Pediatric cerebral edema and intracranial hypertension syndrome

Introduction

Introduction to cerebral edema and intracranial hypertension syndrome in children

Intracranial hypertension (intracranialhypertension) refers to a series of clinical manifestations of increased brain volume and weight caused by increased brain parenchymal fluid. In pathology, the accumulation of free fluid in the interstitial space of brain cells is called brain edema, and the brain The increase of intracellular fluid is called brain swelling, but in actual clinical work, the two are difficult to distinguish, or they are different stages of the same pathological process, and often exist at the same time in the later stage, so they are often called brain edema. Obvious and persistent cerebral edema causes intracranial hypertension, which is more common in certain pediatric diseases, especially acute infectious diseases. Early diagnosis and timely treatment of intracranial hypertension are one of the important measures to control brain edema, prevent cerebral palsy, reduce mortality and morbidity.

basic knowledge

Sickness ratio: 0.0001%

Susceptible people: children

Mode of infection: non-infectious

Complications: respiratory failure

Pathogen

Pediatric cerebral edema and the cause of intracranial hypertension syndrome

(1) Causes of the disease

The intracranial hypertension syndrome is divided into acute and chronic.

1. The cause of intracranial hypertension: The cause of acute cranial hypertension in children is mainly brain edema:

(1) Acute infection: cerebral edema can occur 24 hours after infection.

1 intracranial infection: such as encephalitis caused by various pathogens, meningitis, meningoencephalitis, brain abscess, otogenic intracranial infection, etc., is the most common cause of acute brain edema in children.

2 extracranial infections: toxic dysentery, severe pneumonia, sepsis, acute severe hepatitis.

(2) cerebral hypoxia: severe hypoxia for several hours, can occur cerebral edema, such as craniocerebral injury, cardiac arrest, asphyxia, shock, heart failure, respiratory failure, pulmonary encephalopathy, status epilepticus, severe anemia, Drowning, sputum, etc. can be caused.

(3) intracranial hemorrhage: intracranial malformation of blood vessels or aneurysms, subarachnoid hemorrhage, infant vitamin K deficiency, brain leukemia, hemophilia, thrombocytopenic purpura, aplastic anemia, etc. Internal bleeding, occasionally vascular ulceration caused by intracranial vasculitis.

(4) Poisoning: carbon monoxide or cyanide poisoning, lead, mercury or other heavy metals, food (such as ginkgo), pesticides (such as organic phosphorus), veterinary drugs (such as chlorophenol), alcohol, drugs (such as sodium phenobarbital) , tetracycline, vitamin A, vitamin D) and other poisoning.

(5) water and electrolyte balance disorder: acute hyponatremia, water poisoning, acidosis caused by various reasons.

(6) intracranial space-occupying lesions: rapidly developing brain tumors and large intracranial hematoma, intracranial parasitic diseases (cerebral cysticercosis, cerebral schistosomiasis, cerebral paragonimiasis, cerebral malaria, Brain abscess caused by Miba protozoa).

(7) Others: such as hypertensive encephalopathy, Wright's syndrome, various metabolic diseases.

2. The cause of chronic intracranial hypertension can be found in hydrocephalus, intracranial tumors, chronic subdural hematoma, intracranial vein embolism, and narrow cranial cavity.

(two) pathogenesis

1. Physiological and pathological features

(1) Normal intracranial pressure: The brain, meninges, blood vessels and cerebrospinal fluid are contained in the solid skull cavity, and the volume is basically kept constant. The space available for compensation in the adult cranial cavity is about 10%. Under normal circumstances, The circulation of blood and cerebrospinal fluid maintains the dynamic balance of intracranial pressure. The intracranial pressure is closely related to the volume of the contents of the cranial cavity, but the two are not proportional. As shown by the capacity pressure curve of Langifitt, the intracranial pressure is normal or slightly increased. At the time, due to the certain compliance of the cranial cavity, the volume change has little effect on the intracranial pressure. However, when the intracranial pressure is significantly increased, the slight increase or decrease in the volume can significantly increase or decrease the intracranial pressure.

