neonatal asphyxia
Introduction
Introduction to neonatal asphyxia Neonatal asphyxia (asphyxiaofthenewborn) refers to the respiratory and circulatory disturbances caused by intrauterine distress or delivery during the period of prenatal, postpartum or postpartum various causes, resulting in hypoxia in the fetus, resulting in no spontaneous breathing within 1 min after birth. Failure to establish regular breathing, with hypoxemia, hypercapnia and acidosis as the main pathophysiological changes, is the most common symptom of newborns and one of the main causes of disability and death. Need to race against time to rescue care. basic knowledge The proportion of illness: 1% Susceptible population: newborn Mode of infection: non-infectious Complications: neonatal seizures coma respiratory failure brain stem injury pneumothorax
Cause
Causes of neonatal asphyxia
The essence of suffocation is hypoxia. Any factor that can cause the decrease of blood oxygen concentration in the fetus or newborn can cause asphyxia. One cause can affect the body through different ways, and multiple causes can also act simultaneously. The neonatal asphyxia is mostly prenatal. Or due to factors of birth, postpartum factors are less, the common causes are as follows:
Pregnancy factor (30%)
(1) pregnant mothers with hypoxic diseases: such as respiratory failure, cyanotic congenital heart disease, severe anemia and CO poisoning.
(2) diseases of placental circulation disorders: such as congestive heart failure, pregnancy-induced hypertension syndrome, chronic nephritis, blood loss, shock, diabetes and infectious diseases.
(3) Others: pregnant mother drug use, smoking or passive smoking, or pregnant mother age 35 years old, <16 years old and multiple pregnancy, etc., the incidence of fetal asphyxia is high.
Fetal factors (30%)
(1) Premature delivery: premature infants, small for gestational age, giant children, etc.
(2) Malformation: various deformities such as posterior nostril atresia, throat, lung insufficiency, congenital heart disease and damage to the nervous system caused by intrauterine infection.
(3) Airway obstruction: Meconium inhalation causes obstruction of the airway.
Placental abnormality (15%)
Such as placenta previa, placental abruption and placental insufficiency.
Umbilical cord abnormality (10%)
If the umbilical cord is compressed, too short, too long to around the neck or around the body, prolapse, torsion or knotting.
Childbirth factor (10%)
Such as dystocia, high position forceps, breech position, fetal head suction is not smooth; anesthesia, analgesics and oxytocin used improperly during labor.
Pathogenesis
A series of pathophysiological changes occur as a result of various causes of suffocation:
1. Cellular damage and hypoxia after asphyxiation can lead to cell metabolism and dysfunction and structural abnormalities, and even death. It is a process of cell damage from reversible to irreversible. Different cells have different susceptibility to hypoxia, and brain cells are most sensitive. Second, myocardial, liver and adrenal cells, while fiber, epithelial and skeletal muscle cells are more tolerant to hypoxia.
(1) Reversible cell damage: The energy required by cells is mainly supplied by ATP produced by mitochondria. The lack of oxygen is firstly caused by cellular aerobic metabolism, ie, mitochondrial oxidative phosphorylation, which reduces or even stops ATP production. Oxygen, leading to cellular metabolism, functional and morphological abnormalities:
1 glucose anaerobic glycolysis enhanced: anaerobic glycolysis increased glucose and glycogen consumption, prone to hypoglycemia; also increased lactic acid, causing metabolic acidosis.
2 cell edema: due to lack of energy, the sodium pump actively transports the barrier, allowing sodium and water to remain.
3 calcium into the cell flow: due to the calcium pump active transport barrier, the calcium flow into the cell increased.
4 nuclear protein shedding: due to the nucleus protein detached from the rough endoplasmic reticulum, the synthesis of proteins and enzymes is reduced. If the blood flow perfusion and oxygen supply can be restored at this stage, the above changes can be completely restored, generally leaving no sequelae.
(2) irreversible cell damage: prolonged or severe hypoxia, will lead to irreversible cell damage.
1 Severe mitochondrial morphology and dysfunction: oxidative phosphorylation is not possible, ATP is impaired, and mitochondrial capacity is interrupted.
2 cell membrane severe damage: loss of its barrier and transport function.
3 lysosomal rupture: due to lysosomal membrane damage, lysosomal enzymes diffuse into the cytoplasm and digest various components in the cell (autolysis). Even if blood flow perfusion and oxygen supply are restored at this stage, the above changes cannot be completely restored. Survivors often left different degrees of sequelae.
