Neonatal persistent pulmonary hypertension

Introduction to neonatal persistent pulmonary hypertension Persistent pu1monary hypotension of newborn (PPHN) refers to the continuous increase of pulmonary vascular resistance after birth, pulmonary artery pressure exceeds systemic arterial pressure, which causes the transition from fetal circulation to normal "adult" type circulatory disorder, resulting in atrial and (or) right-to-left shunt of blood at the level of the arterial catheter, clinical symptoms such as severe hypoxemia. The disease is more common in term infants or expired children. basic knowledge The proportion of illness: 0.003% Susceptible people: infants and young children Mode of infection: non-infectious Complications: heart failure

Causes of persistent pulmonary hypertension in neonates

Intrauterine factors (45%):

Such as uterus - placental insufficiency leading to chronic hypoxia, sputum, no brain, expired production, oligohydramnios syndrome, etc., such as mother taking aspirin or indomethacin during pregnancy.

Childbirth factor (35%):

There are suffocation and inhalation (amniotic fluid, meconium, etc.) syndrome.

Post-delivery factors (20%):

Congenital lung disease, pulmonary dysplasia, including pulmonary parenchyma and pulmonary vascular dysplasia, respiratory distress syndrome (RDS); cardiac insufficiency, etiology including perinatal asphyxia, metabolic disorders, intrauterine catheter closure, etc.; In the case of sepsis, the contraction of the heart caused by bacteria or viruses, endotoxin, etc., pulmonary microvascular thrombosis, increased blood viscosity, pulmonary vasospasm, etc.; central nervous system disorders, neonatal scleredema.

In addition, many chemicals affect the expansion and contraction of blood vessels, and thus are related to the continuous circulation of the fetus. In short, except for a small number of primary pulmonary arterioles, excessive muscle development and loss of relaxation, any other hypoxia and acidosis can lead to increased pulmonary artery pressure. It even leads to a right-to-left shunt of the arterial catheter and the foramen ovale.

Pathogenesis

The decline of pulmonary vascular resistance after birth is an important transition process from intrauterine to extrauterine physiological changes. The pulmonary vascular resistance of normal newborns decreases significantly within 12 to 24 hours after birth, and can be reduced by 80% at 24 hours after birth. In PPHN patients, this There is an obstacle in the transformation process, pulmonary hypertension continues to rise, and there is a right-to-left shunt at the level of the arterial catheter and/or the foramen ovale. The increase in pulmonary artery pressure increases the right ventricular afterload and oxygen consumption, leading to the right ventricle and left ventricle. Posterior wall and right subventricular hypothalamic ischemia, papillary muscle necrosis, tricuspid dysfunction, and finally due to increased right heart load, ventricular septum biased to the left ventricle, affecting left ventricular filling, reducing cardiac output, some children after birth Pulmonary vascular resistance only increased temporarily, and decreased rapidly after the removal of the predisposing factors; however, the vasoconstrictor response of neonatal pulmonary vessels was more obvious than that of adults, and the vascular structure was easily changed under the stimulation of hypoxia, and muscle thickening appeared. Due to these factors, The pulmonary circulation is highly reactive to various stimuli, and sometimes the pulmonary vasospasm cannot be relieved after the factors causing pulmonary vascular response are removed.

There are at least three pathological types in PPHN clinically:

1. Pulmonary vascular hypoplasia (underdevelopment) refers to the airway, the number of alveolar and related arteries decreased, the blood vessel area decreased, the pulmonary vascular resistance increased, can be seen in congenital diaphragmatic hernia, lung dysplasia, etc.; its treatment effect is the worst.

2. pulmonary dysplasia (maldevelopment) refers to the intrauterine growth of smooth muscle from the prealveoli (prealveoli) to normal smooth muscle in the intra-alveoli artery, and the number of pulmonary arterioles is normal, due to vascular smooth muscle hypertrophy, Decreased lumen causes blood flow to be blocked, chronic intrauterine hypoxia can cause pulmonary remodeling and middle muscle hypertrophy; early closure of intrauterine fetal catheter (such as mother application of aspirin, indomethacin, etc.) can be secondary Pulmonary vascular hyperplasia; for these patients, the treatment effect is poor.

