Neonatal apnea

Introduction to neonatal apnea Neonatal apnea is defined as a cessation of respiratory airflow 20 s with or without heart rate slowing or < 15 s, accompanied by a slow heart rate. In premature infants, breathing pauses for 10 to 15 s, and periodic breathing, which is not accompanied by slow heartbeat, is normal. The type of neonatal apnea. (1) Centrality - no airflow due to central nervous system causes airflow to stop; (2) obstructive - respiratory motion exists without airflow in the respiratory tract; (3) mixed. basic knowledge The proportion of sickness: 1%-5% (the incidence rate of newborns is about 1%-5%, more common in Apagar scores less than 7 points) Susceptible population: newborn Mode of infection: non-infectious Complications: renal failure, sepsis, neonatal hypoxic ischemic encephalopathy

Causes of neonatal apnea

(1) Causes of the disease

1, primary - premature infants due to incomplete development of the respiratory center;

2, symptomatic

(1) Hypoxia: asphyxia, pneumonia, hyaline membrane disease, congenital heart disease and anemia;

(2) infection: sepsis, meningitis, etc.;

(3) Central nervous system disorders: intraventricular hemorrhage and hypoxic ischemic encephalopathy;

(4) The ambient temperature is too high or too low;

(5) metabolic disorders: hypoglycemia, hyponatremia, hypocalcemia and hyperammonemia;

(6) stomach, esophageal reflux, necrotizing enterocolitis;

(7) due to excessive anterior curvature of the neck, airflow obstruction, apnea is more common in premature infants, the incidence can be as high as 50% to 60%, the smaller the gestational age, the higher the incidence.

(two) pathogenesis

Many clinical phenomena are associated with neonatal apnea, some of which may be the cause of apnea. An important feature of various apneas is that they usually occur when the newborn is awake, and the onset of apnea is usually frequent and continuous. Newborns often find a cause, and repeated apneas in premature infants have no obvious lesions. Some mechanisms have been proposed to explain the occurrence of neonatal apnea, central nervous system regulation, peripheral respiratory muscle movement during ventilation, and Maintaining a smooth airway so that there is a fine balance between the gas exchanges, if this balance is broken, it can cause apnea.

The immature development of the brainstem respiratory center is the key to apnea. In the central and mixed apnea episodes, the respiratory center's output to each respiratory muscle is reduced, and the respiratory central neurons do not have the self-discipline of sinus node. The electrophysiological activity of the reticular activity of the spinal cord plays an important role in maintaining the rhythmic release of impulses in the respiratory central nervous system. The afferent impulses from superior (cortical activity) and subordinate (peripheral nerve receptors, reflex arcs) constitute This neural connection can be excitatory or inhibitory, and many neurotransmitters and neuroregulatory secretions (such as endorphins, prostaglandins, and adenosine) can inhibit respiratory center activity, but become older with age. Less important, the output of the respiratory center is the combination and balance of the above-mentioned influencing factors. In the newborn, there will be strong and weak periodic changes in regular ventilation. The apnea episode is the period of least ventilation during this cycle. It may also be an unstable manifestation of the respiratory regulation system. It is confirmed by auditory evoked response that children with apnea have no apnea. Premature infants in the control group had longer brainstem conduction time, suggesting a delay in the maturation of the central nervous system and supporting the view that as the brain matures, the complex connections between dendrites and synapses increase, and the stability of central respiratory drive is obtained. perfect.

The basic chemical drive is relatively ineffective for neonates, especially premature babies. Premature infants with gestational age less than 33 weeks have lower sensitivity to ventilating and respiratory muscles to carbon dioxide, and premature infants with apnea, response to carbon dioxide. A line curve shows that the response of ventilation to carbon dioxide increase does not change much, but with the increase of gestational age and postnatal age, the sensitivity to carbon dioxide increases. In premature infants, hypoxia leads to transient hyperventilation, followed by ventilation. Insufficient and sometimes apneas, in addition, hypoxia reduces the premature babies' responsiveness to elevated carbon dioxide, which explains why apneas do not end up quickly being stimulated by hypoxia or hypercapnia, This is also the reason for oxygenation to improve critical hypoxemia, or to lose red blood cells to treat anemia to reduce the onset of apnea.

