intracranial hemorrhage in neonates

Introduction

Introduction to neonatal intracranial hemorrhage Neonatal intracranial hemorrhage (intracraninal hemorrhage of newborn) is a common serious disease in neonates. It is a common brain injury caused by birth injury and hypoxia. It is also one of the main causes of perinatal neonatal death, including subdural Hemorrhage, subarachnoid hemorrhage, subventricular ventriculo-intraventricular hemorrhage, cerebellar hemorrhage, and parenchymal hemorrhage. Subventricular-intraventricular hemorrhage is the most common, and the prognosis is poor. In recent years, due to the advancement of obstetric techniques, subdural hemorrhage caused by birth injury has been significantly reduced, and periventricular-intraventricular hemorrhage caused by hypoxia in premature infants has become a new life. The most common type of intracranial hemorrhage, high mortality of neonatal intracranial hemorrhage, is one of the main causes of early neonatal death. Some surviving children often have severe sequelae of various nervous systems, such as hydrocephalus and cerebral palsy. Epilepsy and mental retardation should be actively controlled. basic knowledge The proportion of illness: 0.001% Susceptible population: newborn Mode of infection: non-infectious Complications: epilepsy, coma, hearing impairment, ataxia

Cause

Causes of neonatal intracranial hemorrhage

(1) Causes of the disease

Hypoxia-ischemia

All prenatal, postpartum and postpartum can cause fetal or neonatal hypoxia, asphyxia, ischemic factors, hypoxic ischemic encephalopathy often leads to hypoxic intracranial hemorrhage, premature infants are more common, the incidence of gestational age is smaller The higher, due to intrauterine distress, intrapartum and postpartum asphyxia, umbilical around the neck, placental abruption, etc., metabolic acidosis occurs during hypoxia-ischemia, resulting in increased permeability of the blood vessel wall, blood spillage, mostly oozing Or point-like hemorrhage, the amount of bleeding is often small and the bleeding range is wide and scattered, resulting in subependymal hemorrhage, parenchymal hemorrhage, subarachnoid hemorrhage.

2. Injury

Squeezing the fetal head is an important cause of birth traumatic intracranial hemorrhage. It is more common in full-term children. It can be caused by too large fetal head, too small birth canal, no head basin, breech production, and too much resistance to the birth canal. , emergency production, high position forceps, suction device, etc., so that the head is squeezed, pulling and causing intracranial blood vessel tears, bleeding, bleeding sites more common in the subdural.

3. Other

Intracranial congenital vascular malformations or systemic hemorrhagic diseases, such as decreased expression of certain coagulation factors can also cause intracranial hemorrhage or exacerbation of IVH, such as vitamin K-dependent clotting factor deficiency, thrombocytopenia, etc., can cause intracranial hemorrhage, rapid expansion, input Hypertonic fluids, excessive blood pressure fluctuations, improper mechanical ventilation, inspiratory peak pressure or excessive end-expiratory positive pressure also promote intracranial hemorrhage to a certain extent.

(two) pathogenesis

1. Traumatic intracranial hemorrhage: excessive pressure on the fetal head during childbirth, uneven local pressure or deformed over-speed in a short period of time can cause subdural hemorrhage, mainly caused by birth trauma, cerebral palsy, The cerebellum canopy tears, the cerebral veins or the upper cerebral veins rupture, the blood pooling at the bottom of the brain can compress the brain, promote death, parietal bone, occipital squamous and skull base fractures, and cranial nerve with subdural hemorrhage The venous tear of the surface of the brain is often accompanied by subarachnoid hemorrhage.

Among the children with breech delivery, the most serious type of birth injury is occipital separation with posterior cranial fossa hemorrhage and cerebellar tear. The premature infant has a soft skull. External pressure compression of the occiput can also cause the occipital bone to move forward. Distorted sinus and occipital sinus, causing cerebellar hemorrhage, which often occurs in breech traction, forceps delivery, and application of mask compression ventilation.

Epidural hemorrhage is rare, mainly due to the rupture of the middle meningeal artery when the intracranial plate is separated from the dura mater.

2. Hypoxic ischemic intracranial hemorrhage

(1) Increased capillary permeability: Hypoxia and acidosis directly damage capillary endothelial cells, causing increased permeability or rupture.