3. Maladaptation refers to the rapid decline of pulmonary vascular resistance after birth, and the number of pulmonary arterioles and the anatomy of the muscle layer are normal, often due to perinatal stress, such as acidosis, hypothermia, hypoxia , meconium inhalation, hypercapnia, etc.; these patients account for the majority of PPHN, its pulmonary vascular resistance is reversible, often respond to drug treatment.

Neonatal persistent pulmonary hypertension prevention

1. Fetal asphyxia: The cause is mostly related to hyaline membrane disease, meconium aspiration pneumonia, neonatal asphyxia and other diseases, so it should actively prevent fetal asphyxia and hypoxia.

2. Pregnant women use caution: Dr. Ostrea of Wayne State University in Detroit, USA, reports that pregnant women use NSAIDs and neonatal persistent pulmonary hypertension (PPHN), and take NSAID-ibuprofen during pregnancy. Naproxen, aspirin, is potentially harmful to the fetus and will have serious consequences for healthy full-term newborns. Pregnant women should take these over-the-counter medications with caution. At the same time, the side effects of these drugs must be clearly marked. Continuous use of SSRI antidepressants in the later stages of pregnancy increases the risk of respiratory disorders in newborns and should be used with caution.

Neonatal persistent pulmonary hypertension complications Complications heart failure

Concurrent cerebral ischemia and hypoxia damage, myocardial damage, heart failure and so on.

Neonatal persistent pulmonary hypertension symptoms common symptoms systolic murmur suffocation blood pressure drop right ventricular hypertrophy shock

PPHN often occurs in the small arteries of the pulmonary arterioles with good development of the smooth muscles and expired births. Premature infants are rare, often have a history of amniotic fluid contaminated by meconium, and often show normal after birth, except for short-term distress; More than 12 hours after birth, there were symptoms such as general bruising and rapid breathing, but no apnea and tri-concavity, and there was no correlation between respiratory distress and the severity of hypoxemia. Most children after high concentration of oxygen were absorbed. The symptoms of bruising are still not improved, and it is difficult to distinguish clinically from cyanotic congenital heart disease.

About half of the children can hear systolic murmurs on the left sternal border, second, tricuspid blood reflux, but the systemic blood pressure is normal, when there is a serious right-to-left shunt of the arterial catheter level, the right upper extremity arterial blood Oxygen partial pressure is greater than the umbilical artery or lower extremity arterial partial pressure. When combined with cardiac insufficiency, it can be heard and galloping with blood pressure, poor peripheral perfusion and other symptoms, ECG can be seen in right ventricular hypertrophy, electrical axis right deviation or ST -T changes; chest X-ray examination can be manifested as enlarged heart, hilar congestion and primary lung disease; echocardiographic assessment of pulmonary artery pressure is significantly increased, and the presence of transarterial catheter or foramen ovale can be found Diversion.

Examination of persistent pulmonary hypertension in neonates

1. If the blood picture is caused by meconium aspiration pneumonia or sepsis, it is an infectious blood picture, the blood viscosity is increased, the red blood cell count and hemoglobin amount are increased.

2. Blood gas analysis Arterial blood gas showed severe hypoxia, PaO2 decreased, and the partial pressure of carbon dioxide was relatively normal.

3. The proportion of chest X-ray film chest and chest can be slightly increased. About half of the children's chest X-ray film shows heart enlargement, pulmonary blood flow is reduced or normal. For simple idiopathic PPHN, lung field is often clear and blood vessels are less; Other causes of PPHN are often normal or associated with primary lung disease, such as meconium aspiration pneumonia and other X-ray features.

4. The electrocardiogram shows that the right ventricle is dominant, and myocardial ischemia can also occur.

5. Ultrasound Doppler examination excludes the presence of congenital heart disease, and a series of hemodynamic assessments are recommended.

(1) Indirect signs of pulmonary hypertension:

1 The ratio of right ventricular systolic and right ventricular systolic time can be measured by M-ultrasound or Doppler method. The normal rate is generally about 0.35, and the chance of pulmonary hypertension is >0.5.

The Doppler method was used to measure the acceleration time of pulmonary blood flow and the ratio of acceleration time/right ventricular ejection time. The measured value was reduced, suggesting pulmonary hypertension.

3 Doppler was used to measure the mean blood flow velocity of the left or right pulmonary artery. The decrease of the flow velocity indicated an increase in pulmonary vascular resistance and pulmonary hypertension.