Overactivity of the upper respiratory tract reflex in the neonatal period is also an important factor in the onset of apnea. There are a large number of nerve endings in the nasal wall, nasopharynx, oropharynx and larynx, which can respond to various chemical and mechanical stimuli. Negative pressure suction or insertion into the nasogastric tube stimulates the posterior pharyngeal wall, often induces apnea and reflex bradycardia, and secretions, fluid or stomach contents accumulate in the throat can induce apnea, with age and development The central nervous system has enhanced ability to inhibit these high reactivity.

Incompatibility and disconnection between the thoracic respiratory muscles (the diaphragm and the intercostal muscles) and the upper respiratory tract (pharyngeal, larynx) muscles that maintain the open airways can lead to ineffective ventilation, and the pharyngeal airways lack an internal rigid support. The neck flexion, the mandibular posterior movement and the hyoid bone are easily collapsed. When inhaling, the diaphragm contraction produces a negative pressure in the pharynx, which aggravates the closure of the airway. The collapsed airway wall obstructs the airway due to the adhesion of mucus. Reopening, dispelling airway obstruction requires airway dilatation muscles such as facial muscle contraction or neck extension to expand the airway. In the inhalation process, before the diaphragm contraction, the upper airway respiratory muscles are excited early, this pair of peak airflow It is important to promote ventilation when passing through the upper airway resistance. For the stimulation of high carbonic acid, the upper airway respiratory muscle is a curve reaction, with only a slight increase at the beginning, only a significant increase in the high carbon dioxide level. The reaction of high carbonic acid is expressed as a proportional or nearly linear rise. Therefore, the respiratory muscles of the airway do not respond to hypercapnia, the response is small or slow, and the response of the thoracic muscle is sensitive, which is a straight rise. Uncoordinated can lead to instability of the upper airway, partial or complete airway obstruction, which can induce airway infarction after central apnea, and explain why short-term apnea is mostly central. Longer apneas are mixed.

The thoracic and pulmonary stretch receptors provide information on the extent of thoracic dilatation and lung expansion, through the vagus nerve into the center, thereby adjusting the intensity and duration of the respiration, with the increase in lung capacity, strong lung stretch reflex (Hering-Breuer reflex) The effect is to inhibit inhalation and prolong exhalation; however, as the maturity increases, the reflex is weakened. Conversely, when the lung capacity decreases, the expiratory time is shortened to maintain the lung volume, and the inspiratory process is prolonged. The ability of the duration of the inspiratory action is a compensatory mechanism to reduce airway occlusion. In response to end-tidal airway occlusion, the inspiratory action of preterm infants without apnea is significantly longer than that of premature infants with apnea. It is suggested that the more mature the respiratory reflex, the stronger its ability to respond to occlusion.

Newborn's breathing is significantly affected by sleep. Rapid sleep eye (REM) dynamic sleep predominates in premature infants and may be associated with brain development. Apnea occurs more frequently during REM sleep, when tidal volume and respiratory rate All of them are obviously irregular. In addition to strong central respiratory regulation inhibition during REM sleep, there is still inhibition of intercostal muscle movement. When the intercostal muscles do not move and the diaphragm changes, the result is chest deformation (contradictory breathing). Lead to ineffective ventilation and reduce lung capacity, compensatory increase in diaphragmatic movement, can cause diaphragmatic fatigue and upper airway obstruction, chest deformation can also cause intercostal-sputum inhibition and reflection, limiting the impulse of the phrenic nerve, the final result is Apnea.