The normal value of intracranial pressure in children changes with age, the newborn is 0.098 ~ 0.196 kPa (10 ~ 20mmH2O), the baby is 0.294 ~ 0.784kPa (30 ~ 80mmH2O), the child is 0.392 ~ 1.47kPa (40 ~ 150mmH2O), the elderly 0.588 ~ 1.76kPa (60 ~ 180mmH2O), it is generally believed that the intracranial pressure of 1.47 ~ 2.67kPa (11 ~ 20mmHg) is a slight increase, 2.80 ~ 5.33kPa (21 ~ 40mmHg) is a moderate increase, > 5.33kPa (40mmHg) To be seriously increased.

(2) characteristics of brain capillaries: brain capillaries have their morphological and functional characteristics, and the differences with whole body capillaries include:

1 Endothelial cells are connected to each other by tight junctions, forming a continuous layer of endothelial cells throughout the brain capillaries, effectively separating plasma and interstitial fluid, and fat-soluble substances and narcotic gases can pass through cerebral vascular endothelial cells. However, water-soluble macromolecular substances cannot pass through the blood-brain barrier at a rapid rate.

2 There are only a few vesicles in the endothelial cells, so plasma proteins cannot enter the brain.

3 The mitochondrial content in endothelial cells is 3 to 5 times higher than that of any capillary endothelial cells in the whole body, so the brain capillary can obtain more ATP to supply energy metabolism of brain tissue.

4 It has the function of actively transporting potassium and certain specific amino acids, and plays an important role in maintaining the concentration of potassium, calcium, glycine and other aminotransmitters.

5 surrounded by a basement membrane, the width of this basement membrane is equivalent to 25% of endothelial cells, the main function is to maintain the integrity of brain capillaries under adverse conditions.

6 When the brain is open, the brain capillaries are open. When the brain metabolism increases sharply, the blood flow of the brain capillaries cannot be increased accordingly.

(3) Characteristics of the cerebral circulation: The extracellular space of the brain only accounts for 3% to 5% of the brain volume, so the vascular capacity of the brain is limited, and the characteristics of the cerebral circulation include:

1 The anastomosis between the meninges and microvessels is limited to between the arterioles, the anastomosis between the venules, and there is no shunting anastomosis between the arterioles and the venules, so the arteriovenous short circuit in the brain tissue is limited, while in the brain capillary bed Inside, there is a wide range of vascular anastomoses between the posterior arterioles and venules less than 25 m in diameter.

2 cerebral blood flow is rich, normal adult is 750 ~ 850ml / min, equivalent to 15% of cardiac output, cerebral blood flow averages 44ml / 100g brain tissue per minute, blood flow in the gray matter is higher than white matter 3 ~ 4 times.

3 The normal value of cerebrovascular resistance is 0.21 kPa/min [1.6 mmHg/(ml blood·100 g brain tissue)], and when the intracranial pressure is increased, the cerebral vascular resistance increases.

4 The energy reserve of brain tissue is very small. Oxygen and glucose are consumed after 3 hours of hypoxia. The glucose required for oxidative metabolism of brain tissue is mostly transported by systemic blood circulation. When anaerobic metabolism occurs, due to the existence of blood-brain barrier, It is not easy to rapidly transport the produced lactic acid to the whole body blood circulation, so it is prone to intracellular lactic acidosis.

