Persistent pulmonary hypertension of newborns

Persistent pulmonary hypertension of newborns is a persistence or return to the state of constriction of the arterioles of the lungs, which causes a significant decrease in blood flow in the lungs and a right-left discharge of blood. Symptoms and signs include tachypnea, the entrainment of malleable areas of the chest and pronounced cyanosis or a decrease in oxygen saturation that do not respond to oxygen therapy. The diagnosis is based on anamnesis, examination, radiography of the chest and response to the oxygen subsidy. Treatment includes oxygen therapy, the fight against acidosis, nitric oxide or, if not effective drug therapy, extracorporeal membrane oxygenation.

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What causes persistent pulmonary hypertension in newborns?

Persistent pulmonary hypertension of newborns (PGHN) is a violation of the vascularization of the lungs, which is observed in full-term and transferred infants. The most common causes are perinatal asphyxia or hypoxia (in the anamnesis often the meconial staining of amniotic fluid or meconium in the trachea); hypoxia provokes a return or persistence of a pronounced restriction of arterioles in the lungs, which is normal in the fetus. Additional reasons are premature closure of the arterial duct or oval aperture, which leads to an increase in pulmonary blood flow in the fetus and can be provoked by the mother's intake of NSAIDs; polycythemia, in which the flow of blood is disturbed; congenital diaphragmatic hernia, in which the left lung is significantly hypoplastic, which causes most of the blood to go to the right lung; neonatal sepsis, apparently due to production by activation of the cyclooxygenase pathway with bacterial phospholipids of prostaglandins with a vasoconstrictor effect. For any reason, high blood pressure in the pulmonary artery causes abnormal development and hypertrophy of the smooth muscles of the walls of pulmonary arteries of small caliber and arterioles, as well as right-left blood discharge through the arterial duct or oval window, which leads to persistent systemic hypoxemia.

Symptoms of persistent pulmonary hypertension in newborns

Symptoms and signs include tachypnea, the entrainment of malleable areas of the chest and pronounced cyanosis or a decrease in oxygen saturation that do not respond to oxygen therapy. In infants with a right-left shunt through the open arterial flow, oxygenation in the right brachial artery is higher than in the descending aorta; so cyanosis can be different, i.e. Oxygen saturation on the lower limbs is about 5% lower than on the upper right.

Diagnosis of persistent pulmonary hypertension in newborns

The diagnosis should be suspected in any children born on or near the time, who have arterial hypoxemia and / or cyanosis, especially with the appropriate anamnesis, and there is no increase in oxygen saturation with respiration of 100% oxygen. The diagnosis is confirmed by echocardiography with dopplerography, which can confirm an increase in pressure in the pulmonary artery and simultaneously exclude congenital heart disease. In lung radiography, pulmonary fields may be normal or may have changes corresponding to the cause of the disease (meconium aspiration syndrome, neonatal pneumonia, congenital diaphragmatic hernia).

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Treatment of persistent pulmonary hypertension in neonates

Oxygenation Index [average pressure in the airways (see water) oxygen fraction in the inspired air 100 / PaO2] more than 40 is associated with a lethality of more than 50%. The overall lethality varies from 10 to 80% and is directly related to the oxygenation index, and also depends on the cause. In many patients (about 1/3) who have experienced persistent pulmonary hypertension of newborns, developmental delay, hearing impairment and / or functional disorders are noted. The frequency of these disorders may not differ from that in other serious diseases.

The oxygen therapy, which is a potent vasodilator for pulmonary vessels, begins immediately to prevent the progression of the disease. Oxygen is supplied with a bag and mask or with hardware ventilation; mechanical stretching of the alveoli promotes vasodilation. FiO2 in the beginning should be equal to 1, but then it should gradually decrease to maintain Ra between 50 and 90 mm Hg. To minimize lung damage. When PaO2 stabilizes, you can try to take the child off with ventilation, reducing FiO2 by 2-3% at a time, and then reducing the inspiratory pressure; the changes must be gradual, since a significant decrease in PaO2 can again cause the constriction of the pulmonary artery. High-frequency oscillatory ventilation dilates and ventilates the lungs, while minimizing barotrauma, and should be borne in mind for children with lung diseases as causes of persistent pulmonary hypertension in newborns whose atelectasis and incompatibility of ventilation and perfusion (H / P) may exacerbate hypoxemia.

Nitric oxide when inhaled relaxes the smooth muscles of the vessels, expanding pulmonary arterioles, which increases blood flow in the lungs and rapidly improves oxygenation in 1/2 patients. The initial dose is 20 ppm, which then decreases to the required level to maintain the desired effect.

Extracorporeal membrane oxygenation can be used in patients with severe hypoxic respiratory failure, which is defined as an oxygenation index of more than 35-40, despite maximum respiratory support.

Normal levels of fluid, electrolytes, glucose, calcium should be maintained. Children should be in the optimal temperature environment and receive antibiotics before the results of the crop are obtained due to the possible presence of sepsis.