumothorax, or underlying dilating lesions such as congenital cystic adenomatous malformation (CCAM) or diaphragmatic hernia can cause premature external respiration. However, central diaphragmatic events rarely occur in the neonatal period, but may occur later with external respiration and cyanosis [5].

Usually, by the end of the first week, and in some cases he is out of breath for the second week, due to the above causes. If the disease persists, diagnosis is usually made by clinical signs and tests, such as a chest x-ray, a detailed cross-sectional echocardiogram, and relevant blood tests. After the first week of life, however, some babies exhibit external respiration that persists or develops beyond the neonatal period. In some cases, there may be significant clinical signs, but in others there may be minimal or subtle signs, or no signs other than exhalation. How to proceed The purpose of this article is to discuss the many causes of external respiration beyond the neonatal period, ranging from those requiring early surgical intervention to those requiring only continuous observation [6].

Polycythaemia

External breathing in infants usually indicates a serious medical condition. It is not uncommon in newborns. Hyaline membrane disease in preterm infants, transient external respiration (TTN) in neonates, and respiratory distress syndrome (RDS) caused by meconium aspiration often result in varying degrees of external respiration. Breathing assistance may be required as oxygen levels in the environment increase [7]. There is usually an improvement over the next few days, and the baby begins to breathe room air as usual. Rarely, extrapulmonary breathing on day 1 or 2 may be accompanied by massive extrapulmonary aortic outflow with still high pulmonary vascular resistance. For example, large arteriovenous fistulas in the brain, so-called galenic fistulas, and in some cases congenital anomalies such as the liver. Occasionally, neonates develop heart failure due to ventricular failure or “pump failure” caused by cardiomyopathy or acute myocarditis. Persistent patency of the ductus arteriosus may delay the onset of external respiration in the ductus arteriosus-dependent systemic circulation, including: B. Stenosis without early ventricular decompensation and severe aortic stenosis. If the ducts begin to close, ventricular insufficiency can cause the baby to breathe outside, and rapid closure of the ducts can also cause cardiogenic shock. In contrast, hospital-dependent pulmonary circulation, pulmonary atresia, or severe Fallot syndrome tend to be associated with early cyanosis. External respiration, caused by communication between the systemic and pulmonary circulation, may take time to develop. Due to the high pulmonary vascular resistance in neonates, left-to-right shunting is limited by large ventricular septal defects and patent ductus arteriosus. Therefore, such tachypnea in infants usually occurs after the first week or two of life [8].

Rarely, metabolic causes can cause acidosis, which can occur in neonates during the extrarespiratory period after acidosis begins with the onset of oral feeding. In some cases, acidosis can be due to renal failure, such as renal dysplasia. Meconium, blood, or milk aspiration, severe pneumothorax, or occult dilating lesions such as congenital cystic adenomatous malformation (CCAM) or diaphragmatic hernia can cause premature external respiration. However, central diaphragmatic events rarely occur in the neonatal period, but may occur later with external respiration and cyanosis [9].

It is normal for the above reasons to cause shortness of breath at the end of the first week, but in some cases it may still occur during the second week. If the disease persists, diagnosis is usually based on clinical signs and tests, such as: Chest radiograph, detailed crosssectional echocardiogram, and relevant blood tests. After the first week of life, however, some babies exhibit external respiration that continues or develops beyond the neonatal period. In some cases, there may be significant clinical signs, while in others there may be minimal or subtle signs or no signs other than exhalation. The purpose of this article is to discuss the many causes of external respiration beyond the neonatal period, ranging from those requiring early surgical intervention to those requiring only continuous observation [10].

Discussion

Interstitial lung disease and atypical infections, such as B. pneumocystis jirovezi (PJP), are rare causes of external respiration. Shortness of breath is usually pronounced and accompanied by a need for additional oxygen. Chest radiographs often show extensive alveolar or interstitial changes. A chest CT scan and bronchoscopy are usually required. A lung biopsy or genetic testing is often needed to confirm the presence or type of interstitial lung disease. PJP is rare in immunocompetent infants and is diagnosed by PCR of bronchoalveolar lavage.

Some of the causes of external respiration in early infancy have been discussed above. Then, what is the explanation for Baby A’s gradual improvement in external respiration, which then became sporadic, and finally slowed down around 2 months of age? There were no abnormal findings other than external respiration. He ate well, had good weight gain, and had normal growth. Vomiting did not occur unless the milk flowed out of the bottle too quickly. Despite his mother having gestational diabetes, his neonatal period was uneventful except for a short period of time immediately after his birth when he externally breathed. A previous chest x-ray was normal, and a repeat electrocardiogram and echocardiogram were normal to ensure nothing was missed the first time. The baby has been fine since then. It is possible that baby A had a silent aspiration, but this seemed unlikely because she was neurologically intact and had an exposed chest. Furthermore, his early onset, normal oxygen saturation, and normal chest radiograph tended to rule out disorders such as infantile neuroendocrine hyperplasia and pulmonary interstitial glycogenesis. .

For unknown reasons, is the respiratory center slightly elevated in infants like Baby A? As it matures over several months, the center is “reset”, external respiration ceases, and respiratory rate returns to normal levels. If external respiration had stopped, further investigation would certainly have been required. Further research is needed to clarify the basis of external respiration in infants like Baby A, which may avoid concerns and the need for extensive investigation.

Conclusion

There are serious causes that can cause persistent external respiration in early infancy, forewarned by prior fetal examinations and confirmed by subsequent clinical examination and appropriate evaluation, but may be associated with symptoms. In addition, there is another group of infants who present with clinically subtle symptoms. Signs may indicate external breathing. Again, if a serious cause is suspected, additional investigation may lead to a diagnosis. Finally, some infants who are “easily ventilated” spontaneously increase their respiratory rate, do well, have normal examinations, and then gradually taper off over the next several months. . Further research could lead to a better understanding of the causes of their extra-breathing, potentially alleviating existing concerns and avoiding the need for large-scale studies.

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