(3) blood flow reperfusion injury: after resuscitation, blood flow reperfusion can lead to intracellular calcium overload and oxygen free radicals, causing further damage to the cells.
2. Asphyxiation development process
(1) Primary apnea: When hypoxia, hypercapnia and acidosis occur in the fetus or newborn, the secretion of catecholamines increases, the respiration and heart rate increase, and the blood flow of the body is redistributed. Selective vasoconstriction reduces blood flow to secondary tissues and organs such as lungs, intestines, kidneys, muscles, skin, etc., while blood flow to major vital organs such as the brain, heart muscle, and adrenal glands increases, blood pressure increases, and cardiac output increases. If hypoxemia and acidosis persist, respiratory arrest occurs, called primary apnea.
(2) Secondary apnea: If the cause is not relieved, hypoxemia persists, blood flow to the lungs, intestines, kidneys, muscles and skin is severely reduced, and blood flow to the brain, heart muscle and adrenal glands is also reduced. Can cause damage to the function and morphology of various organs of the body, such as brain and myocardial damage, shock, stress ulcers, etc., after the primary apnea, several wheezing-like respirations occur, followed by respiratory arrest, the so-called secondary Apnea.
Both types of apnea have no respiratory and heart rate below 100 beats/min, so it is difficult to identify clinically. In order not to delay the rescue time, those who have no breathing after birth should be identified and treated according to secondary apnea.
3. Blood biochemical and metabolic changes after asphyxia In the asphyxiating stress state, the release of catecholamines and glucagon increases, making early blood glucose normal or increase; when hypoxia continues, the use of sugar increases, glycogen storage is empty, hypoglycemia occurs Increased blood free fatty acids promote calcium-protein binding to hypocalcemia. In addition, acidosis inhibits the binding of bilirubin to albumin and reduces the activity of enzymes in the liver, resulting in high indirect bilirubinemia; Increased atrial natriuretic peptide secretion, resulting in hyponatremia and so on.
Prevention
Neonatal asphyxia prevention
1. Perinatal health care: strengthen perinatal care and timely treatment of high-risk pregnancy.
2. Fetal monitoring: strengthen fetal monitoring, avoid and timely correct intrauterine hypoxia, for intrauterine hypoxic fetus, can understand the degree of meconium-stained amniotic fluid through amniocentesis, or take fetal scalp blood when the fetal head is exposed to the cervix Blood gas analysis to estimate the degree of intrauterine hypoxia, PG and SP-A are low near birth, or L/S, PG, SP-A are very low, the risk of RDS is very high, and measures must be taken actively.
3. Avoid dystocia: closely monitor pregnant women in labor and avoid dystocia.
4. Proficiency in resuscitation techniques: training the delivery personnel to master the resuscitation technique.
5. Equipped with resuscitation equipment: Resuscitation equipment should be equipped in the hospital delivery room. Persons with mastery of resuscitation techniques must be present during high-risk pregnancy delivery. Care should be taken during clinical resuscitation. Before the airway is cleaned (especially meconium-contaminated children), avoid irritation. The newborn makes it cry so that the inhalation in the airway is not further inhaled into the lungs.
Complication
Neonatal asphyxia complications Complications neonatal seizures coma respiratory failure brainstem injury pneumothorax
Oxygen deficiency during asphyxia is not limited to the heart and lungs, but the multiple organs of the system are damaged. In severe cases, complications are often accompanied.
1. Brain: Hypoxia ischemic encephalopathy (HIE) is the main complication of neonatal asphyxia. Due to the blood-brain barrier involved in asphyxia and hypoxia, plasma protein and water cause cerebral edema and swelling through extravascular permeability. The cells compress the cerebral blood vessels, reduce blood flow, cause tissue ischemia to aggravate hypoxia, and eventually lead to neuronal necrosis in the brain tissue. In hypoxia, it is often accompanied by hypercapnia, resulting in decreased pH and cerebral vascular regulation dysfunction. Arterial blood pressure is lowered, causing insufficient blood supply, causing white matter infarction. The white matter, such as the parasagittal region, at the end of the blood supply to the anterior, middle, and posterior cerebral ventricles of the cerebral ventricle, which is farthest from the heart, may cause vascular infarction, and the white matter is softened, so HIE is hypoxic. The ischemic mutual causal lesions, clinical diagnosis basis and indexing criteria (1989 Jinan Conference) are:
(1) Have a clear history of perinatal hypoxia, especially perinatal severe asphyxia (Apgar score 1 minute <3 points, 5 minutes <6 points, or spontaneous breathing after 10 minutes of rescue; or need a trachea The inner cannula is under positive pressure for more than 2 minutes).
