bubble_chart Overview

Intracranial hemorrhage is a common and severe condition in newborns, and one of the leading causes of perinatal neonatal death. Subependymal and intraventricular hemorrhages are the most frequently seen types.

bubble_chart Etiology

It can be divided into two types: the hypoxic type occurs when capillaries increase permeability due to hypoxia, leading to blood leakage, which can happen before birth, during birth, or after birth. The injury type occurs exclusively during birth. In reality, a significant number of intracranial hemorrhages occur due to injury on the basis of hypoxia and tissue dysfunction.

Traumatic intracranial hemorrhage increases with higher birth weight. In very low birth weight infants during difficult delivery, intracranial hemorrhage is primarily injury-related, whereas in natural childbirth, it is mainly hypoxic. The proportion of injury-related cases is significantly higher in difficult deliveries compared to natural childbirth. Analysis by birth weight shows the general pattern: the smaller the birth weight, the more hypoxic cases occur, while larger birth weights correlate with more injury-related cases. The more severe the hypoxia, the more prone to injury. Due to reduced clotting factors in newborns during the first week of life, there is a tendency for bleeding, which can worsen the severity and consequences of intracranial hemorrhage. A few cases are caused by iatrogenic factors such as vitamin K deficiency, rupture of intracranial vascular malformations, or rapid intravenous injection of sodium bicarbonate or volume expanders.

bubble_chart Pathological Changes

All cerebral hypoxic lesions develop in a centripetal manner. Premature infants are most susceptible to capillary injury due to hypoxia. The smaller the gestational age, the more abundant the primitive neural cells in the subependymal germinal layer tissue and the blood vessels with only a single layer of endothelial cells. These small vessels lack connective tissue support and exhibit a unique U-shaped blood flow direction, making them highly sensitive to hypoxia, hypercapnia, and acidosis. Under circulatory disturbances and increased venous pressure, they are prone to rupture, allowing blood to enter the ventricles from the subependymal region and also to spill from the fourth ventricle into the subarachnoid space. Near-term infants have more mature ventricles and greater resistance to hypoxia, but survivors may develop numerous cavities in the white matter and marginal areas of the cerebral cortex. The cerebral cortex of full-term infants remains sensitive to hypoxia; with circulatory failure or sustained venous hypertension, the marginal zones of the white matter are prone to infarction and/or hemorrhage. Rupture of choroid plexus vessels can lead to intraventricular hemorrhage.

Subdural hemorrhage is mainly caused by birth trauma, such as tears in the tentorium cerebelli or falx cerebri, or rupture of the great cerebral vein or superior cerebral veins. Blood pooling at the base of the brain can compress the medulla oblongata, leading to death. Fractures of the parietal bone, squamous part of the occipital bone, or skull base often injure cranial nerves and are accompanied by subdural hemorrhage.

Epidural hemorrhage is rare and is primarily caused by the separation of the inner table of the skull from the dura mater during forceps delivery, resulting in rupture of the middle meningeal artery.

bubble_chart Clinical Manifestations

In extremely severe cases, death may occur during delivery or shortly after birth with only a faint heartbeat, and despite aggressive resuscitation, the outcome remains fatal.

Most cases experience asphyxia at birth, with slow recovery from resuscitation, difficulty in establishing respiration, and symptoms of cortical stimulation and increased excitability within 12 hours, such as dysphoria, restlessness, moaning, refusal to feed, weak crying, hypothermia, hyperactive Moro reflex, muscle tremors, spasms, staring, strabismus, nystagmus, unequal pupil size, absent light reflex, and respiratory disturbances. Due to the unfused cranial sutures in newborns, signs of increased intracranial pressure are often less obvious. The anterior fontanelle may be tense but rarely bulging or accompanied by projectile vomiting, and opisthotonos is uncommon. Subsequently, cortical inhibitory symptoms may appear, such as drowsiness, unconsciousness, decreased muscle tone in the limbs, weakened or absent Moro reflex, and irregular breathing. Severe cases and premature infants may exhibit only inhibitory symptoms without excitatory signs. Generally, traumatic intracranial hemorrhage presents earlier and more severely than hypoxic-ischemic injury. A few cases may show symptoms only 2–3 days after birth, and in rare instances, intracranial hemorrhage due to vitamin K deficiency may manifest 1–2 months postpartum.

