Pulmonary edema in newborns
PathophysiologyLung edema develops as a result of the transfer of protein-rich fluid from the pulmonary capillary system through the endothelium to the interstitial space, exceeding the capacity of the lymphatic system to return it to the venous bed.
The following pathogenetic mechanisms determining the development of pulmonary edema are listed:
Pressure increase in pulmonary capillaries
- Cardiac insufficiency
- Excessive fluid injection
- Pulmonary flow intensification
- Reduction of the blood flow of the lung
Decreased osmotic blood pressure in hypoproteinemia
- Dropsy congenital
- Excessive fluid administration
- Increased protein loss
- Inadequate nutrition
- Lesion of the lymphatic system
- Lesion of the lymphatic system
- Interstitial emphysema
- Bronchopulmonary dysplasia
- High central venous pressure
Damage to the endothelium of the capillaries
- Hyaline-membrane disease
- Toxic oxygen effect
- Pulmonary emboli
Conditions in which increasesintravascular hydraulic pressure or osmotic pressure of blood, cause the transition of fluid from the capillaries to the interstitial spaceGUSTs. Disturbance of lymph drainage or damage to the endothelium of the capillaries also contribute to the development of edema. When the volume of accumulated fluid exceeds the capacity of interstitial, the protein-rich liquid begins to enter the alveoli through the epithelium, which normally limits the passage of the liquid. This sequence of events explains the two main definitions of pulmonary edema: interstitial and alveolar.
In each separate clinical case, several pathogenetic mechanisms can be simultaneously acted upon. For example, preterm infants may have increased pressure in a small circle of circulation, as a result of which fluid is filtered. The cause of this is hypoxia and non-proliferation of the ductus arteriosus. With prematurity, hypoproteinemia is often noted. In addition, oxygen therapy and barotrauma with mechanical ventilation can adversely affect the lymph flow and damage the endothelium of the capillaries.
A number of conditions that cause pulmonary edema are described below. Many of these conditions have similar pathogenetic mechanisms.
Pulmonary edema associated with asphyxiaThere is much in common between the syndromes of TTN, pulmonary edema due to asphyxia and persistent pulmonary hypertension. In addition to the classical weakly expressed form of TTN, Holliday described a severe form associated with perinatal asphyxia, a high oxygen demand( more than 60%), generalized myocardial insufficiency, and echocardiographic signs of pulmonary hypertension in 1981.The pathophysiology of pulmonary edema with perinatal asphyxia is described by Adamson and co-authors. The authors showed that a significant amount of blood plasma passes into the interstitial space. The lymphatic drain increases again and lasts for a long time at a high level, and then gradually decreases in the post-fixation period. Unlike TTN, more active therapeutic measures are required, often mechanical ventilation is required.
Massive hemorrhage to the lungsFrequency .Massive pulmonary hemorrhage occurs with a frequency of 0.2-1.8 per 1000 births. The outcome is almost always lethal;Pulmonary hemorrhage was detected in 9% of cases with pathoanatomical examination. It is described in connection with premature birth, significant prematurity, multiple birth, pelvic presentation of the fetus, caesarean section, rhesus conflict, maternal blood aspiration, perinatal asphyxia, hypothermia, bacterial or viral infection, HMB, toxic oxygen exposure, arterial duct failure, congenital malformationheart, blood clotting disorders and congenital hyperamonia. With these conditions, the frequency of pulmonary hemorrhage increases.
Pathogenesis of .In most cases, massive hemorrhage into the lungs is a form of fulminant hemorrhagic edema with the transition of blood plasma and red blood cells from the capillaries to the alveolar spaces. The most likely cause of increased pressure in the pulmonary capillaries is left ventricular failure in asphyxia. This is facilitated, on the one hand, by factors that cause increased fluid filtration( hypoproteinemia, massive transfusions, surfactant deficiency) and, on the other hand, factors that provoke damage to lung tissue( infection, mechanical ventilation, oxygen therapy).The pressure in the pulmonary capillaries can grow to such an extent and so quickly that bleeding occurs due to rupture of the capillaries. Pathomorphologic hemorrhage may be interstitial( early stage) and alveolar( late stage).
Clinical features of .The catastrophe develops suddenly: the skin is pale, cyanosis of the lips, bradycardia, a drop in blood pressure, apnea. Hemorrhagic edematous fluid, often foamy, with a hematocrit less than 10%, gets into the trachea in almost every second case;this is the most pathognomonic sign. On the roentgenograms, a granular-mesh or large-nodular pattern of the lungs is visible. In severe cases, a homogeneous darkening of both pulmonary fields is observed. These signs of the disease appear within the first 24 hours after birth, and most of the deaths occur 48 hours after birth.
Treatment of .Treatment can be successful if you urgently begin artificial ventilation with high pressure at the end of exhalation and transfusion of fresh blood or freshly frozen plasma. If blood clotting defects are found, appropriate measures are needed. Despite active supportive therapy, the outlook is extremely pessimistic.
