OVERVIEW

What is hypoxic-ischemic encephalopathy?

Hypoxic-ischemic encephalopathy (HIE) refers to brain damage caused by insufficient blood flow and oxygen supply to brain tissue due to various reasons.

Who is prone to hypoxic-ischemic encephalopathy?

Newborns, patients with cardiovascular or cerebrovascular diseases, suicidal individuals, those at risk of cardiac or respiratory arrest, people susceptible to suffocation, etc.

SYMPTOMS

What are the symptoms or manifestations of hypoxic-ischemic encephalopathy?

• Main manifestations include: impaired consciousness, excessive excitement, lethargy, or even coma; changes in limb muscle tone, such as increased or decreased tone, or even flaccidity; abnormal primitive reflexes, such as hyperactive, weakened, or absent Moro reflex, and weakened or absent sucking reflex.

• In severe cases, seizures may occur, and increased fontanelle tension due to cerebral edema.

• Adults may exhibit impaired consciousness, mental disorders, or epileptic seizures after a clear history of brain tissue hypoxia.

• Severe cases may present with brainstem damage symptoms, such as irregular breathing, slowed breathing, or apnea (central respiratory failure), constricted or dilated pupils, sluggish or absent light reflex, and some patients may experience nystagmus.

How is the severity of hypoxic-ischemic encephalopathy classified in pediatric patients?

Pediatric cases are divided into three degrees based on severity:

• Mild manifestations: Irritability and excitement, most noticeable within the first day, resolving within 2–3 days; normal or slightly increased limb muscle tone, increased spontaneous movements; normal or slightly hyperactive primitive reflexes; no seizures or increased fontanelle tension. Prognosis is usually favorable.

• Moderate manifestations: Predominantly depressive symptoms, such as drowsiness or lethargy, weak crying; decreased limb muscle tone, reduced spontaneous movements; weakened primitive reflexes, incomplete Moro reflex, and poor feeding. Some patients may exhibit increased intracranial pressure and seizures. Most symptoms resolve within a week, but prolonged symptoms may indicate potential sequelae.

• Severe manifestations: Coma predominates, with absent limb muscle tone (flaccidity), no spontaneous movements, and absent primitive reflexes. Most patients have increased intracranial pressure and seizures, which may be frequent and difficult to control even with adequate sedation. Some show brainstem symptoms, such as irregular breathing, apnea, constricted or dilated pupils, and sluggish or absent light reflex. Some patients die within a week, and survivors often have severe sequelae.

How is the severity of hypoxic-ischemic encephalopathy classified in adult patients?

Adults are classified based on the degree of impaired consciousness (Glasgow Coma Scale, GCS). Lower GCS scores indicate more severe impairment.

• A maximum score of 15 indicates clear consciousness;

• Scores of 12–14 indicate mild impairment;

• Scores of 9–11 indicate moderate impairment;

• Scores ≤8 indicate coma.

CAUSES

Hypoxic-ischemic encephalopathy is commonly seen in newborns. What are its main causes?

Neonatal hypoxic-ischemic encephalopathy is a brain lesion caused by hypoxia in perinatal (from the 28th week of pregnancy to one week after birth) newborns. Common causes include fetal distress due to various factors (such as umbilical cord around the neck, abnormal amniotic fluid, etc.), as well as asphyxia and hypoxia during delivery or after birth.

Newborns with a history of asphyxia may exhibit changes in consciousness, muscle tone, and respiratory rhythm after resuscitation, and may even experience convulsions.

Can hypoxic-ischemic encephalopathy occur in non-neonates?

Hypoxic-ischemic encephalopathy can occur in anyone whose brain experiences ischemia or hypoxia. While it is most common in newborns, it can also occur in other age groups.

How does hypoxic-ischemic encephalopathy develop? What is its pathogenesis?

Under hypoxic conditions, the metabolic function of brain cells is impaired, and the autoregulation of cerebral blood vessels is reduced, making cerebral blood flow perfusion more susceptible to systemic blood pressure drops.

Swelling of perivascular astrocytes and bubble-like degeneration of vascular endothelial cells narrow or even occlude the lumen. Even after blood flow is restored, blood cannot reach these ischemic areas, leading to regional ischemia or infarction and potentially irreversible brain damage.

Hypoxia increases vascular permeability, causing certain metabolites to accumulate in tissues. Factors such as increased antidiuretic hormone secretion contribute to cerebral edema, raising intracranial pressure and further reducing cerebral blood flow. This leads to severe metabolic dysfunction in brain cells, eventually resulting in brain atrophy.

Under what circumstances do non-neonatal patients typically develop hypoxic-ischemic encephalopathy?

In non-neonates, hypoxic-ischemic encephalopathy occurs due to severe brain ischemia or hypoxia caused by various factors, such as respiratory or cardiac arrest (e.g., asphyxia, hanging, drowning), as well as shock, carbon monoxide poisoning, status epilepticus, or myasthenia gravis.

Any process causing systemic ischemia or hypoxia can lead to this condition, which may also be an intermediate or terminal stage of certain diseases.

Therefore, it is not an independent disease but a severe manifestation during disease progression. For example, chronic renal failure can cause hyperkalemia, cardiac arrest, and respiratory failure, leading to hypoxic-ischemic encephalopathy—a critical factor in mortality. Timely treatment may restore the patient to their pre-onset condition; otherwise, death or sequelae may occur.

Can hypoxic-ischemic encephalopathy be prevented by oxygen therapy alone?