Mild cases or those with minor periventricular parenchymal hemorrhage may exhibit symptoms later, alternating between excitation and inhibition—appearing intermittently dull or irritable—and are easily overlooked. Some cases, termed "silent," present with even fewer symptoms, often only reduced activity, hypotonia, and decreased hematocrit, which may draw attention. Recent studies using modern CT imaging for intracranial hemorrhage detection have identified cases even in normal control groups, indicating that very mild forms of the disease may be asymptomatic and go unnoticed. Burstion et al. reported that among premature infants weighing less than 1500g with subependymal hemorrhage, 68% showed no clinical symptoms.

Infratentorial hemorrhage manifests as brainstem compression with respiratory and circulatory disturbances, indicating a more severe condition. Cerebral hemorrhage presents with excitability, high-pitched crying, irritability, and seizures. Subdural hemorrhage may be asymptomatic in mild cases, while severe cases may involve hemiplegia or focal spasms. Posterior fossa hematoma or cerebellar hemorrhage manifests as medullary compression, with rapid progression.

Overall, the clinical presentation of this disease varies widely depending on the cause, type, location, and extent of hemorrhage. In atypical cases, neurological symptoms are often overshadowed by respiratory dysfunction and irregular breathing.

bubble_chart Diagnosis

1. Medical History: Gestational age less than 32 weeks, weight under 1500g, prone to subependymal hemorrhage and intraventricular hemorrhage, with an incidence rate of 40-50%. Most cases occur within 3 days.

2. Clinical Manifestations: Often lacks an excitatory phase, with prominent inhibitory symptoms such as refusal to feed, drowsiness, low responsiveness, hypotonia, and absence of the Moro reflex. Paroxysmal irregular respiratory rhythms and apnea frequently occur, accompanied by cyanosis. In advanced stages, convulsions and unconsciousness may appear. Complexion is pale, anterior fontanelle bulging, eyes staring, pupils unequal or dilated and fixed, with loss of light reflex.

3. Auxiliary Examinations:

(1) Hemoglobin, platelet count, and hematocrit decrease. Prothrombin time is prolonged, indirect bilirubin increases, blood gas analysis shows metabolic and respiratory acidosis, and hypoxemia.

(2) Cerebrospinal fluid: Subarachnoid and intraventricular hemorrhage, cerebrospinal fluid appears bloody, and microscopy reveals shrunken red blood cells.

(3) Others: Changes in the anterior fontanelle and head circumference can be dynamically observed. Skull transillumination, cranial B-ultrasound, and CT scans can be performed as needed. CT can accurately determine the type, location, and severity of hemorrhage, aiding in prognosis assessment. Specific grading is as follows: Grade I: Subependymal hemorrhage; Grade II: Intraventricular hemorrhage without ventricular dilation, with over 90% survival; Grade III: Intraventricular hemorrhage with ventricular dilation; Grade IV: Intraventricular hemorrhage with parenchymal hemorrhage, with a mortality rate of 50%.

bubble_chart Treatment Measures

1. Prevent continued bleeding by keeping warm, maintaining quiet, limiting activity, and providing oxygen. Avoid crying to prevent exacerbating hemorrhage, and centralize nursing care. Ensure airway patency. For those without vomiting, elevate the upper body by 15–30 degrees to reduce intracranial pressure. For those with vomiting, to avoid aspiration, it is advisable to lie flat with the head turned to one side and feed via a gastric tube. Intravenous fluid intake should be restricted to 60 ml/kg/day, adjusted based on vomiting, cardiac, and renal function. Administer vitamin K₁5 mg intramuscularly or intravenously once daily for 3 days (reduce dosage for premature infants) and supplement with vitamin C. Other hemostatic agents such as etamsylate may also be used. A small amount of fresh blood or fresh frozen plasma (10 ml/kg) can be transfused to replenish clotting factors and correct anemia.