(2) The following abnormal neurological symptoms occur within 12 hours after birth: disturbance of consciousness, such as excessive excitement (physical trembling, long blinking time, gaze, etc.), lethargy, lethargy, and even coma; changes in limb muscle tone, such as weakened tension, soft; The original reflection is abnormal, such as the hug reflection is too active, weakened or disappeared, and the sucking reflex is weakened or disappeared.
(3) When the condition is severe, there may be convulsions. Attention should be paid to the characteristics of neonatal seizures, such as facial, irregular limbs, unsteady rhythmic tics, eye gaze, tremor accompanied by apnea, and complexion.
(4) In severe cases, there are central respiratory failure, pupillary changes, and intermittent extensor tension enhancement.
2, heart: due to hypoxia affect the conduction system and myocardial, atrioventricular conduction is prolonged in mild cases, T wave flattened or inverted, arrhythmia or slow in severe cases, often can hear systolic murmur, myocardial contraction during acidosis The weakening of the force and the decrease in output and blood pressure decreased further affected the perfusion of coronary and cerebral arteries. Finally, heart failure occurred. The Pediatric Hospital of Shanghai Medical University reported a heart failure rate of 22.5% after asphyxia, and the right atrial level was seen by echocardiography. Distraction to the left is an important basis for heart failure after asphyxia. Doppler measurement of cardiac output can observe the degree of cardiac dysfunction and its recovery.
3, lung: mainly manifested as respiratory disorders, easy to secondary pneumonia on the basis of amniocentesis, after active recovery, still need to pay attention to pneumothorax, pulmonary edema and pulmonary vasospasm may be associated with ventilation dispersal disorders, pulmonary artery pressure can promote arteries Reopening of the catheter restores the fetal circulation, aggravating hypoxia can cause damage to the lung tissue and pulmonary hemorrhage.
4, liver: suffocation hypoxia can reduce the binding force of bilirubin and albumin, so that jaundice deepens, prolonged time, but also due to liver damage and II, V, VII, IX and X and other coagulation factors are easy to develop DIC.
5, other: severe asphyxia children with low renal function can easily cause hyponatremia, gastrointestinal tract by the redistribution of blood is easy to produce necrotizing enterocolitis, due to anaerobic metabolism of glycogen consumption increased, prone to hypoglycemia, calcium The regulation function is weakened and it is prone to hypocalcemia.
Symptom
Neonatal asphyxia symptoms common symptoms arrhythmia skin pale breath slow slow breathing inhibition neonatal cyanotic neonatal heart failure wheezing after birth "four concave sign" asphyxia neonatal convulsion
1. The baby is delivered to the back and the skin of the whole body is blue-purple or pale, and the lips are dark purple.
2. Breathing superficial, irregular or no breathing or only breathing like a weak breath.
3. Heartbeat rules, heart rate 80-120 beats / minute or irregular heartbeat, heart rate <80 times / minute, and weak.
4. Respond to external stimuli, muscle tension is good or no response to external stimuli, muscle tension is relaxed.
5. The laryngeal reflex exists or disappears.
Examine
Neonatal asphyxia check
[Laboratory Inspection]
1. Blood gas analysis: For the most important laboratory examination, the arterial blood oxygen partial pressure (PaO2), carbon dioxide partial pressure (PaCO2) and pH value must be measured during respiratory therapy. In the early stage of the disease, PaO2<6.5kPa (50mmHg), PaCO2 >8kPa (60mmHg), pH<7.20, BE<-5.0mmol/L, should consider hypoxemia, hypercapnia, metabolic acidosis, no improvement by oxygen or assisted ventilation, can be converted into airway Intubation and ventilator treatment to avoid severe respiratory failure, usually 1 to 3 hours after starting mechanical ventilation, and every 12 to 24 hours after 2 to 3 days, you need to check the arterial blood gas value to determine the outcome of the disease and regulate breathing Machine parameters to maintain proper ventilation and oxygen supply.