(4) The main factors affecting the cerebral circulation are:

1 Carbon dioxide partial pressure: Carbon dioxide can freely pass through the blood-brain barrier, affecting the pH of cerebrospinal fluid and brain tissue, and its diffusion into the cell is faster than oxygen. It is one of the main factors controlling cerebral blood flow. When the partial pressure of carbon dioxide is increased, Cerebrovascular dilatation, increased cerebral blood flow, increased intracranial pressure, decreased carbon dioxide partial pressure, cerebral vasoconstriction, decreased cerebral blood flow, and decreased intracranial pressure. This is the main theoretical basis for reducing intracranial pressure by using hyperventilation. When the partial pressure of carbon dioxide is 2.67~5.33kPa (20~40mmHg), the cerebral blood flow can be reduced by 4% for every 0.133kPa (1mmHg). When the partial pressure of arterial carbon dioxide is greater than 5.33kPa (40mmHg), each increase is 0.133kPa (1mmHg). ), cerebral blood flow can increase by 2.5%, arterial carbon dioxide partial pressure changes the limits of vasoconstriction and expansion are 1.33 ~ 2.67kPa (10 ~ 20mmHg) and 10.7 ~ 13.3kPa (80 ~ 100mmHg), arterial carbon dioxide partial pressure is less than 2.67 At kPa (20 mmHg), secondary vasodilation is caused by cerebral ischemia and hypoxia, and cerebral blood flow is increased.

2 Oxygen partial pressure: The effect of oxygen partial pressure on cerebral blood flow is opposite to that of carbon dioxide partial pressure, and the effect is small. Mild hypoxemia does not cause cerebral blood flow changes. When the blood oxygen partial pressure is less than 6.67 kPa (50 mmHg), Cerebrovascular dilatation, increased cerebral blood flow, increased intracranial pressure, increased blood oxygen partial pressure, cerebral vasoconstriction, decreased cerebral blood flow, decreased intracranial pressure, and 100% pure oxygen, which can increase cerebral vascular resistance by 30%. Severe hypoxia can cause cerebral microvascular lumen stenosis, intravascular thrombosis, increased permeability of brain blood vessel wall and blood-brain barrier, which can lead to brain cell edema after hypoxia, and the oxygen consumption of gray matter is more than three times higher than white matter. Gray matter is less tolerant to hypoxia.

3 blood pressure: in order to keep the cerebral blood flow uniform, blood pressure at 8.00 ~ 10.7kPa (60 ~ 180mmHg), through the automatic adjustment function to change the diameter of the cerebral vessels, can control cerebral blood flow, even if blood volume, blood pressure or perfusion pressure changes The cerebral blood flow is not affected. This is the Bayliss effect. When the blood pressure is lower than 8.00 kPa (60 mmHg) or higher than 10.7 kPa (180 mmHg), the autoregulation function is lost. When the blood pressure is lower than 4.00 kPa (30 mmHg), the brain A decrease in blood flow of more than 1/2 will affect brain function; when cerebral blood flow is less than 15% of cardiac output, neuronal function will be irreversibly damaged. When severe acidosis occurs, Bayliss effect is weakened or even disappeared.

4 intracranial pressure: cerebral perfusion pressure = mean arterial pressure - intracranial pressure, so increased intracranial pressure or decreased blood pressure to reduce cerebral perfusion pressure, increased intracranial pressure, decreased cerebral perfusion pressure, increased cerebral vascular resistance, brain Blood flow is rapidly reduced, and cerebral ischemia and hypoxia occur.

5 neurotransmitters: Unlike other parts of the body, there are few adrenergic receptors and cholinergic receptors in the blood vessels of the brain, so the autonomic nervous system has a weak regulation of the cerebral circulation. Therefore, the regulation of cerebral blood vessels mainly depends on Autoregulation, but there are abundant autonomic nerve fibers on the surface of the brain and the basal part of the blood vessels. The neuromodulation effect is obvious. In addition, the production of cerebrospinal fluid is related to the autonomic nervous system. When the adrenergic receptors on the choroid plexus are stimulated, Reduced cerebrospinal fluid production.