2. Symptomatic treatment: Dysphoria and spasms may worsen bleeding. Administer chlorpromazine (2 mg/kg/dose) and phenobarbital sodium (5–8 mg/kg/dose) alternately via intramuscular injection every 3–4 hours. Gradually reduce the dosage after symptoms are controlled. Alternatively, a loading dose of phenobarbital sodium (20 mg/kg IV) followed by a maintenance dose (2.5 mg/kg every 12 hours) may be used. Combining with diazepam enhances the anticonvulsant effect. For cases with bulging fontanelle and significantly increased intracranial pressure, administer mannitol as a dehydrating agent—initial dose 0.5–0.75 g/kg IV, followed by 0.25 g/kg four times daily. Dexamethasone (0.5–1 mg/kg IV, 2–4 times daily) may enhance efficacy. Severe cases may require furosemide (1 mg/kg/dose) until intracranial pressure decreases and cerebral edema is controlled, then gradually taper and discontinue. The usual treatment course is 2–3 days.

For persistent cyanosis despite oxygen therapy, weak or irregular breathing, assist with a ventilator and correct acidosis to maintain adequate perfusion.

In cases of subdural hematoma, perform repeated subdural punctures for fluid drainage. If effusion persists after 3 weeks, surgical removal of the fluid-filled sac may be necessary.

3. Protect brain tissue by administering cytochrome C, coenzyme A, and ATP in 10% glucose solution via IV drip for 1–2 weeks. Additionally, glutamate, gamma-aminobutyric acid (GABA), vitamin B6, citicoline, cerebrolysin, and piracetam may aid in restoring brain cell function.

4. Administer antibiotics to prevent infection.

bubble_chart Prognosis

First, a clear diagnosis must be made. Mild intracranial hemorrhage has an almost 100% survival rate, with sequelae ranging from 0% to 10%. Moderate cases have a mortality rate of 5% to 15%, with sequelae between 15% and 25%. Severe cases have a mortality rate of 50% to 65%, with sequelae ranging from 65% to 100%. Common sequelae include hydrocephalus, porencephalic cyst formation, motor and intellectual impairments, quadriplegia, epilepsy, hypotonia, and others.

bubble_chart Prevention

Before birth, measures should be taken to prevent premature labor and avoid asphyxia. Pregnant women must maintain absolute bed rest to reduce uterine contractions, and β-adrenergic agonists such as hydroxyephedrine (Ritodrine) can be used to delay childbirth. During labor, fetal monitoring should be conducted, and immediate rescue measures should be taken if intrauterine hypoxia or birth asphyxia is detected. Efforts should be made to avoid birth trauma during childbirth, and a cesarean section should be performed if necessary. For pregnant women at risk of premature labor, dexamethasone should be administered within 3 days before childbirth to promote lung maturation and reduce the risk of respiratory distress syndrome. To prevent bleeding tendencies, phenobarbital 50mg can be slowly administered intravenously 10 hours before childbirth, and vitamin K 15–30mg should be given orally 4–15 hours before delivery.

For premature infants weighing less than 1500g, phenobarbital can be administered within 6 hours after birth to reduce cerebral metabolic rate, clear free radicals, decrease cerebral blood flow, and suppress sudden increases in blood pressure.

For breastfeeding mothers, they should be advised to consume more leafy greens and fresh fruits. For those who frequently experience diarrhea or take antibiotics, vitamin K 50–100μg/day should be given, or vitamin K 1mg can be injected monthly. Infants with obstructive jaundice or hepatitis should be given vitamin K ₁ to prevent intracranial hemorrhage caused by deficiency.

bubble_chart Differentiation

In cases of cerebral hypoxia due to intracranial hemorrhage, shallow and irregular breathing or pauses are more common; whereas pulmonary hypoxia is primarily characterized by shortness of breath, nasal flaring, and three-concave signs, with cyanosis improving after oxygen administration or crying. Cardiac hypoxia often presents with increased respiratory depth, and cyanosis persists even after oxygen therapy. Spasm should be differentiated from conditions such as cerebral edema after asphyxia hypoxia, hypoglycemia, hypocalcemia, hyponatremia, hypomagnesemia, vitamin B₆ dependency, intracranial malformations, infections, and kernicterus. Hypotonia should be distinguished from Down syndrome, myasthenia gravis, congenital hypotonia syndrome, and glycogen storage diseases of the cardiac or muscular type, as well as abdominal mass diseases.