(2) Autonomous regulation of dysfunction: hypoxia and acidosis damage the cerebral vascular autoregulation function, forming a pressure passive brain current. When the systemic circulation pressure increases, the cerebral blood flow increases, causing the capillary to rupture. On the contrary, when the blood pressure drops, Cerebral blood flow is reduced and ischemic changes, and hemorrhagic foci may be present in the ischemic necrosis area.

(3) Premature delivery: All brain hypoxic lesions are developed according to centripetal, premature infants are most likely to cause capillary damage due to hypoxia, 32 weeks premature infants in the lateral ventricles of the brain and the subventricular membrane around the fourth ventricle And the outer granular layer under the cerebellar subbrain retains the embryonic germinal matrix, and the smaller the gestational age, the more abundant the primitive nerve cells of the subependymal layer and the blood vessels with only one layer of endothelial cells, the tissue is an immature The capillary network has only one layer of endothelial cells in the blood vessel wall. These small blood vessels lack connective tissue support, lack collagen tissue support, small capillary fragile, and have a unique U-shaped blood flow direction, for hypoxia, hypercapnia and Acidosis is extremely sensitive. When the arterial pressure suddenly rises, it can cause capillary rupture and hemorrhage. The blood in the ependymium can penetrate the ependymal membrane and cause intraventricular hemorrhage. At the same time, it can also overflow from the fourth ventricle into the subarachnoid space. The fibrinolysis system around the cerebral ventricle is active, so it can spread to the white matter and cause parenchymal hemorrhage. The venous system around the ventricle is U-shaped. When hypoxia or blood pressure drops, the blood flow changes direction, which is easy to cause blood. The fluid stagnant, the capillary bed pressure increased and ruptured; some full-term children still have a germinal matrix under the ependymal membrane, so bleeding may also occur, and most of the intraventricular hemorrhage comes from the choroid plexus.

The cerebral ventricle is mature in recent months and is more resistant to hypoxia. However, in the dead, the white matter and the margin of the cerebral cortex can form many cavities. The cerebral cortex of term infants is still sensitive to hypoxia, when circulatory failure or Continuous high blood pressure, infarcts and/or hemorrhage in the marginal zone of white matter, rupture of choroid plexus can cause intraventricular hemorrhage.

3. Iatrogenic intracranial hemorrhage: excessive movement of the baby, infusion of hypertonic fluid or infusion too fast, frequent attraction and pneumothorax can cause a sharp rise in blood pressure leading to changes in cerebral blood flow and cause intracranial hemorrhage.

Prevention

Neonatal intracranial hemorrhage prevention

Prevent premature birth and avoid suffocation before birth.

1. Do a good job in maternal health care, avoid premature birth, improve obstetric techniques, reduce neonatal asphyxia and birth injury, and promptly treat pregnant women with bleeding disorders. Pregnant women must be absolutely bedridden to reduce uterine contractions, and can use -adrenalin. A class of drugs such as Ritodrine to delay delivery.

2, improve the quality of care, to avoid a variety of factors that may lead to iatrogenic intracranial hemorrhage, the monitoring of the fetus during the labor process, such as seeing intrauterine hypoxia and asphyxia at birth, are promptly rescued, try to avoid birth injury during childbirth, necessary When doing cesarean section.

3, for pregnant women who may be premature birth, dexamethasone should be applied within 3 days before delivery to promote lung maturation and reduce the risk of respiratory asphyxia syndrome, to prevent bleeding tendency, can be slowly intravenous injection of 50 mg of phenobaramine 10 hours before delivery, and 4 to 15 hours before delivery, take vitamin K 15 ~ 30mg.

4, there is no proof that pregnant women or neonates can be given prophylaxis with dexamethasone, stop bleeding, VitE and other drugs can prevent the development of germinal matrix - intraventricular hemorrhage, for 1500g of immature children within 6 hours after birth can be used phenobarbital Reduce brain metabolic rate, scavenge free radicals, reduce cerebral blood flow, and inhibit blood pressure from rising sharply.

For breastfeeding, breastfeeding should be directed to eat more green leafy vegetables and benzene and fresh fruit. For those who take antibiotics for frequent diarrhea, vitamin K50~100g/day, or monthly injection of vitamin K1mg, obstructive jaundice or infant hepatitis should be maintained. Intracranial hemorrhage caused by a deficiency of K1.