2. Mechanism of occurrence of intracranial hypertension The main description of acute infectious diseases caused by intracranial hypertension, cerebral edema classification methods, according to its mechanism can be divided into:

(1) vasogenic cerebral edema: mainly due to damage to the blood-brain barrier, damage to the cerebral vascular wall, destruction of endothelial cells or tight junctions, increased permeability of the blood-brain barrier, and exudation similar to plasma components The fluid leaks to the extracellular space, thus forming cerebral edema. The cells in the white matter area are arranged more gray than loose, the interstitial space is larger, and the resistance is smaller, so the edema is more obvious. When the intravascular pressure is greater than the interstitial space pressure, the water is more likely to be outside the blood vessel. Leakage, common in brain trauma, central nervous system infection, brain tumor, brain abscess, cerebral hemorrhage or infarction, due to edema between the brain tissue and the ventricle, there is a hydrostatic pressure difference, part of the fluid can enter the ventricular system through the ependymal membrane, and with the cerebrospinal fluid It is absorbed by the circulation, which is the main way to dissipate the edema fluid.

(2) Cellular cerebral edema: characterized by fluid accumulation in cells, common in cerebral hypoxia, ischemia, various intracranial inflammation, chemical poisoning, Wright's syndrome, etc., brain tissue can not use fat and protein, Glucose is the only source of energy. 1mmol of glucose is aerobicly oxidized to produce 38mmol ATP to maintain the normal life activities and physiological functions of brain cells. When various pathological conditions cause cerebral hypoxia, 1mmol glucose anaerobic glycolysis can only produce 2mmol. ATP, the brain cell energy supply is insufficient, the sodium pump can not operate, sodium ions can not be transferred from the cell to the outside of the cell, resulting in accumulation of sodium ions in the brain cells, membrane potential function can not be maintained, nerve impulse conduction is temporarily stopped, negatively charged chlorine The ions can pass through the cell membrane freely, and combine with sodium ions to form sodium chloride. The increase of intracellular sodium chloride leads to an increase in osmotic pressure, and a large amount of water enters the cells, so as to maintain the balance of osmotic pressure inside and outside the cells, so that the brain cells are swollen and the volume is increased. The outer gap is reduced, even the cells are ruptured, the resistance of the glial cell membrane is small, and the intracellular edema is easy to occur first, and anaerobic metabolism is caused. Acid accumulation, decreased intracellular pH, enhanced cell membrane permeability, enhanced hydrophilicity of cytoplasmic proteins, and promoted the development and development of edema in brain cells. This type of cerebral edema is present in both white matter and gray matter, sodium in edema fluid and The chloride ion content is quite high.

(3) osmotic cerebral edema: various pathogenic factors cause the osmotic pressure of brain extracellular fluid to decrease, causing brain edema caused by increased intracellular water content, common in acute water poisoning, hyponatremia, diabetic acidosis and resistance When the secretion of diuretic hormone is increased, the edema fluid of this type of cerebral edema is water. The water mainly accumulates in the white matter and gray matter glial cells, and the white matter is more obvious. The sodium ion concentration in the edema area is slightly lower, and the potassium ion concentration is significantly reduced.

(4) Interstitial cerebral edema: seen in a variety of causes of traffic or non-communicating hydrocephalus, also known as hydrocephalus cerebral edema, mainly due to cerebrospinal fluid secretion, absorption disorders or circulatory disorders, so that the cerebrospinal fluid too much Gathered in the ventricles, the enlarged intraventricular pressure increases, the ependymal membrane is compressed to flatten the cells, and even tear. The cerebrospinal fluid enters the white matter around the ventricles through the ventricular wall, causing interstitial cerebral edema, so the edema fluid is cerebrospinal fluid. When the hydrocephalus is severe, the cerebrospinal fluid can be dispersed to the whole white matter, so that the cells are separated from the nerve fibers, and there is gliosis. The capillaries in the edema tissue are normal, and the capillaries around the ventricles can absorb the extravasated cerebrospinal fluid, so the intracranial pressure sometimes Normal, sometimes increased, ventricular enlargement persists for too long, can make the cerebral cortex compressed and thin, and even brain atrophy.