In short, newborns, especially premature infants, are prone to apnea due to immature respiratory center development, easy to cause respiratory regulation disorder, neonatal respiratory system anatomy is not perfect, physiological function is unstable, physiological information can not be transmitted correctly, and respiratory rhythm is not complete Periodic breathing and apnea have a common pathophysiological basis. Apnea is further developed on the basis of the pathogenesis of periodic breathing. Respiratory dysfunction exists in the respiratory center, central chemoreceptors, peripheral chemoreceptors and lung reflexes, possibly multiple The factors play a role, and the respiratory control center of the apnea infant is in a state of inhibition. The tidal volume of the infant is small, the alveolar ventilation is low, the PaCO2 of the alveoli is high, the pressure in the esophagus during respiration is less, and the ventilation response is poor when PaCO2 is elevated. The respiratory center is immature, and its impulse is weak, which is related to the poor function of the central nervous system.

Neonatal apnea can be caused by hypoxia, hypoxia can inhibit the physiological function of the neonatal respiratory center, and can reduce the neonatal response to CO2, the more severe the hypoxia of the baby, the worse the response to CO2, which is exactly the same as adult hypoxia In contrast, in addition to hypoxia, such as changes in body temperature, hypoglycemia, acidosis, etc. can inhibit the respiratory center, causing apnea.

In addition, the accumulation of respiratory secretions and swelling of the bronchial mucosa increase the resistance of the respiratory tract, and even cause a certain degree of airway obstruction. It is necessary to increase the work of breathing to compensate. The compensatory ability of neonatal respiratory work is very poor, when the respiratory load is increased. At the time, it is not possible to effectively prolong the inspiratory time, change the esophageal pressure and increase the effective elasticity for compensation. This imperfection of respiratory reflex function is one of the causes of apnea easily occurring in neonates with respiratory diseases.

Neonatal apnea prevention

Children with apnea often have unfavorable perinatal factors, which are associated with increased mortality and prevalence, and there is a link between simple obstructive apnea and neurodevelopmental dysplasia. These children may have apnea due to intraventricular hemorrhage, rather than apnea due to immature.

1. Actively correct hypoxemia When using a mask to absorb oxygen, the lower edge of the mask should be placed on the ankle. If placed under the armpit, the trachea can be compressed to cause apnea; the arterial oxygen partial pressure is maintained at 6.65 to 9.31 kPa ( 50 ~ 70mmHg), can reduce the onset of apnea; avoid excessive ventilation of mechanical respiration, because alkali poisoning is often the result of unnecessary hyperventilation, will affect the sensitivity of the respiratory center, thus causing apnea, at this time should reduce the machinery Per minute ventilation of breathing makes PaCO2 gradually increase. Clinically, hypocapnia is seen in patients with mechanical respiration or metabolic acidosis combined with compensatory respiratory alkalosis.

2. Active prevention and treatment of various neonatal diseases, neonatal sepsis, intracranial hemorrhage, open arterial catheter or necrotizing enterocolitis, can inhibit the respiratory center, apnea, medication with apnea often invalid, need Mechanically assisted ventilation.

Neonatal apnea complications Complications, renal failure, sepsis, neonatal hypoxic ischemic encephalopathy

Due to the lack of oxygen supply, complications of other organs may occur. Excessive hypoxia may cause serious complications such as renal failure. If not treated promptly, it may die due to severe hypoxia, due to the defense of patients with acute respiratory distress syndrome. The ability to infect lungs is low, and bacterial pneumonia often occurs during the course of illness. Attention to abnormalities in body temperature, purpura, heart, lungs and nervous system, children with apnea within 24 hours after birth may often have sepsis.

Neonatal apnea symptoms Common symptoms Respiratory slow irregular irregular purpura central apnea heart failure hyperleptic sepsis

(1) The following medical history is a high-risk child prone to apnea:

1. Premature infants with a birth weight of 1800g (32 weeks pregnant);

2. Infants whose siblings have sudden death syndrome;

3. Infants with nervous system and various diseases mentioned above.

(2) Clinical manifestations:

Neonatal respiratory airflow stopped 20s, with or without heart rate slowdown or <15s, accompanied by heart rate slowing.