2. Determination of serum electrolytes: often serum potassium, sodium, chlorine, calcium, phosphorus, magnesium and blood sugar are reduced, detecting arterial blood gas, blood sugar, electrolytes, blood urea nitrogen and creatinine and other biochemical indicators, according to the needs of the disease can also selectively measure blood sugar Blood sodium, potassium, calcium, etc., early blood sugar is normal or increased, when hypoxia continues, blood sugar drops, blood free fatty acids increase, hypocalcemia, indirect bilirubin increased, blood sodium decreased.
3. PG and SP-A: can be used as an auxiliary index to judge lung maturation, the two are close to pre-natal low, suggesting that the lung is immature, in the lung immature fetus, if L/S, PG, SP-A are very Low, the risk of RDS is very high, the determination of airway aspirate, or the above indicators of early gastric juice after birth, can also help determine the effect and outcome of RDS treatment, there are also research using microscopic microbubble counting method to detect airway cleaning solution Or the ratio of microbubbles to large bubbles in gastric juice, indirectly judge the content and activity of endogenous pulmonary surfactant, can help to quickly determine the extent of RDS disease and treatment effect.
[Auxiliary inspection]
1. X-ray examination: chest X-ray can be characterized by unclear margins, plaque-like shadows of varying sizes, sometimes partial or total atelectasis, focal emphysema, similar pneumonia changes and pleural effusion.
2. Electrocardiogram examination: the PR interval is prolonged, the QRS wave is broadened, the amplitude is decreased, the T wave is increased, and the ST segment is decreased.
3. Skull B-ultrasound or CT: The location and extent of intracranial hemorrhage can be found.
4. Amniocentesis: For intrauterine hypoxic fetuses, the degree of meconium-contaminated amniotic fluid can be understood by amniocentesis, or the fetal scalp blood can be taken for blood gas analysis when the fetal head is exposed to the cervix to estimate the degree of hypoxia in the uterus.
Diagnosis
Diagnosis and diagnosis of neonatal asphyxia
diagnosis
1. Newborn face and body skin bruising.
2. Breathing is superficial or irregular.
3. Heartbeat rules, strong and powerful, heart rate 80-120 beats / min.
4. Respond to external stimuli and have good muscle tone.
5. Laryngeal reflex exists.
6. With the above performance as mild asphyxia, Apgar scored 4-7 points.
7. The skin is pale and the lips are dark purple.
8. No breathing or only breathing like a weak breath.
9. The heartbeat is irregular, the heart rate is <80 beats/min, and weak.
10. No response to external stimuli, muscle tension is relaxed.
11. Throat reflex disappears.
12. With 7-11 items for severe asphyxia, Apgar scores 0-3 points.
Judging the degree of asphyxia: Apgar scoring is a classic and simple method for clinical evaluation of the degree of birth asphyxia. The 1 min postnatal score can distinguish the degree of asphyxia. After 5 min, the score is helpful for prognosis.
1. Time: Regular scores were taken at 1 min and 5 min after birth. The 1 min score was related to arterial blood pH, but not completely consistent. For example, an anesthetic or analgesic used in the mother's delivery to make neonatal respiratory depression, although the Apgar score is low. , but no intrauterine hypoxia, blood gas changes are relatively light, if the 5min score is less than 8 points, should be scored once per minute until 2 consecutive scores greater than or equal to 8 points; or continue Apgar score until 20 minutes after birth .
2. Apgar score judgment: 1min Apgar score 8 ~ 10 is normal, 4 ~ 7 is divided into mild asphyxia, 0 ~ 3 is divided into severe asphyxia.
3. Significance of evaluation: The 1min score reflects the severity of asphyxia. In addition to the severity of asphyxia, the 5min and 10min scores can also reflect the effect of recovery.
4. Note: The assessment should be objective, rapid and accurate; the premature infants with small gestational age have low maturity, although there is no asphyxia, but the score is lower.
Differential diagnosis
(a) Neonatal hyaline membrane disease.
(two) neonatal wet lung
More common in full-term cesarean section, there is a history of intrauterine distress, often within 6 hours after birth, shortness of breath and cyanosis, but the general condition of the child is good, the symptoms disappear within about 2 days, the two lungs can be smelled and wet Luoyin, low breath sounds, lung X-ray showed thickening of lung texture, small pieces of granules or nodular shadows, pleural or pleural effusion between the leaves, often emphysema, but the recovery of lung lesions Ok, often disappear within 3 to 4 days.
(iii) Neonatal inhalation syndrome.
(4) Neonatal esophageal atresia
Newborn esophageal atresia is more commonly used in the classification of Gross five types:
Type 1: The upper and lower segments of the esophageal atresia are two blind ends.