In clinical work, the above cerebral edema often exist at the same time, it is difficult to separate, it is difficult to accurately classify cerebral edema, for example, children with tuberculous meningitis are prone to cranial hypertension, the reason is comprehensive, meningeal congestion, Edema, inflammatory exudate can directly increase the contents of the cranial cavity; if the choroid plexus is involved, the secretion of cerebrospinal fluid increases, and when the arachnoid granules are involved, the absorption of cerebrospinal fluid is reduced, which can cause hydrocephalus; for the skull base adhesion or ventricle membrane Inflammation causes intraventricular obstruction, which causes cerebrospinal fluid circulation obstruction, which can cause non-communicative or traffic hydrocephalus; when combined with occlusive cerebral endarteritis, it can cause vasogenic cerebral edema due to cerebral ischemia and hypoxia. Cellular cerebral edema; and increased secretion of antidiuretic hormone caused by central nervous system infection, which can cause water retention, hyponatremia and osmotic cerebral edema.

3. Pathological changes: The pathological changes of cerebral edema are mainly congestion and edema.

(1) Gross specimen: visible brain swelling, brain tissue becomes tender, it seems to have fluidity, meninges are congested, cerebral sulcus is shallow, the gray matter and white matter of the cut surface are unclear, the white matter is obviously swollen, the gray matter is compressed, and the lateral ventricle volume is reduced. Or in the form of a fissure, in theory, the intercellular fluid of vasogenic cerebral edema increases, the brain tissue is soft, the profile is moist, called "wet brain", the cell cerebral edema is mainly intracellular edema, and the extracellular fluid is reduced. The toughness of the brain tissue is increased, and there is no obvious liquid exudation in the section, which is called dry brain. In fact, when the two kinds of brain edema develop to a certain extent, mixed brain edema may occur successively, or one of them may be dominant.

(2) Histological changes:

1 Extracellular edema: The space around the cells and microvessels was significantly widened. The HE staining showed pink edema fluid. The white matter water content increased in a sponge shape. Under the electron microscope, the extracellular space between the myelin fiber bundles of white matter was widened and transparent. The capillary junction of the capillary endothelial cells is open, the basement membrane is broadened with a decrease in electron density, and the exudate is an electron dense floc.

2 intracellular edema: gray matter and white matter cells swelling, especially the most prominent astrocyte, nuclear staining, vacuoles in the cytoplasm, sometimes the nucleus is pyknosis, nerve fiber myelin swelling, deformation or fracture, axis The cord can be bent, broken or disappeared, the microvascular expansion, the swelling and even necrosis of endothelial cells, the late stage of cerebral edema, the involvement of microglia in repair, and the formation of scars. Under the electron microscope, the astrocyte glial cells with increased glycogen granules can be seen in the gray matter. It can involve neurites or dendrites or even cell bodies before or after contact with cell processes, stellate cells in white matter, oligodendrocytes and axons are swollen, and acidic metabolites increase after cerebral hypoxia, which promotes intracerebral cells. The lysosomal-bound acidic hydrolase is activated to autolysis the cells.

(3) Cerebral palsy formation: When the volume and weight of the swollen brain tissue continue to increase, the intracranial pressure continues to increase, forcing the more easily displaced brain tissue to be squeezed into lower space or pores to form cerebral palsy, the most common The hippocampus in the cranial fossa is smashed into the cerebellar lobes, forming a cerebellar stenosis (the sacral sulcus is back, if the cerebral edema continues to develop, or the cerebellar edema, which is mainly cerebellar swelling, continues to increase, so that The cerebellar tonsils in the posterior cranial fossa are inserted into the occipital foramen, which form the cerebellar tonsil sputum, also called the occipital foramen, which causes the brain stem to be stressed and endangered.

