What Is Persistent Pulmonary Hypertension of the Newborn?

Neonatal persistent pulmonary hypertension refers to the persistent increase in pulmonary vascular resistance after birth. Pulmonary arterial pressure exceeds systemic arterial pressure, which impedes the transition from fetal-type circulation to normal "adult" -type circulation and causes atrial and / or arterial catheters. Levels of right-to-left shunting of blood level, clinical symptoms such as severe and difficult to correct hypoxemia. The disease is more common in term or postpartum infants. Neonatal persistent pulmonary hypertension is not a single disease but a clinical syndrome caused by multiple factors. It has a dangerous incidence and a high mortality rate.

Basic Information

English name: persistent pulmonary hypertension of newborn
Visiting department: Pediatrics
Multiple groups: Newborn

Common causes: Diaphragmatic hernia, anencephaly, postpartum, asphyxia at birth, lung hypoplasia, etc.
Common symptoms: Whole body bruising and dyspnea etc.

Causes of persistent pulmonary hypertension in newborns

The neonatal pulmonary arteriolar muscularis is over-developed before birth. When hypoxemia and acidosis are caused by certain causes, pulmonary arteriolar spasm can be caused, resulting in increased pulmonary artery pressure and persistent pulmonary vascular resistance after birth. . The causes of hypoxemia in the utero or after birth are as follows:

Intrauterine factor

Such as utero-placental insufficiency leading to chronic hypoxia, diaphragmatic hernia, anencephaly, postpartum birth, oligohydramnios syndrome and so on. Another example is mother taking aspirin or indomethacin during pregnancy.

2. Delivery factors

Severe asphyxia at birth and aspiration (especially inhalation of amniotic fluid contaminated with meconium, etc.) syndrome.

3. Post-natal factors

Congenital lung diseases, pulmonary dysplasia, including pulmonary parenchyma and pulmonary vascular dysplasia, respiratory distress syndrome (RDS); cardiac insufficiency, etc. Etiology includes perinatal asphyxia, metabolic disorders, closure of intrauterine arterial ducts, etc .; cardiac contraction due to bacteria or virus, endotoxin, etc. during pneumonia or sepsis, pulmonary microvascular thrombosis, increased blood viscosity, pulmonary vasospasm, etc. ; Central nervous system disorders, neonatal scleredema, etc. In addition, many chemicals affect the expansion and contraction of blood vessels, and are therefore associated with continued fetal circulation. In short, except for a few primary pulmonary arteriolar muscularis overdevelopment and loss of relaxation, any severe hypoxia and acidosis can lead to increased pulmonary artery pressure and even right-to-left shunting of arterial ducts and oval foramen.

Clinical manifestations of neonatal persistent pulmonary hypertension

Neonatal persistent pulmonary arteries often occur in term infants and term infants with well-developed smooth muscles in the middle layer of the pulmonary arterioles. Preterm infants are rare. Severe asphyxia or inhalation of amniotic fluid contaminated with meconium after birth. Symptoms such as bruising and dyspnea, which are difficult to correct throughout the body due to severe hypoxia, occur more than 12 hours after birth. The symptoms of bruising cannot be improved after inhaling high concentration of oxygen, and it is difficult to distinguish clinically from cyanotic congenital heart disease. About half of the children can hear systolic murmurs on the left edge of the sternum, which is caused by blood regurgitation of the mitral and tricuspid valves but normal systemic blood pressure. When there is a severe right-to-left shunt at the level of the arterial catheter, the partial pressure of blood oxygen in the right upper limb is greater than the partial pressure of umbilical or lower limb arteries. Symptoms such as adverse and shock, ECG can show right ventricular hypertrophy, right axis deviation or ST-T changes; chest X-ray examination can show heart shadow enlargement, hilar congestion and primary lung disease manifestations; echocardiography estimates pulmonary artery pressure Significantly increased, and right-to-left shunting through arterial ducts or oval holes was found.

Neonatal persistent pulmonary hypertension

Blood image

If caused by meconium aspiration pneumonia or sepsis, it presents infectious haematological manifestations. Increased blood viscosity increased red blood cell counts and hemoglobin levels.

2. Blood gas analysis

Arterial blood gas showed severe hypoxia, PaO ₂ decreased, and carbon dioxide partial pressure was relatively normal.

3. Chest X-ray

The cardiothoracic ratio can be increased slightly. About half of the children's chest X-rays show an enlarged heart and reduced or normal pulmonary blood flow. For pure idiopathic neonatal persistent pulmonary hypertension, the lung field is often clear and there are few vascular shadows; others are related to primary lung diseases, such as X-ray characteristics such as meconium aspiration pneumonia.

4. ECG

It can be seen that the right ventricle is dominant, and myocardial ischemia can also appear.

5. Ultrasound Doppler

The presence of congenital heart disease can be ruled out and hemodynamic assessment can be performed.

Echocardiography displays and measures the direction of open catheters and shunts and calculates pulmonary artery pressure. Pulmonary hypertension can be diagnosed when the pulmonary arterial systolic pressure is 75% of the systemic systolic blood pressure.

Diagnosis of persistent pulmonary hypertension in newborns

With proper ventilation, severe cyanosis, hypoxemia, and chest radiography that cannot explain the degree of hypoxia in early neonates, and those with pneumothorax and congenital heart disease should be excluded. The possibility of neonatal persistent pulmonary hypertension should be considered.

1. The child has a history of severe asphyxia during perinatal period, or severe meconium aspiration syndrome.

Diagnostic test

(1) Pure oxygen test The high oxygen test head box or mask inhales 100% oxygen for 5-10 minutes, and there is no improvement if hypoxia.

(2) Hyperoxic hyperventilation test For those who still have cyanosis after the hyperoxic test, the frequency of skin ventilation under tracheal intubation or mask is 100 to 150 times / min to reduce the partial pressure of carbon dioxide to the "critical point" (20 to 30mmHg) of blood. The oxygen partial pressure can be greater than 100mmHg.

(3) Blood oxygen partial pressure difference Check the arterial blood oxygen partial pressure difference before and after the arterial catheter opening. When the difference between the two is greater than 15-20mmHg or the difference in percutaneous oxygen saturation of the two places is> 10%, congenital heart disease can be ruled out at the same time.

(4) Echocardiography is one of the most important diagnostic methods for this disease. Not only for qualitative diagnosis, but also for providing valuable quantitative data on pulmonary artery pressure.