The normal value of the above indicators varies greatly, but the series of dynamic observations have certain significance for evaluating the therapeutic effect of PPHN.

(2) Direct signs of pulmonary hypertension:

1 shows open catheter and shunt: two-dimensional color Doppler ultrasound shows an open arterial catheter in the high left sternal section, and right-to-left shunt, bidirectional shunt or left-to-right shunt can be determined according to the blood flow direction of the catheter level. The Doppler sampling point can also be placed in the arterial catheter, and the pulmonary artery pressure can be calculated by simplifying the Bernoulli equation (pressure difference = 4 x speed 2) according to the flow rate with reference to the systemic circulation pressure.

2 pulmonary hypertension: using tricuspid regurgitation in patients with pulmonary hypertension, continuous flow rate measured by continuous Doppler to simplify the Bernoulli equation, calculate pulmonary artery pressure: pulmonary systolic blood pressure = 4 × tricuspid regurgitation blood flow maximum Speed 2 CVP (assuming CVP is 5 mmHg), pulmonary hypertension can be diagnosed when pulmonary systolic blood pressure is 75% systemic systolic blood pressure.

3 Confirm right-to-left shunt: Directly observe the right-to-left shunt through the foramen ovale by color Doppler. If it can not be displayed, you can also use 2~3ml normal saline through the upper limb or scalp vein (better central vein). Bolus, if you see the "snowflake" shadow from the right room into the left room, you can confirm the right to left shunt.

Diagnosis and differential diagnosis of neonatal persistent pulmonary hypertension

Diagnostic criteria

Under proper ventilation, severe cyanosis, hypoxemia, chest radiographs and hypoxia are not parallel in the early stage of neonatal, and those with pneumothorax and congenital heart disease should be considered. The possibility of PPHN should be considered. The diagnostic method, the ideal diagnosis should be non-invasive, painless, sensitive and specific, but there is no single diagnostic method to meet the above requirements.

1. Physical examination If the child has a history of perinatal asphyxia, the systolic murmur caused by tricuspid regurgitation may be heard at the left or lower sternal border.

2. Diagnostic test

(1) Pure oxygen test: high oxygen test head or mask inhalation of 100% oxygen for 5 to 10 minutes, such as no improvement in hypoxia, suggesting the presence of PPHN or cyanotic heart disease caused by right to left blood shunt.

(2) Hyperoxia and hyperventilation test: For those who are still sputum after hyperoxia test, the air is inflated under the tracheal intubation or mask, the frequency is 100-150 times/min, and the partial pressure of carbon dioxide is reduced to the "critical point" (20~ 30mmHg), PPHN blood oxygen partial pressure can be greater than 100mmHg, and the increase of blood oxygen partial pressure in cyanotic heart disease is not obvious, if higher ventilation pressure (>40cmH2O) is required to reduce the partial pressure of carbon dioxide to the critical point, it indicates the pulmonary hypertension The child has a poor prognosis.

(3) blood oxygen partial pressure difference: before the opening of the arterial catheter (usually taking the right iliac artery) and the artery after the opening of the arterial catheter (usually the left iliac artery, umbilical artery or lower extremity artery), the blood oxygen partial pressure difference, when the two If the difference is greater than 15-20mmHg or the difference of percutaneous oxygen saturation between the two places is >10%, and the congenital heart disease can be excluded at the same time, the child is prompted to have PPHN, and there is a right-to-left shunt at the level of the arterial catheter because the egg A right-to-left shunt can also occur at the level of the round hole, and the negative test does not completely exclude PPHN.

Differential diagnosis

In the diagnosis of continuous fetal circulation, it must be differentiated from central cyanosis caused by other diseases in the neonatal period. It is especially necessary to distinguish from neonatal cyanotic congenital heart disease, and distinguish it from cyanosis secondary to lung disease. Physical examination, combined with electrocardiogram, X-ray findings, can help to detect the primary disease of the heart or lungs, combined with pure oxygen test, can understand the existence of shunt, and initially identify intracardiac shunt or intrapulmonary shunt, ultrasound Cardiogram technology has become one of the most important diagnostic methods for this disease. It can not only be used for qualitative diagnosis, but also provide valuable quantitative data of pulmonary artery pressure, which is an indispensable differential diagnosis method.

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