Prevention

Cerebral edema and prevention of intracranial hypertension syndrome in children

1. Actively prevent various water and electrolyte disorders.

2. Actively prevent and treat various hypertensive encephalopathy, intracranial hemorrhage, etc.

3. Actively prevent and cure various poisoning, such as lead or other metals, food, drugs (vitamin A, D, phenobarbital, etc.), pesticides and other poisoning.

Complication

Pediatric cerebral edema and complications of intracranial hypertension syndrome Complications, respiratory failure

1. Cerebellum incision

The hippocampus in the cranial fossa of the skull is plunged into the cerebellar lobes and oppresses the midbrain. It can be unilateral or bilateral. The oculomotor nucleus located in the midbrain is compressed and causes the pupil to become small and small. If the light reflection is weakened or disappeared, the oculomotor nerve also occupies part of the eye muscle. After the injury, one or both sides of the eyelids may sag, squint or gaze, etc., and the respiratory center of the midbrain is compressed, and double inhalation occurs. Sighing or sobbing breathing, central respiratory rhythm disorders such as mandibular movement and apnea, and involvement of the dura mater at the cerebellar fissure, can cause significant neck rigidity, and the 1 or 2 lateral midbrain and cerebral peduncle are compressed At the time, there is a unilateral (condylar cerebral palsy) or bilateral pyramidal tract sign and/or limb paralysis.

2. Occipital macropores

For the posterior cranial fossa cerebellum into the occipital foramen, acute cerebral edema caused by cerebral palsy, more than the first small cerebellar incision, and then the occipital foramen magnum; sometimes cerebral edema is rapidly aggravated, clinically not Can observe the performance of the former, and mainly the occipital foramen, the coma of the child is rapidly deepened, the pupils of both sides are dilated, the response to light disappears, the eyeball is fixed, and the respiratory arrest is often caused by central respiratory failure. The large occipital condyle of the occipital lesions occurs after the cerebellar incision, but the subsegmental space-occupying lesions directly cause the large occipital condyle without concomitant cerebellar incision.

3. Brain death

When the intracranial pressure rises to the intracranial mean arterial pressure level, the cerebral blood flow blockage state may occur, which is called brain packing. At this time, the brain circulation stops. If it is not corrected within a short period of time, the brain cells may become irreversible. Damage, often accompanied by clinical brain death.

Symptom

Symptoms of cerebral edema and intracranial hypertension syndrome in children Common symptoms

The clinical manifestations of acute intracranial hypertension are closely related to the primary pathogenic nature, location, development rate and comorbidities of the intracranial hypertension. The main manifestations are:

Headache

Increased intracranial pressure causes the meninges, blood vessels and cranial nerves to be pulled and inflammatory changes to stimulate the nerves and cause headaches. At the beginning, it is paroxysmal, and later develops into persistence. The forehead and the bilateral sacral side are mainly, and the weight is different. Often coughing, sneezing, sneezing, stretching when bending or standing up, when the brain edema is serious, there may be a tear-like feeling, infants often can not self-report headaches, more manifestations of irritability, screaming, and even beat head Department, sometimes due to compression of the vestibular nerve of the cochlea, causing tinnitus and dizziness, infants due to anterior and posterior foramen ovale and cranial sutures, can partially relieve the craniocerebral pressure, so the headache is not as serious as adults.

2. Jet vomiting

Cranial hypertension stimulates the vomiting center of the fourth ventricle and the medulla of the medulla to cause jet vomiting, rarely nausea, and has nothing to do with diet, and is heavier in the morning.

3. Head signs

The anterior hernia is swelled, the fracture of the bone is split, the head circumference is enlarged, the superficial venous engorgement of the head and face, the positive sign of the broken pot sound is a subacute or chronic compensatory mechanism, and the cranial suture of the infant is not completely closed, the skull bone It is related to softness and certain elasticity. Such compensation mechanism often makes early symptoms atypical.

