Definition of neonatal hypoxic ischemic encephalopathy
Hypoxic-ischemic encephalopathy (HIE) of the newborn refers to a series of encephalopathy manifestations which are caused by perinatal asphyxia and lead to hypoxic-ischemic damage of the baby’s brain. This disease is not only a serious threat to the life of newborn babies, but also one of the most common causes of postnatal disability.
There is no specific treatment for this disease. We should focus on preventing fetal distress and improving the resuscitation level of neonatal asphyxia. During the delivery process to closely monitor the fetal heart rate, early detection of intrauterine distress, choose the best way to end childbirth as soon as possible. Neonates with postnatal asphyxia Should race against the clock to establish effective respiration and perfect circulatory function so as to minimize the damage to brain cells caused by postnatal hypoxia. Neonates after resuscitation from asphyxia should closely observe neurological symptoms and monitor vital signs. Once abnormal neurological symptoms such as disturbance of consciousness, weakening of limb tension and difficulty in eliminating primitive reflexes are found, the diagnosis of the disease should be considered and early treatment should be given to reduce the incidence of sequelae in survivors.
Causes of neonatal hypoxic-ischemic encephalopathy
Hypoxic-ischemic encephalopathy (HIE) is a fatal and dangerous disease, which can easily cause brain damage in newborns. Neonatal hypoxic-ischemic encephalopathy is mostly caused by perinatal asphyxia.
Perinatal asphyxia is the main cause of neonatal hypoxic-ischemic encephalopathy. Anyone who causes obstruction of blood circulation and gas exchange between mother and fetus and lowers the concentration of blood oxygen can cause asphyxia. Among them, 50% were caused by intrauterine asphyxia, 40% suffocated during delivery, and 10% were caused by congenital diseases.
There are many factors that cause neonatal hypoxic-ischemic brain damage.
(1) Perinatal asphyxia: including antenatal, intrapartum and postpartum asphyxia, intrauterine hypoxia, placental dysfunction, umbilical cord prolapse, compression and around the neck; abnormal childbirth such as rapid delivery, delayed delivery, abnormal fetal position; fetal abnormalities such as premature delivery, postpartum delivery and intrauterine growth retardation.
(2) apnea: recurrent apnea can cause hypoxic-ischemic brain damage.
(3) Severe pulmonary infection: neonates with severe respiratory diseases, such as severe pulmonary infection can also cause this disease.
(1) Severe circulatory diseases: cardiac arrest and bradycardia, severe congenital heart disease, severe heart failure and so on.
(2) massive blood loss: massive blood loss or shock.
(3) severe intracranial diseases such as intracranial hemorrhage or brain edema.
Neonatal asphyxia is the main cause of hypoxic-ischemic encephalopathy in neonates. Antenatal and intrapartum asphyxia accounted for 50% and 40% respectively, and other causes accounted for about 10%.
Pregnant women should be on time during pregnancy, prenatal care should be actively communicated with medical personnel, to maximize avoid perinatal asphyxia leading to neonatal hypoxic-ischemic encephalopathy.
Neonatal hypoxic ischemic encephalopathy symptoms
Hypoxic-ischemic encephalopathy (HIE) of the newborn is caused by perinatal asphyxia. The appearance and performance of the newborn are different from that of the normal full-term infants after delivery. There are a series of symptoms in neonates with hypoxic ischemic encephalopathy.
1, most of them are full-term suitable for gestational age, with obvious history of intrauterine distress or asphyxia during labor.
2, different degrees of consciousness disorder, light only irritation or lethargy; heavy obvious inhibition, coma.
3, the front fontanelle is full, the seams are separated, the head circumference is enlarged, and there are cerebral edema.
4. Convulsions: Most cases are moderate or severe. Convulsions can be atypical focal or multifocal, clonic or tonic myoclonic. Attack frequency varies, mostly in 24 hours after birth, within 24 hours the incidence of sequelae increased significantly.
5, increased or decreased muscle tone.
