How to prevent hypoxic-ischemic encephalopathy

How to prevent hypoxic-ischemic encephalopathy

Speaking of hypoxic-ischemic encephalopathy, I believe many friends are not familiar with this type of disease. In fact, hypoxic-ischemic encephalopathy is one of the more common brain damage diseases caused during the perinatal period. This type of disease is divided into three types: mild, moderate, and severe according to the severity of the disease. In addition, the main manifestations are cerebral palsy, learning difficulties, and even coma. How to prevent hypoxic-ischemic encephalopathy?

In fact, the causes of hypoxic-ischemic encephalopathy are very complicated. In addition to the maternal factors that account for a large part, it also includes fetal factors, abnormal fetal position during delivery, and even surgical reasons during delivery. How to prevent hypoxic-ischemic encephalopathy?

Causes of Hypoxic-Ischemic Encephalopathy

Perinatal asphyxia is the main cause of this disease. Anything that causes obstruction of blood circulation and gas exchange between the mother and fetus, resulting in a decrease in blood oxygen concentration, can cause suffocation. 50% are caused by intrauterine asphyxia; 40% are caused by asphyxia during delivery; and 10% are caused by congenital diseases.

(1) Maternal factors: pregnancy-induced hypertension, heavy bleeding, cardiopulmonary disease, severe anemia or shock, etc.

(ii) Placental abnormalities: placental abruption, placenta previa, placental dysfunction or structural abnormalities, etc.

(III) Fetal factors: intrauterine growth retardation, premature birth, post-term birth, congenital malformations, etc.

(iv) Umbilical cord blood blockage: such as umbilical cord prolapse, compression, knotting or wrapping around the neck, etc.

(V) Factors during delivery: such as delayed labor, precipitous labor, abnormal fetal position, surgery or use of anesthetics, etc.

Pathological changes

1. Brain edema: intracellular edema caused by decreased ATP and extracellular edema caused by increased vascular permeability (both vascular edema can compress blood vessels and aggravate hypoxia-ischemia). Brain edema can be seen in bulging anterior fontanelle, widened bone sutures, tense meninges, flat and wide gyri, shallower cerebral grooves and narrowed ventricular cavity.

2. Selective neuronal necrosis: Necrosis of neurons in the cerebral and cerebellar cortex leads to gyral atrophy and glial fiber proliferation. Common sequelae of this type of brain injury are movement disorders, intellectual disability and convulsions. It is a hypoxic injury and is more common in full-term infants.

3. Marble degeneration of the basal ganglia: Marble-like patterns appear in the basal ganglia and thalamus. Microscopic examination revealed massive neuronal loss, gliosis, and excessive myelination. Clinically, it manifests as extrapyramidal dysfunction, which is related to athetosis. It is hypoxic brain damage.

4. Neuronal damage in the parasagittal area of ​​the brain: Ischemic cerebral infarction occurs in the band-shaped area on both sides of the sagittal sinus, which is equivalent to the central nervous system projection area of ​​the shoulder and pelvis. Clinically, there is weakness of the shoulder and iliac joints, and cortical blindness may also occur. More common in full-term infants.

5. Periventricular white matter transformation: This ischemic injury is more common in premature infants. The lesions are located in the deep white matter area around the lateral ventricles, which softens and necrotizes. When the softening area is large, it can liquefy into a cyst, which is called syrinx. Clinical manifestations include spastic paralysis, mental retardation and hydrocephalus.

Disease prevention

To prevent neonatal asphyxia, pregnant women should have regular prenatal check-ups, and high-risk pregnancies should be treated promptly to avoid premature birth and surgical delivery; obstetric techniques should be improved; fetal heart rate monitoring should be performed during delivery for high-risk pregnancies to detect fetal intrauterine distress early and treat it; during delivery, after the fetal head is delivered, the mucus in the mouth and nose should be squeezed out immediately, and the oral and nasopharyngeal secretions should be squeezed out or sucked out again after birth, and all preparations for neonatal resuscitation should be made.

Regarding hypoxic-ischemic encephalopathy, in fact, in order to prevent the occurrence of this type of disease, in addition to the need for pregnant women to undergo various examinations before delivery, if it is a high-risk pregnancy, it is also necessary to use instruments to monitor the fetal heartbeat, etc. Once fetal intrauterine distress is detected, it should be dealt with in a timely manner, which can greatly reduce the occurrence of hypoxic-ischemic encephalopathy in newborns.

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