4. Disorder of consciousness

Intracranial hypertension causes extensive damage to the cerebral cortex and damage to the reticular formation of the brain stem, causing the child to have varying degrees of consciousness, agitation or mania. If the brain edema cannot be controlled in time, the disturbance of consciousness rapidly deepens and enters a coma.

5. High blood pressure

When the intracranial pressure is increased, the compensatory pressure reaction of the medullary vasomotor center increases the blood pressure, and the systolic blood pressure can rise above 2.67 kPa (20 mmHg), and the pulse pressure is widened and the blood pressure tone is enhanced.

6. Muscle tone changes and convulsions

The intracranial hypertension on the brainstem, basal ganglia, cerebral cortex and some extrapyramidal oppression of the cerebellum can significantly increase muscle tone, mostly manifested as paroxysmal or persistent upper extremity internal rotation, lower extremity stretched and straight, sometimes appearing Extensor or horn arch reversal, all of which are manifestations of denervation to the brain. If the compression is mainly above the midbrain, it is characterized by one or two upper extremity spasm, which is in a semi-flexed state, and even the arms cross in front of the chest. With cortical tonic with lower extremity extensibility, cerebral cortex or inflammation can stimulate cerebral cortex, which can cause convulsions and even epileptic seizures.

7. Respiratory disorders

The brain stem is compressed or axially displaced, which can cause respiratory rhythm irregularity, pause, tidal breathing, mandibular movement, etc., and most of them are prodromal symptoms of cerebral palsy.

8. Cycling disorders

The intracranial hypertension affects the nerve tissue baroreceptors, causing the surrounding blood vessels to contract, manifesting as pale skin, pale, and toe cyanosis. Hypoxia during brain stem displacement can cause slow pulse, but it is rare in children.

9. Temperature regulation disorder

Because of the hypothalamic body temperature regulation center (the front part is the cooling center, the posterior part is the warming center), the heat production increases when the muscle tension increases, and the sympathetic nerve is damaged, the sweat function is weakened, and the surface heat dissipation is poor. In a short period of time, the body temperature rises sharply and is persistent. It is difficult to control high fever or super high fever. Because the peripheral blood vessels contract, the rectal temperature can be significantly higher than the body surface temperature. When the body temperature rises sharply, it is often accompanied by breathing, circulation and muscle tension. Change.

10. Eye performance

Eye changes are more likely to suppress the midbrain.

(1) Eyeball protrusion: Increased intracranial pressure through the supracondylar fissure on the cavernous sinus in the orbit, the eyelid venous return is limited, so two eyes can be prominent.

(2) Double vision: The extension of the nerve in the skull is long, and it is easy to be double-viewed by the pulling or squeezing of the intracranial hypertension, but the baby cannot express it.

(3) Visual field changes: manifested as blind spot enlargement and concentric view, but patients with acute intracranial hypertension have many disturbances, so they cannot check the visual field.

(4) Fundus examination: optic disc edema is the main symptom of chronic intracranial hypertension, which is caused by obstruction of fundus venous return. It is rare in acute cerebral edema. It is rare in infants and young children, sometimes the retinal radiance is enhanced, and the fundus is small. Venous stenosis, small arterial thinning, severe optic disc edema can cause secondary optic atrophy, disturbance of consciousness, dilated pupils and increased blood pressure with slow pulse called Cushing triad, a crisis of cranial hypertension, often a precursor to cerebral palsy.

Examine

Examination of cerebral edema and intracranial hypertension syndrome in children

Measuring intracranial pressure Using biophysical methods to directly measure intracranial pressure is a more accurate method for diagnosing intracranial hypertension. Because these methods are mostly invasive, brain damage and co-infection are often difficult to avoid, and the advantages and disadvantages should be weighed in clinical application. Note that when measuring intracranial pressure, the child must be in a quiet state, relax the neck, chest and abdomen so that they are not under pressure, and then record the reading is more reliable.