First of all, the diagnosis is clear, almost all of the light intracranial hemorrhage survives, the sequelae are 0 to 10%; the medium mortality rate is 5% to 15%, the sequela is 15% to 25%; the severe mortality rate is 50% to 65%, and the sequela is 65% to 100%. Common sequelae include hydrocephalus, brain penetrating cystic changes, motor and intellectual disabilities, quadriplegia, epilepsy, and low muscle tone.

Complication

Neonatal intracranial hemorrhage complications Complications, epilepsy, coma, hearing impairment, ataxia

1. Often combined with hyaline membrane disease, pulmonary hemorrhage.

2. Frequent paroxysmal respiratory rhythm irregularities and apnea, accompanied by convulsions, convulsions and coma in the late stage, pale complexion, anterior bulging, gaze in both eyes, pupils are not equal or loose, light reflection disappears, extremely severe can die There is only a weak heartbeat during or after birth, and although it is actively recovered, it will still be invalid.

3. Different degrees of neurological sequelae occur, survivors often have epilepsy, cerebral palsy, mental retardation, vision or hearing impairment, ataxia and other sequelae.

Symptom

Newborn intracranial hemorrhagic symptoms Common symptoms Face pale wood stiff breath Irregular intracranial pressure increased drowsiness to the brain strong straight hair sputum sputum full convulsions coma

1. Common clinical manifestations of intracranial hemorrhage

The clinical manifestations of intracranial hemorrhage are related to the location of bleeding and the degree of hemorrhage. The main manifestations are the excitation of the central nervous system and the inhibition of symptoms, which occur within 3 days after birth.

(1) Excitatory symptoms: early common: increased intracranial pressure such as anterior iliac crest, cranial suture widening, head circumference increased; ideology change, irritability, excessive excitement, irritability, brain scream, convulsions, etc.; Symptoms such as gaze, strabismus, difficulty in turning the eyeball, nystagmus; early increase in muscle tone.

(2) Inhibition state: As the disease progresses, the disturbance of consciousness appears to be inhibited, such as apathy, lethargy, coma, low muscle tone, weakening or disappearing of the hug reflex; often pale, bruising, full or bulging, double pupil The size varies or the light reflection disappears and disperses; the breathing disorder changes, the breathing rhythm increases from slow to slow, irregular or apnea; the original reflection weakens or disappears.

(3) Others: such as anemia and jaundice that can be explained without reason.

2. Clinical features of bleeding at various sites

The different clinical features of various types of intracranial hemorrhage are as follows.

(1) subdural hemorrhage: characterized by a majority of birth injuries, large amounts of bleeding, birth trauma caused by a canopy, acute cerebral palsy tears and cerebral superficial venous rupture, acute nervous system in a few minutes or hours Symptoms worsen, respiratory cessation and death; subacute patients, symptoms appear 24 hours after birth, mainly convulsions, focal cerebral signs, such as hemiplegia, oblique to the temporal side of the eye; also symptoms are not obvious in the neonatal period, Chronic subdural effusion occurs after several months of birth, with seizures, developmental delays and anemia.

The episode of hemorrhage on the cerebellum is characterized by irritation, brain screaming, gaze and convulsions in both eyes, and further development of the disease. The state of inhibition may occur. The subarachnoid hemorrhage may cause dysfunction and irregular breathing due to the pressure of the hemorrhage. Paroxysmal apnea or even respiratory arrest, muscle tension is low.

(2) subarachnoid hemorrhage: more common in premature infants, often with a history of asphyxia, can be primary, but also intraventricular hemorrhage or subdural hemorrhage caused by blood into the subarachnoid space, primary subarachnoid Cavity bleeding, bleeding originated from the bridge vein in the subarachnoid space, the typical symptoms are seizures on the second day after birth, the interval is good, most of the prognosis is good, individual cases may have hydrocephalus sequelae due to adhesions, a small amount Bleeding is asymptomatic, or only irritability, low muscle tone, often recover within 1 week, more bleeding symptoms are obvious, convulsions can occur, but convulsions are conscious, subarachnoid hemorrhage is not easy to oppress brain stem Therefore, the prognosis is good, but severe bleeding can also rapidly deteriorate or even die in a short period of time. The main sequelae are traffic or obstructive hydrocephalus.