The causes of hypoxic-ischemic encephalopathy include ischemia, hypoxia, or both. Oxygen therapy only increases oxygen supply. For example, in cases of asphyxia, providing oxygen alone will not prevent hypoxic-ischemic encephalopathy.

DIAGNOSIS

How is hypoxic-ischemic encephalopathy diagnosed? Can a history of hypoxia-ischemia alone confirm the diagnosis?

A definitive history of hypoxia-ischemia combined with subsequent acute neurological damage may be considered for diagnosis.

If the duration of hypoxia-ischemia is too brief, the body can generally compensate and recover. The critical duration depends on whether it is complete or incomplete hypoxia-ischemia, as well as the age of the individual.

Simply put, the greater the brain's demand for blood and oxygen, the more susceptible it is to damage, especially in newborns. Acute poisoning, cerebrovascular diseases, hypoglycemic coma, etc., should also be ruled out.

What tests are needed for hypoxic-ischemic encephalopathy?

Tests include head CT or MRI, blood biochemistry (enzyme levels), blood glucose measurement, blood gas analysis, brain natriuretic peptide levels, electroencephalogram (EEG), etc. Head CT often shows cerebral edema and demyelination.

What should be noted during these examinations for hypoxic-ischemic encephalopathy?

For patients with sudden cardiac or respiratory arrest, if vital signs are still unstable during resuscitation, aggressive testing may pose risks. A head CT can be performed within 48 hours if necessary, with full preparation based on the patient's condition. MRI takes longer and is better suited for assessing recovery potential once the patient is stable.

What is the Apgar score for hypoxic-ischemic encephalopathy? What is its significance?

The Apgar score is a simple method to assess whether a newborn has asphyxia and its severity. It corresponds to the first letters of the evaluated criteria: Activity (muscle tone), Pulse (heart rate), Grimace (reflex irritability), Appearance (skin color), and Respiration. The score reflects the degree of neonatal asphyxia, helping clinicians promptly evaluate the condition and guide resuscitation efforts.

If the Apgar score is low in hypoxic-ischemic encephalopathy, will the newborn definitely develop complications later?

Apgar score results: 8–10 indicates no asphyxia, 4–7 mild asphyxia, and 0–3 severe asphyxia. A score of 8 or above is generally considered normal. For infants with lower scores, long-term outcomes depend on their specific growth and development.

TREATMENT

How to treat hypoxic-ischemic encephalopathy?

In the early stages of hypoxic-ischemic encephalopathy, maintain vital signs, identify the cause, and provide hypothermic brain protection if possible. Hyperbaric oxygen therapy should be administered as soon as possible to improve cerebral ischemia and hypoxia. Other awakening-promoting methods, such as Xingnaojing and Butylphthalide, as well as traditional Chinese medicine and acupuncture, can also be used.

Do all hypoxic-ischemic encephalopathy patients require tracheotomy?

Patients who regain consciousness quickly do not need it, but those who remain unconscious for an extended period should undergo tracheotomy as early as possible. This is especially important for elderly patients with chronic bronchitis, as phlegm blockage and hypoxia may occur, reducing the likelihood of recovery.

Is early rehabilitation suitable for hypoxic-ischemic encephalopathy?

If the patient's condition is stable in the early stages, rehabilitation training should begin as soon as possible to restore limb function and other abilities promptly.

DIET & LIFESTYLE

How to Care for Patients with Hypoxic-Ischemic Encephalopathy?

• When the patient is in a coma, professional airway care is required to prevent bedsores. Pay attention to the management of incontinence, ensure energy supply, and prevent lung infections and deep vein thrombosis.

• For conscious patients, initiate rehabilitation training as early as possible, provide psychological counseling (especially for those with suicidal tendencies), and follow a gradual approach during recovery. Prevent recurrence of hypoxic-ischemic encephalopathy.

What Dietary Considerations Should Patients with Hypoxic-Ischemic Encephalopathy Follow?

A light diet is generally recommended, especially for obese individuals or those with underlying cardiovascular diseases. Patients whose condition is triggered by allergies must strictly avoid allergens.

Can Hypoxic-Ischemic Encephalopathy Be Caused by Babies Sleeping Face Down?

Generally not. Most infants adjust their heads sideways to breathe while sleeping face down, so hypoxic-ischemic encephalopathy is unlikely. However, cases may occur if a mother holds the baby too tightly during breastfeeding or accidentally blocks the infant’s nose and mouth, leading to suffocation and hypoxia.

PREVENTION

How to Prevent Hypoxic-Ischemic Encephalopathy?

• Before birth, monitor for high-risk factors (abnormal conditions that may lead to fetal intrauterine hypoxia-ischemia, such as umbilical cord entanglement around the neck or body, placenta previa or placental abruption; severe maternal gestational hypertension syndrome; severe intrauterine distress; prolonged labor, etc.). Correct these issues promptly and terminate the pregnancy if necessary to reduce the occurrence of HIE.

• If asphyxia occurs during delivery, provide timely and proper resuscitation. After resuscitation, protect vital organ functions, especially maintaining normal cardiovascular function, to ensure proper brain metabolism and function.

• Patients with allergies should avoid exposure to allergens.

• Patients with cardiovascular or cerebrovascular diseases should receive early prevention, and those with suicidal tendencies should undergo active intervention.

• In particular, immediate cardiopulmonary-cerebral resuscitation is crucial during disease onset to minimize brain damage and functional impairment.