Pediatric guide: neonatal hypoxic-ischemic encephalopathy

Hypoxic-ischemic encephalopathy (HIE) refers to various brain diseases such as mental retardation, epilepsy, cerebral palsy, ataxia, etc., which are caused by partial or complete hypoxia, reduction or suspension of cerebral blood flow and permanent neurological dysfunction. Most of them occur in asphyxiated full-term infants, but the incidence of premature infants is significantly higher than that of full-term infants. HIE is one of the main causes of neonatal acute death and chronic nervous system injury.

Etiology and pathogenesis

I. Etiology The core of the disease is hypoxia, and the main reason is perinatal asphyxia. In addition, lung disease, heart disease, severe blood loss and anemia after birth can also lead to brain damage.

Second, the pathogenesis

1. Cerebral blood flow regulation function decreased. Normal newborns' cerebral vessels relax and contract to regulate blood flow into brain tissue. When the blood flow decreases, the cerebral blood vessels relax, and when the blood flow increases, the cerebral blood vessels contract. With this function, blood pressure fluctuates greatly and blood flow changes greatly, but at this time, the regulation function of cerebral blood vessels has declined. When blood pressure drops and blood flow decreases, the cerebral vessels fail to relax in time, resulting in insufficient cerebral perfusion. When blood pressure rises and blood flow increases, the cerebral vessels fail to contract in time and turn into hyperperfusion, which is the most prone to brain edema and intracranial hemorrhage. In addition, hypoperfusion itself can also lead to hypoxic-hemorrhagic encephalopathy.

2. Abnormal metabolism of brain tissue The metabolism of human organs and tissues depends on the amount of oxygen and glucose needed by the brain. Insufficient energy supply during hypoxia and ischemia affects brain tissue metabolism, which is also manifested in:

① Oxygen boasting (O2-) damages cell membrane due to peroxidation, and when capillary wall cells are damaged, the permeability increases, leading to brain edema.

② The calcium channel on the cell membrane was opened, and extracellular Ca++ flowed into the cell, which destroyed the survival of the cell.

③ The increase of enkephalin bark in brain tissue directly inhibits respiration and aggravates the degree of hypoxia.

④ Metabolic and respiratory acidosis occurs during hypoxia and ischemia. The above-mentioned abnormal metabolism of brain tissue leads to brain tissue softening, necrosis, bleeding and cavity formation.

3. Areas of the brain that are sensitive to hypoxia and ischemia

① Fetuses and newborns with different gestational ages have different brain mature parts and different susceptibility to hypoxia and ischemia. Areas with rich cells, many blood vessels and high metabolic rate have high oxygen demand and are most sensitive to hypoxia and ischemia. The susceptible area of premature infants is the subependymal mucus layer, because the cell metabolism in this area is the most active at 28 weeks, and the capillaries in this area lack the support of connective tissue, so it is easy to bleed. After 32-34 weeks of pregnancy, the active cells in the mucus layer gradually moved to the cerebral cortex, and the left mucus layer was replaced by white matter. However, due to insufficient blood supply, it can still be affected by hypoxia and ischemia. The cerebral cortex of full-term infants has become a susceptible area because of the migration of active cells.

② The area around the artery is prone to hypoxia and ischemia due to insufficient blood supply and low blood pressure. The temporal area of the parietal lobe of full-term infants is the boundary area between the ends of the anterior, middle and posterior arteries of the brain, and the white matter around the ventricles of premature infants is also the peripheral area of the arteries, which is prone to tissue softening.

pathological change

The distribution and range of lesions mainly depend on the maturity, severity and duration of brain injury. After hypoxia and ischemia, the brain first appears edema, softening, bleeding and necrosis, and then forms a cavity. Hemorrhage can occur in the ventricles, omentum and subdural, and the brain can shrink in the course of the elderly.

1. Brain lesions Most of the cerebral cortex of full-term infants has lesions, except edema and hemorrhage and necrosis. After forming a small cavity, it is called polycystic brain, and if forming a large cavity, it is called spongiform brain.

2. Intracranial hemorrhage Premature infants are mostly bleeding in subependymal and ventricle, and full-term infants are mostly bleeding in brain parenchyma (IPH). Others such as subdural hemorrhage (SDH) and subarachnoid hemorrhage (SAH) can occur in full-term and premature infants.

3. Brain stem lesions heal in the brain stem nucleus or white matter. Brain stem can also appear secondary atrophy due to cerebral cortex lesions.

4. Premature infants showed periventricular leukomalacia (PVLM).

clinical picture

Acute injuries and lesions in both hemispheres of the brain often occur within 24 hours after birth, and 50%-70% of them may have convulsions, especially in full-term infants. The most common manifestations of convulsions are mild seizures or multifocal clonus, and there are symptoms and signs of brain edema such as anterior fontanelle uplift. If the lesions are in the brain stem and thalamus, symptoms such as central respiratory failure, pupil contraction or expansion, intractable convulsions may occur, and they often die within 24-72 hours. Some patients have developed hypoxic-ischemic brain damage in utero, and the Apagar score is normal at birth, and the multiple organ damage is not obvious, but the symptoms of nervous system damage gradually appear within weeks or months after birth. According to the condition can be divided into three degrees:

1, mild symptoms are excessive excitement, restlessness, limb tremor, normal or increased muscle tone, mild active hug response and sucking reflex, generally no convulsion, regular breathing and no change in pupils. Symptoms improved within one day and the prognosis was good.

2. Moderate children have drowsiness, slow response, decreased muscle tone, weakened Moro reflex and sucking reflex, frequent convulsions, irregular breathing, and possibly narrowed pupils. Symptoms are obvious within three days and disappear in a week or so, and survivors may have sequelae.

3. Severe children are unconscious, their muscle tone becomes soft, Moro reflex and sucking reflex disappear, they repeatedly twitch, their breathing is irregular, their pupils are asymmetrical, their light reaction disappears, and their mortality rate is high, most of them are killed by one blow. Survivors' symptoms will last for weeks, leaving sequelae.

Laboratory and other inspections

A, blood biochemical examination

1, serum creatine phosphokinase isoenzyme (CPK-BB), normal value < 10U/L, increased when brain tissue was damaged.

2. The normal value of neuron-specific enolase (NSE) is less than 6U/L, and the activity of NSE in plasma increases when neurons are damaged.

Second, the imaging examination

1. Head B-ultrasound examination: coronal and sagittal sector ultrasound examination was performed with the infant's front chimney as the window. It can be operated by bed, not affected by radiation, and can be tracked many times, with many advantages. Can clearly show brain edema, brain parenchymal lesions, ventricular enlargement.

2. Computerized scanning photography (CT) examination of the head: take multi-level photos of the horizontal cross section of the head. The display of subdural hemorrhage and subarachnoid hemorrhage is clearer than that of B-ultrasound, and the complementary examination of CT and B-ultrasound can improve the diagnostic rate.

3. EEG and EEG power spectrum can show abnormal spikes in EEG, and EEG can find power reduction or dislocation, which is helpful to judge the degree of brain lesions, prognosis and distinguish convulsions.

Fourth, cerebrospinal fluid examination In order to reduce the interference to children, cerebrospinal fluid examination should be avoided, and this examination should only be carried out when suppurative meningitis needs to be ruled out. It is worth noting that a very small amount of red blood cells may enter the cerebrospinal fluid of normal newborns, or the cerebrospinal fluid may be yellowish because of jaundice. Doesn't mean there's intracranial hemorrhage.