(3) Cerebral parenchymal hemorrhage: mostly premature infants, mostly due to venule thrombosis, increased capillary pressure, rupture and bleeding, such as bleeding in the brain stem, early pupil changes, respiratory irregularities and bradycardia The sacral tension may not be high. The main sequelae are cerebral palsy, epilepsy and mental retardation. Because the nerve conduction bundle that innervates the lower limbs is adjacent to the lateral ventricle, the lateral conduction is the trunk, the upper limb, and the facial nerve. Therefore, the lower extremity dyskinesia is more common. The bleeding site can liquefy the cyst, such as the cyst and the ventricle are called brain penetrating cysts.

(4) Periventricular and intraventricular hemorrhage: more common in premature babies and those with a history of asphyxia at birth, most of them occur within 3 days of birth, the symptoms are different, the most common symptoms are the disappearance of Moro reflex, low muscle tone, apathy and apnea In severe cases, it can be rapidly deteriorated. In a few minutes or hours, it will enter a coma, convulsions, low muscle tension in the limbs, fullness of the front sputum, disappearance of the pupils on the light, apnea, etc., and the amount of bleeding is anemia, blood pressure does not rise.

According to the CT image of the skull, it can be divided into 4 levels:

Grade 1I: subventricular hemorrhage.

Grade 2II: intraventricular hemorrhage, no ventricular enlargement.

Grade 3III: intraventricular hemorrhage with ventricular enlargement.

Grade 4IV: intraventricular hemorrhage with hemorrhage of the brain parenchyma.

Small amount of I, II bleeding can be asymptomatic, the prognosis is better; III, IV bleeding, the nervous system symptoms progress quickly, in a few minutes to several hours, the state of consciousness changes from dull to coma, pupillary fixation, disappearance of photoreaction, convulsions and Go to the state of brain tonic and blood pressure; bradycardia, respiratory arrest and death.

Some children have a good interval in the course of the disease, and some children are no longer aggravated, and some have new symptoms after the stable period. Survivors often have hydrocephalus and other neurological sequelae.

(5) Epidural hemorrhage: common in the production of forceps, often with skull fractures, symptoms of increased intracranial pressure, severe cases of brain stem dysfunction gradually worsened or even died.

(6) intracranial hemorrhage: characterized by premature and very low birth weight infants with gestational age <32 weeks, frequent apnea.

Acute onset, cerebellar hemorrhage can be manifested as apnea, bradycardia, anemia and brainstem dysfunction, the condition often worsens, the child usually has a history of breech dystocia, most of the clinical symptoms begin within 2 days after birth, after Symptoms of brain stem compression, such as stupor, coma, abnormal brain, frequent apnea, bradycardia or angulation, and death due to respiratory failure.

Examine

Examination of neonatal intracranial hemorrhage

[Laboratory Inspection]

Blood picture

If the bleeding is severe, there may be anemia, hemoglobin, platelets, and hematocrit.

2. Blood test

Biochemical examination has increased CPK-BB activity, plasma thromboxane B2 and 6-keto-prostaglandin ratios are helpful for diagnosis, blood gas analysis is metabolic and respiratory acidosis and hypoxemia, others may have indirect bilirubin increase , prothrombin time prolonged and so on.

3. Cerebrospinal fluid examination

It can be positive in subarachnoid hemorrhage and intraventricular hemorrhage. Clinically, cerebrospinal fluid examination reveals uniform blood cerebrospinal fluid and suggests subarachnoid hemorrhage. It is characterized by homogeneous blood, wrinkled red blood cells, early cerebrospinal fluid red blood cell count and protein content. Increased, in some cases, white blood cells increased, and the cerebrospinal fluid became yellow and glucose decreased.

However, in some cases, the cerebrospinal fluid is not bloody, such as the diagnosis of subdural hemorrhage and brain parenchymal hemorrhage, and may induce cerebral palsy. Therefore, the lumbar puncture examination can not rule out the disease, and it is not suitable for this operation when the condition is critical. Therefore, lumbar puncture can not be used as a diagnostic method for IVH.

[Auxiliary inspection]

1. Cranial transillumination: Cranial transillumination has a certain significance in the diagnosis of subdural hematoma, brain penetrating malformation or hydrocephalus.