It is not difficult to diagnose apnea according to the above symptoms. The key is to identify primary and symptomatic. Therefore, children with apnea should undergo detailed and comprehensive physical examination, paying special attention to hypothermia, purpura, heart, lung and Abnormal manifestations of the nervous system, children with apnea within 24 hours after birth may often have sepsis; premature infants with apnea 3d to 1 week after birth can be considered as the original occurrence after excluding other diseases; respiratory occurs 1 week after birth Suspended premature babies should look for the cause and rule out the symptoms. All apneas in full-term children are symptomatic.

Neonatal apnea check

Laboratory inspection

1. Blood routine and blood test Hematocrit can identify anemia; suspected sepsis should check blood routine, platelets, C-reactive protein and blood culture; serum bilirubin should be measured with jaundice; blood glucose and blood calcium should be measured Etc., can exclude electrolyte disorders and metabolic disorders.

2. Blood gas analysis to determine whether there is hypoxemia, hypercapnia, arterial oxygen partial pressure maintained at 6.65 ~ 9.31kPa (50 ~ 70mmHg), can reduce apnea episodes, PaCO2 <4.65kPa (35mmHg) is low Carbonation.

Auxiliary inspection

1. Image inspection

(1) X-ray examination: chest X-ray can detect the nature and extent of lung disease, such as pneumonia, hyaline membrane disease, etc., and can help the diagnosis of congenital heart disease. Abdominal radiograph can exclude necrotizing small intestine colon inflammation.

(2) Head CT: It is helpful for diagnosing neonatal intracranial hemorrhage and central nervous system disorders.

(3) Ultrasound examination: Ultrasound examination of the head can exclude intraventricular hemorrhage, and cardiac ultrasound examination can help diagnose congenital heart disease.

2. Polysomnography (polysomnography) can not only distinguish between different types of apnea, but also indicate the relationship between apnea and sleep phase, which helps to diagnose the cause of apnea.

3. EEG monitoring There are rhythmic delta waves in the EEG during convulsive apnea episodes.

Neonatal apnea diagnosis

When examining the presence or absence of bruising in newborns, it is necessary to correctly distinguish between peripheral cyanosis and central cyanosis, lips and oral mucosa, which is the most reliable and sensitive part of true cyanosis. The obvious local cyanosis is still needed in some newborns. Skin pigmentation, such as the difference between the birth and the birth of the baby, the common skin pattern is often seen in the newborn, more obvious in the cold environment, due to the autoregulation instability of the skin vasomotor, the baby exposed on the face is exposed to the head and face due to stress Caused by congestion, edema, local skin and even lips can be blue-purple, should be distinguished from central cyanosis.

1. Physiological phenomena Newborns born newborns have irregular breathing and sometimes even apnea, which is a common phenomenon in newborns, especially premature babies. This is related to the immature development of the nervous system and poor regulation. The time is generally no more than 10s, and there are no other abnormal symptoms, which can be a normal physiological phenomenon.

2. Primary and secondary apnea According to the above definition, the diagnosis of apnea is not difficult, the key is to identify primary and secondary apnea, the cause of neonatal apnea is more complicated, premature infants are mostly primary Sexuality, also secondary; all apnea occurs in the full-term apnea, pay attention to timely detection of the underlying disease, a detailed, comprehensive physical examination of children with apnea, pay special attention to hypothermia, cyanosis, heart Abnormal manifestations of the lungs and nervous system, children with apnea within 24 hours after birth may often have sepsis; premature infants with apnea within 3 days to 1 week after birth, may be considered as primary after exclusion of other diseases Sexually; premature infants who develop apnea after 1 week of birth should seek the cause and exclude secondary.

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