Ischemic hypoxic encephalopathy

Introduction to hypoxic ischemic encephalopathy Hypoxic-ischemic encephalopathy (HIE) is a brain lesion caused by hypoxia in perinatal neonates, mainly caused by intrauterine distress, neonatal asphyxia, and a small number of brain damage caused by other causes. basic knowledge The proportion of illness: 0.0035% Susceptible population: perinatal newborn Mode of infection: non-infectious Complications: cerebral palsy, hydrocephalus, epilepsy

Causes of hypoxic ischemic encephalopathy

Cause

It is not fully understood and needs to be further studied. It is speculated that it is related to the following reasons:

1. The cerebral blood flow regulation function reduces the blood flow of the normal neonatal cerebral blood vessels to dilate and contract to regulate the blood flow into the brain tissue. When the blood flow decreases, the cerebral vasodilation, and when the blood flow increases, the cerebral blood vessels contract, with this function The flow into the brain tissue is relatively stable. The blood pressure fluctuates greatly during hypoxia-ischemia, and the blood flow changes more. However, the regulation function of the cerebral blood vessels has decreased. When the blood pressure is reduced and the blood flow is reduced, the cerebral blood vessels fail to be timely. Diastolic, forming a low perfusion of the brain, when the blood pressure is increased, the blood flow is increased, the cerebral blood vessels fail to contract in time, and become high perfusion. During this transformation, cerebral edema and intracranial hemorrhage are most likely to occur, and the low perfusion itself is also Can lead to hypoxic encephalopathy.

2. Abnormal metabolism of brain tissue The metabolism of various organs of the human body requires the highest amount of oxygen and glucose required by the brain. The energy supply is insufficient during hypoxia-ischemia, and the metabolism of brain tissue is also the largest, which is manifested in:

1 Oxygen itself is boasted (O2-), which damages the cell membrane by peroxidation. When the capillary wall cells are damaged, the permeability increases, causing cerebral edema;

2 The calcium channel on the cell membrane is open, and extracellular Ca++ flows into the cell, destroying the survival of the cell;

3 increased brain encephalopathy in brain tissue, directly inhibiting breathing and increasing the degree of hypoxia;

4 Metabolic and respiratory acidosis occurs during hypoxia-ischemia, and abnormal brain metabolism causes brain tissue to soften, necrosis, hemorrhage and cavity formation.

3. The brain is susceptible to hypoxia-ischemia

1 The fetal parts of different gestational ages and neonatal brains are different, and the susceptibility to hypoxia-ischemia is different. The cells are rich, the blood vessels are high, and the areas with high metabolic rate have high oxygen demand and are most sensitive to hypoxia-ischemia. The predisposition of the premature infant is in the germinal layer under the ventricle of the ventricle. Because the cell is most active in the fetus at 28±week, and the capillaries in this area lack the support of connective tissue, it is easy to bleed to 32-34 weeks of gestational age. The active cells of the posterior germinal layer gradually migrate to the cerebral cortex, leaving the germinal layer replaced by white matter. However, due to the lack of blood supply to the distal end of the artery, it can still be affected by hypoxia-ischemia. The cerebral cortex is active in term infants. The cells move in and become susceptible areas;

2 The marginal zone of the arterial tip is due to low blood supply and low blood pressure, which is a good site for hypoxia-ischemia. The apical part of the full-term infant is the junction of the anterior, middle and posterior arteries of the brain. The white matter area around the ventricles is also the end of the arteries, which is prone to tissue softening.

Pathological change

After hypoxia-ischemia, the brain first appears edema, softening, hemorrhage and necrosis, and later forms a cavity, intraventricular, subarachnoid, subdural may be bleeding, the brain may be atrophied in the elderly.

1. Cerebral lesions Full-term children's lesions are mostly in the cerebral cortex. In addition to edema, there is bleeding and necrosis. After forming a small cystic cavity, it is called spelencephaly. If a large cavity is formed, it is called porencephalen.

2, intracranial hemorrhage premature infants with more bleeding sites in the subependy and ventricles, full-term children in the brain parenchyma (IPH), other such as subdural hemorrhage (SDH) and subarachnoid hemorrhage (SAH) in the foot Both children and premature babies can occur.

3, brain stem lesions in the brain stem nucleus or white matter sputum, brain stem can also appear due to lesions of the cortex secondary to atrophy.

Hypoxic ischemic encephalopathy is caused by asphyxia in term infants. The longer the asphyxia, the longer the time, the more serious the brain disease, the higher the incidence of sequelae. The disease can also occur in premature infants, which is characterized by softening of white matter around the ventricles. (Periventricular Leukomalacia, PVLM).