2. Cranial ultrasound: the first choice for the diagnosis of IVH, continuous spiral ultrasound at the bed provides reliable information on the start time, bleeding site and severity of IVH in premature infants, and it is cheap and convenient, no need to move children, no radiation damage Very low birth weight infants are high-risk groups susceptible to IVH. Skull ultrasound should be routinely screened and checked once every 3 days, 1 week, and 1 month after birth.

IVH can be divided into 4 grades by cranial ultrasound. Grade I: bleeding is limited to the subependyum, without intraventricular hemorrhage, grade II: IVH without ventricular dilatation, grade III: IVH (>50% ventricle area) with ventricular enlargement Grade IV: intraventricular hemorrhage combined with parenchymal hemorrhage or periventricular hemorrhagic infarction. Subdural hematoma on the surface of the brain with midline shift was detected. The diagnosis of supratentorial hemorrhage was inferior to CT, and the diagnosis of subarachnoid hemorrhage was inferior to MRI.

3. Cranial CT: CT is an effective means to confirm the location and extent of IVH. For subdural hemorrhage, posterior cranial fossa hemorrhage, subarachnoid hemorrhage and certain brain parenchymal lesions, the diagnostic value of CT is superior to ultrasound, but CT can not be carried out at the bedside, and there is a disadvantage of exposing the child to radiation. The diagnostic value of posterior cranial foveal subdural hemorrhage and cerebellar hemorrhage is inferior to MRI.

4. Skull X-ray: occipital bone separation and skull fracture can be confirmed by X-ray film of the skull.

5. Transcranial brain impedance method: In recent years, transcephalic cerebral impedance and Doppler technique have been used to measure cerebral blood flow velocity to check intracranial effusion and predict therapeutic effect.

6. Head circumference: Continuous observation of the head circumference helps to monitor changes in ventricular volume.

Diagnosis

Diagnosis and diagnosis of neonatal intracranial hemorrhage

diagnosis

1, medical history: gestational age less than 32 weeks, weight less than 1500g, prone to subventricular hemorrhage and ventricular hemorrhage, the incidence rate of up to 40% to 50%, mostly occurred within 3 days.

2, clinical manifestations: often no excitement process, and inhibition symptoms are obvious, such as refusal of milk, lethargy, low response, low muscle tone, hug reflexes disappear, often paroxysmal respiratory rhythm irregularities and apnea, accompanied by convulsions, late convulsions And coma, pale, front bulging, eyes gaze, pupils are not equal or scattered, light reflection disappears.

3, auxiliary examination: IVH diagnosis in addition to combined with perinatal hypoxia or trauma history and relying on clinical manifestations of identification and imaging examination, premature infants with fewer clinical symptoms and signs, imaging examination of skull CT, B-ultrasound is the main IVH Diagnostic methods can accurately understand the type, location and extent of the lesion according to the results of the B-ultrasound or CT examination, and make a graded diagnosis and estimate the prognosis.

Differential diagnosis

1. Cerebral hypoxia of intracranial hemorrhage is more common with irregular or paused breathing; pulmonary hypoxia is mainly caused by shortness of breath, nasal discharge and tri-concave sign, and the improvement of cyanosis after oxygen and crying; The breathing depth is increased, and after the oxygen is taken, it is blue and purple.

2. Twitching should be differentiated from cerebral edema, hypoglycemia, low calcium, low sodium, hypomagnesemia, vitamin B6 dependence, intracranial malformation, infection, and nuclear jaundice after hypoxia.

3. Low muscle tone should be differentiated from congenital stupid type, myasthenia gravis, congenital muscle relax syndrome, heart type or muscle type glycogen accumulation disease.

4. Lumbar puncture injury: blood cerebrospinal fluid is a clue to suggest subarachnoid or intraventricular hemorrhage, but it needs to be differentiated from lumbar puncture injury.

5. Bacterial meningitis: The cerebrospinal fluid of IVH non-acute intracranial hemorrhage is characterized by yellow cerebrospinal fluid, increased red blood cell count and increased protein content, cerebrospinal fluid sugar (30mg/dl), and even as low as 10mg/dl, and sustainable. For weeks or even months, the decrease in sugar in the cerebrospinal fluid may be a mechanism for the transport of glucose to the cerebrospinal fluid by hemorrhagic damage. When the cerebrospinal fluid is reduced in sugar, with lymphocytosis and increased protein content, it is difficult to distinguish it from bacterial meningitis.

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