6. Primitive reflexes: excessively active, weakened or disappeared. Sucking reflex attenuate or disappear.
7. Central respiratory failure occurs with brainstem injury such as irregular respiratory rhythm, apnea, nystagmus and pupil changes. The most important clinical symptoms of HIE are consciousness, muscle tone changes and convulsions, which are the main indicators to distinguish the severity and sequelae of encephalopathy.
In addition, according to different symptoms, neonatal hypoxic ischemic encephalopathy can be divided into three degrees:
Mild: Excessive arousal, irritability, excitement and high excitement (jitter, tremor), normal muscle tone, active cuddle reflex, normal sucking reflex, smooth breathing, no convulsion. The symptoms gradually disappeared within 3 days, and the prognosis was good.
Moderate: depressive state, sleepiness or light coma, low muscle tone, 50% of cases have seizures, apnea and hug, sucking reflex weakened. The decrease of muscle tone in the upper limbs is more serious than that in the lower limbs, suggesting that the lesions involve the sagittal sinus area. Premature infants with lower extremity muscle tone reduction than upper extremity weight, suggesting lesions for periventricular leukomalacia. If symptoms persist for more than 7~10 days, there may be sequelae.
Severe: Children in coma, extremely low muscle tone, soft, hug reflex, tendon reflex disappeared, pupil unequal, poor response to light, anterior fontanel protrusion, frequent convulsions, irregular or suspended breathing, and even respiratory failure. The mortality of severe children is high, and survivors often leave sequela.
Neonatal hypoxic ischemic encephalopathy examination
After a childbirth accident, if the medical staff found that the newborn may have hypoxic-ischemic encephalopathy, it is necessary to give the newborn a physical examination, clear the condition after timely treatment. Neonatal hypoxic ischemic encephalopathy can be examined as follows:
1. Laboratory examination:
1. Biochemical indices: Neurostenolase (NSE), S-100 protein (S-100) and creatine phosphokinase (CK-BB) exist in different parts of nerve tissue. The elevation of NSE and CK-BB in blood and cerebrospinal fluid at 6-72 hours after HIE is positively correlated with the degree of brain damage. They can be used as sensitive markers for early diagnosis and prognosis of HIE.
2. Others: Blood gas analysis, blood glucose, electrolytes, urea nitrogen, platelets, prothrombin time, coagulation time, fibrinogen and other tests were selected according to the condition.
Two. Supplementary examination
1. Chest X-ray: aspiration pneumonia often occurs.
2. Head CT examination.
Mild: scattered, focal low density shadows were distributed in 2 cerebral lobes.
Moderate: low density shadow over 2 cerebral lobes, gray matter contrasting with white matter.
Severe: diffuse low-density, gray matter white matter boundaries disappeared, but the basal ganglia and cerebellum still have normal density. Intracranial hemorrhage is common in moderate and severe cases. Normal neonates, especially premature infants, have excessive brain water, immature myelin sheath development, and may have extensive low density. Therefore, the diagnostic CT value of low density should be below 18. In the acute phase of HIE, brain edema is more obvious, may cover up the damage of brain cells, and the disease is still changing, so early imaging can not reflect the prognosis, need to be reviewed after 2 to 4 weeks.
3. Craniocerebral ultrasound: General echo enhancement, ventricular narrowing or disappearance, suggesting brain edema. Periventricular hyperechoic areas, mostly in the posterior horn of lateral ventricle, suggest that there may be periventricular leukomalacia. Scattered in the hyperechoic area is caused by extensive cerebral ischemia. The localized hyperechoic area indicates ischemic damage in the area of a major cerebral vascular distribution.
4. Magnetic resonance imaging (MRI): not only can detect the presence, distribution and severity of HIE in acute phase, but also can help to judge the prognosis, and can also find whether myelination is delayed or abnormal, in order to judge the neural development.
5. Brain function examination
Electroencephalogram (EEG) examination: rhythmic disorders, spike-slow wave bursts on low-amplitude background waves or persistent diffuse slow activity; the presence of “burst suppression”, “low voltage” or even “resting” is severe HIE. The abnormal degree of EEG is parallel to the severity of the disease. The prognosis of patients with normal EEG or single lesion is good; persistent abnormal EEG (isopotential, low potential, fast wave, burst suppression wave, etc.), especially periodic, multifocal or diffuse changes, is a signal of the sequelae of nervous system.