Hypoxic ischemic encephalopathy prevention

Umbilical cord around the neck, maternal pregnancy-induced hypertension, maternal anemia, umbilical cord prolapse factors can cause perinatal asphyxia, and studies have shown that H IE is closely related to perinatal abnormal factors, therefore, in perinatal examination and labor observation, Timely detection of high-risk factors and timely correction, if necessary, end pregnancy is a protection for perinatal children, must strengthen the obstetrics technology in primary hospitals, there are obstetric abnormalities, vaginal delivery should be timely cesarean section to stop pregnancy, can not delay the opportunity To reduce the incidence of perinatal asphyxia. Once the fetal distress is found, the mother is immediately given oxygen, and the newborn's resuscitation and oxygen supply are prepared. After birth, the child is placed supine, the head is raised slightly, and the disturbance is less.

Hypoxic-ischemic encephalopathy complications Complications cerebral hydrocephalus epilepsy

Common sequelae include cerebral palsy, hydrocephalus, mental retardation, epilepsy, etc., such as white matter softening around the ventricles may have dyskinesia.

Hypoxic-ischemic encephalopathy symptoms Common symptoms Blink coma Neonatal response Low hug Reflex Disappear convulsions Drowsiness Responsive limb tremor Respiratory irregular sucking reflex disappears Muscle tension enhancement

Hypoxic-ischemic intracranial hemorrhage is more common in premature infants. The higher the gestational age, the higher the incidence. The hemorrhage site is most common in the subependymal caudate nucleus, and it is easy to break into the adjacent lateral ventricle and become subventricular. Intraventricular hemorrhage (SEH-IVH), general hypoxic ischemic encephalopathy may have a history of intrauterine distress before birth, fetal heart rate may increase or slow during childbirth, or the second stage of labor is prolonged, amniotic fluid is contaminated by meconium There is a history of asphyxia at birth, there is still consciousness after the recovery, muscle tension, respiratory rhythm, reverse and other changes, and even convulsions, according to the condition can be divided into three degrees:

Mild

Excessive excitement, irritability, limbs can be fibrillated, muscle tension is normal or increased, hug response and sucking reflexes are slightly active, generally no convulsions, breathing rules, no changes in pupils, improved symptoms within one day, good prognosis.

2. Moderate

Children with sleepiness, slow response, decreased muscle tone, weakened hugs and sucking reflexes, often convulsions, irregular breathing, dilated pupils, symptoms are obvious within three days, disappear within about a week, survivors may have sequelae .

3. Severe

The child is unconscious, the muscle tension is soft, the hug reflex and the sucking reflex disappear, the convulsions are repeated, the breathing is irregular, the pupil is asymmetrical, the response to light disappears, the mortality rate is high, and more deaths occur in one shot, and the symptoms of survivors are sustainable. For weeks, there are sequelae.

Examination of hypoxic ischemic encephalopathy

1, imaging diagnosis

Improve the accuracy of the diagnosis.

(1) Skull B-mode ultrasound (B-ultrasound) examination: clear cerebral edema, brain parenchymal lesions and ventricular enlargement.

(2) CT scan of the skull (CT): a multi-level cross-section of the horizontal level of the skull, the display of a small amount of subdural hemorrhage and subarachnoid hemorrhage is clearer than the B-ultrasound examination, so CT and B-super complementary examination can be Improve the diagnostic rate.

2, EEG and EEG power spectrum examination

Abnormal spikes can occur in the EEG, and the EEG power map can be found to have reduced or misaligned power.

3, cerebrospinal fluid examination

In order to reduce the disturbance to the child, cerebrospinal fluid examination should be avoided. This test should be performed only when it is necessary to exclude purulent meningitis. It is worth noting that normal newborn cerebrospinal fluid may have a very small amount of red blood cells entering the cerebrospinal fluid, or cerebrospinal fluid due to jaundice. It is pale yellow and does not indicate a cranial hemorrhage.

Diagnosis and diagnosis of hypoxic ischemic encephalopathy

diagnosis

Diagnosis can be based on medical history, clinical symptoms, and laboratory findings.

Differential diagnosis

The disease needs to be differentiated from diseases such as central nervous system damage and meningitis.

Children with eczema caused by increased intracranial pressure caused by cerebral palsy (the soft part of the baby's head bones are not spliced), the initial symptoms are similar to colds, such as fever, headache and vomiting, followed by drowsiness and neck pain, especially It is pain when stretching your neck forward. Children often feel pain when they have a back of the bow. JE will also have dark red or light purple spots on the whole body. Combined with medical history, it can be identified as encephalitis.

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