Type 2: The upper end of the esophagus is connected to the trachea and the lower end is the end.
Type 3: The upper part of the esophagus is a blind end, and the initial part of the lower part is connected to the trachea.
Type 4: Both the upper and lower esophagus are connected to the trachea.
Type 5: no esophageal atresia, but there is a fistula and trachea communication, it can be seen that in addition to type I, esophageal atresia, the other types of esophagus and trachea have traffic congestion.
When the newborn baby has increased oral secretions, coughing, purpura and asphyxia after feeding, use a soft and moderate catheter, nasal or oral insertion into the esophagus, if the catheter automatically returns, the disease should be suspected, but the diagnosis must be Iodine oil was used for esophagography.
(5) Neonatal nasal posterior atresia
After birth, there is a serious difficulty in inhaling, cyanosis, when the mouth is open or crying, the hair loss is reduced or disappeared. When the mouth is closed and the milk is sucked, there is difficulty in breathing. Due to the difficulty in feeding the baby, the weight is not increased or the malnutrition is severe. According to the above performance, If you suspect this disease, you can use the tongue depressor to press down the base of the tongue. If the child has difficulty breathing, or remove the mouth of the child, use a thin catheter to insert it from the anterior nares to see if you can enter the pharynx or use a stethoscope to aim at the newborn. The left and right nostrils, whether there is air rushing out, you can also use cotton silk in the nose hole to observe whether to swing, to determine whether the nostrils are ventilated, you can also use a small amount of gentian violet or Meilan from the front nostril to observe whether it can flow to the pharynx If necessary, use iodized oil to drip into the nasal cavity and perform X-ray examination.
(6) Newborn jaw fracture, cleft palate
When the baby is born, the mandible is small, sometimes accompanied by a fissure. The tongue is drooping to the pharynx and it is difficult to inhale. Especially in the supine position, the breathing difficulty is significant. When breathing, the head is tilted back, the ribs are sunken, and the inhalation is accompanied by wheezing and paroxysmal. Cyanosis, later ankle deformity and weight loss, sometimes accompanied by other malformations, such as congenital heart disease, clubfoot, and refers to (toe), cataract or mental retardation.
(7) Newborns
After birth, there are dyspnea and persistent and paroxysmal purpura, accompanied by intractable vomiting. During the physical examination, the left side of the chest is weakened. The left side of the percussion is drumy or dull. The auscultation is low or disappears. Sometimes it can be heard. To the bowel sounds, the heart sounds and the apex beats to the right side, showing a scaphoid, X-ray chest and abdomen perspective or photo can be diagnosed.
(8) Congenital throat
After birth, the crying is weak, the voice is hoarse or silent, and the inspiratory is accompanied by throat and chest soft tissue retraction. Sometimes it is difficult to inhale and exhale. The diagnosis depends on laryngoscopy, and the throat can be seen directly.
(9) Congenital heart disease.
(10) Group B hemolytic streptococcus (GBS) pneumonia can be seen in premature delivery, near term and full-term neonates, mothers have a history of infection and premature rupture of amniotic membrane in late pregnancy, clinical signs of the same as premature infant RDS, can have positive bacterial culture X-ray examination of the chest showed signs of inflammation of the lung lobe or segment and signs of alveolar collapse. The clinical signs of infection were 1 to 2 weeks. The treatment was performed with a combination of broad-spectrum antibiotics such as ampicillin plus M. After the application of 7 to 10 days of ampicillin or penicillin, the dose requirements refer to the minimum inhibitory concentration to avoid loss due to low dose.
(11) Hereditary SP-B deficiency, also known as "congenital pulmonary surfactant protein deficiency", was discovered in the United States in 1993, and there are currently more than 100 children diagnosed by molecular biology techniques in the world. The cause of the disease is the mutation of the DNA sequence that regulates the synthesis of SP-B. The clinical manifestation is that children born in full-term have progressive dyspnea. If any treatment intervention is ineffective, there may be a family morbidity. The lung pathology is similar to that of premature infants. Lung biopsy found that SP-B protein and SP-B mRNA were deficient, and may be associated with abnormalities in the synthesis and expression of pre-SP-C. The lung tissue pathology is similar to alveolar proteinosis, and exogenous pulmonary surfactant treatment can only be temporarily relieved. Symptoms, children rely on lung transplantation, otherwise they will die within 1 year of age.