Brainstem auditory evoked potentials (BAEP) are characterized by delayed outflow, prolonged latency, flattened amplitude and wave loss. The amplitude of V wave and the ratio of V/I amplitude were observed dynamically.
Doppler ultrasound cerebral blood flow velocity (CBV) measurement: help to understand the situation of cerebral perfusion, high CBV suggestive of cerebral palsy and lack of autonomic regulation, low CBV suggestive of extensive cerebral necrosis, low perfusion, or even no perfusion.
6. Cerebral metabolic monitoring
Magnetic resonance spectroscopy (MRS): MRS is a non-invasive method to detect chemical components in vivo (such as ATP, creatine phosphate, lactic acid, etc.). It can measure the metabolism of brain tissue in vivo, and can reflect the degree of hypoxic-ischemic brain injury more early and sensitively than MRI.
Near-infrared spectroscopy (NIRS): NIRS is a new optical diagnostic technique developed abroad in recent years. It can directly measure the changes of oxyhemoglobin and reduced hemoglobin in brain tissues. It can actually understand the oxygenation in brain and indirectly reflect the cerebral hemodynamics and intracellular biological oxidation process.
In order to make accurate physical judgment for newborns and prevent hypoxic-ischemic encephalopathy (HIE) caused by perinatal asphyxia, pregnant women should choose hospital delivery as far as possible in order to reduce the damage caused by childbirth accidents to newborns.
Treatment of neonatal hypoxic-ischemic encephalopathy
Once perinatal asphyxia occurs, the neonate is most likely to suffer from hypoxic ischemic encephalopathy. Health care workers need immediate physical examination and treatment. The aim of treatment of neonatal hypoxic-ischemic encephalopathy is to improve the metabolic function of damaged neurons as far as possible and maintain the stability of the internal environment.
1. General treatment:
(1) Correction of hypotension: to ensure adequate cerebral blood flow perfusion, commonly used dopamine 5-10 ug/kg per minute, intravenous drip.
(2) correct metabolic acidosis: slow slow drops after diluted with sodium bicarbonate 2-3mEg/kg10% glucose.
(3) correct hypoxemia and hypercapnia: use respirator when necessary.
(4) intravenous calcium gluconate can be obtained when blood calcium is below 1.9mmol/L.
(5) Adequate glucose supply to meet the energy metabolism needs of brain tissue: 6-8 mg/kg per minute.
(6) limit liquid intake: 50-60ml/kg per day. The infusion speed was less than 4ml/kg/h.
2. Control convulsion:
The first dose of sodium phenobarbital is 15-20mg/kg. If not, add 1-2 times at 5 mg/kg intervals of 5-10 minutes with a total load of 25-30mg/kg. On the second day, 4-5mg/kg was maintained daily (once or two times intravenously). It is better to monitor the blood concentration and stop it for a week after the seizure stops. If convulsion is frequent, it can be added with diazepam or hydrated chloral.
3. Control intracranial hypertension:
Dexamethasone 0.5mg/kg and furosemide 1mg/kg were injected intravenously for 4-6 hours. After 2-3 times, if the intracranial pressure is still high, use mannitol 0.25-0.5g/kg for intravenous injection, intermittent for 4-6 hours. Strive to reduce intracranial pressure within 48-72 hours.
4. Central nervous system stimulants:
Cytochrome C, urea triphosphate, coenzyme A can be used daily intravenous drip, until the symptoms improved significantly; also can be used cytochrome choline 100-125 mg / day, diluted static point, the second day after birth, once a day intravenous drip; Cerebrolysin 5ml diluted with normal saline intravenous drip, can improve brain metabolism.
Treatment must continue until symptoms disappear completely. Moderate HIE should be treated for 10-14 days, and severe HIE should be treated for 14-21 days or longer. The earlier the treatment begins, the better the treatment should begin within 24 hours after birth. Try to avoid all kinds of pathological factors after birth.