Congenital edemaRespiratory distress in congenital edema is due to a number of interacting factors. In many severe cases, it is associated with a deficit of surfactant( premature delivery), in others, the main cause of breathing disorders is pulmonary edema. Anemia and perinatal asphyxia, to which such newborns are predisposed, lead to inadequate heart function. The latter can be complicated by pulmonary edema( the mechanism is described above).To hypostasis predisposes hypoproteinemia, which is closely correlated with the severity of the condition.
Most patients, however, do not have hypervolemia, and phlebotomy is indicated only if central venous pressure remains elevated after resuscitation and metabolic transfusion. These therapeutic measures are aimed at reducing acidosis, hypoxia and anemia.
Functioning arterial ductFrequency .The frequency of the functioning arterial duct( FAP) is inversely related to gestational age and body weight at birth. This pathology is often combined with HMB.FAP is found in only 1 in 2,000 live births. Several medical centers conducted a joint study, which showed that clinically significant FAP is diagnosed in 20% of newborns with birth weight less than 1750 g;this indicator in different clinics varied within 11-36%.
Pathogenesis of .The mechanisms that determine the closure of the arterial duct at birth in full-term newborns, and the reasons for the delay in the preterm are not fully understood.
The initial functional closure of the duct is due to the contraction of its smooth muscles. This is followed by a stage of final closure, during which the endothelium is destroyed, the cells underneath it proliferate, the connective tissue develops and the lumen grows. In preterm, the muscular membrane of the duct is weakly expressed, the subendothelial layer, obliterating the lumen into the constriction phase, may be absent, and the inner elastic membrane remains intact, all this leads to a prolonged functioning of the duct. The tonus of the arterial duct is determined by the ratio of contractile( for example, oxygen) and relaxing effects. The functioning of the duct in prematurity occurs, apparently, due to the hypersensitivity of this vessel to prostaglandins, and not to a decrease in the response to oxygen.
Clinical picture of .The most common symptom is systolic or persistent cardiac noise, which is heard over the entire front surface of the chest. However, according to Valdes, published in 1981, heart murmur is heard only in 50% of newborns with an open arterial duct. Pathophysiological signs of the disease depend on the extent to which the shunting of blood from left to right and changes in the state of the heart and lungs in response to shunting are expressed.
Among the typical symptoms of tachycardia, increased apical impulse, increased pulse pressure or jumping pulse, tachypnea and wheezing in the lungs. Signs of apnea and bradycardia testify to the violation of lung function.
Against the background of mechanical ventilation, newborns often need increased ventilation and increased oxygen supply. X-ray reveals cardiomegaly and signs of pulmonary edema from a moderate decrease in the transparency of pulmonary fields until they are completely darkened.
Diagnosis of .The following echocardiographic parameters are used to assess the cardiac condition in the FAP: the ratio between the diameter of the left atrium and the aortic aorta, the size of the left atrium, the diastolic size of the left ventricle, and the duration of the systolic intervals of the left ventricle. However, echocardiography shows only an increase in the cavities of the heart and indirectly reflects the function of the heart. Limiting the introduction of fluid prevents the expansion of cavities, and auxiliary ventilation reduces pulmonary venous return. Therefore, determining the time interval of systole is the most reliable way to detect hemodynamic disturbances by shunting blood from left to right through the FAP even against the background of mechanical ventilation and restriction of the introduction of fluid.
Treatment of .In cases that do not require auxiliary ventilation, drug treatment is performed until the arterial duct spontaneously closes. When congestive heart failure is limited to the introduction of fluids( up to 75% of the required amount) and, in addition, use diuretics. Slow and careful introduction of erythrocyte mass is necessary to maintain a hematocrit at a level exceeding 40%.
Forecast of .With asymptomatic flow, the condition of newborns with FAP is good even without treatment. However, the FAP worsens and prolongs the course of HMB, so early treatment of FAP with respiratory distress is fully justified. If the duct remains open 3 days after birth( according to contrast echocardiography), the likelihood of a lethal outcome increases, the period of mechanical ventilation lengthens, the risk of bronchopulmonary dysplasia increases. Long-term follow-up of this category of patients did not reveal any late complications of treatment with indomethacin.
Congenital heart defectsSome congenital heart defects manifest in the neonatal period with respiratory disorders, the leading sign of which is congestive heart failure. Congenital cardiac arrhythmias, usually supraventricular tachycardia or complete transverse blockage, can lead to cardiovascular failure immediately after birth. Hypoplasia of the left heart, aortic stenosis, coarctation of the pre-anterior part of the aorta, a common arterial trunk and arteriovenous fistula are common causes of cardiovascular failure in the first week of life. In addition to these reasons, in the later neonatal period, intracardiac shunting of blood from left to right is possible, which manifests itself when the pulmonary vascular resistance decreases. Another group of causes of congestive heart failure that develops at week 2-4 includes so-called white-type defects such as endocardial fibroelastosis, an interventricular septal defect, and blue-type defects such as pulmonary venous return and atresia of the right atrioventriculartricuspid) valve. Serious suspicion of congenital heart disease in newborns with respiratory distress requires appropriate examination and treatment.
Read more about edema of lungs in adults
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