1. Lumbar puncture to measure cerebrospinal fluid pressure

When the normal person is lying on the side, the whole body muscles are relaxed, and the glass pressure measuring tube for lumbar puncture is used. The initial pressure of the cerebrospinal fluid (the original pressure before the cerebrospinal fluid is not released) is equal to the pressure of the ventricle fluid, so it can represent the intracranial pressure, but if the spinal spider When the sub-membrane cavity is blocked, the cerebrospinal fluid pressure measured by lumbar puncture can not represent intracranial pressure. The cerebrospinal fluid pressure during normal breathing can fluctuate from 0.1 to 0.2 kPa (10-20 mmH2O). When the subarachnoid space is blocked, this fluctuation occurs. Disappeared, each time the cerebrospinal fluid pressure changes from 0.02 to 0.05 kPa (2 to 5 mmH2O). When the subarachnoid space is blocked, the viscosity of the cerebrospinal fluid is increased, or the occipital foramen is formed, the pressure changes little or disappears. The pressure of the cerebrospinal fluid of the pulse changes greatly, suggesting that there is traffic hydrocephalus. When the subarachnoid space is blocked, the pressure of the cerebrospinal fluid in the lumbar puncture is not very sensitive to observe the intracranial pressure, and the measured value is lower than the actual intracranial pressure.

2. Lateral ventricle puncture pressure measurement

This method is the most accurate and safe. In the case of monitoring the intracranial pressure, it can also control the drainage of cerebrospinal fluid to achieve the purpose of decompression therapy. The cerebral ventricle puncture is easy for the operation of children with anterior orbital patency. The skull must be drilled. In children with severe intracranial hypertension, due to swelling of the brain parenchyma, the pressure in the ventricle becomes smaller, shifting, and puncture is often not successful.

3. Front pressure measurement

The anterior ankle pressure is directly measured by a non-invasive intracranial pressure monitor, and is suitable for patients with anterior or posterior patency.

4. Direct intracranial pressure monitoring

The sensor is placed in the ventricle of the child, the subarachnoid space, and the epidural. The transducer is connected to a monitor with a pressure monitoring device or a special intracranial pressure monitor to read directly on the screen.

5.X line

Chronic intracranial hypertension on the skull showed signs of finger pressure, thinning of the cortical bone, cracking of the bone, brain atrophy, etc., the above-mentioned performance of acute intracranial hypertension is not obvious.

6.CT scan

According to different absorption coefficients of X-rays of human tissues, CT scan is used to make images. Acute cranial hypertension is characterized by fullness of brain tissue, shallow sulcus back, narrowing or disappearing of lateral fissure, small compression of ventricles, and shifting of midline structure Wait, when the chronic cranial hypertension, external hydrocephalus can be seen, brain atrophy.

7. Magnetic resonance imaging (MRI)

This method is used to check the change of fluid content in the brain compared with CT scan, and the formation of cerebral palsy can be observed. When cerebral edema occurs, T1 and his image value are prolonged, so there is a long T1 low signal or the like on the T1-weighted image. The signal, which is a high signal on the T2-weighted image.

8. EEG

When the cerebellum is incision, it causes brain tissue displacement and circulatory disturbance, and there is a slow wave of temporal temporal lobe, which is caused by dysfunction of the brainstem reticular structure. Sometimes the bilateral frontal and temporal symmetry of the frontal and temporal sacs are synchronous. Amplitude slow wave.

9. Transcranial Doppler ultrasound

Non-invasive detection of blood flow velocity of the large blood vessels of the skull base Willis ring, to understand the changes of cerebral hemodynamics, TCD mainly showed high spectrum of peak blood pressure, decreased blood flow velocity, mainly decreased diastolic flow rate, with resistance index and fluctuation index Increase and so on.

Diagnosis

Diagnosis and differentiation of cerebral edema and intracranial hypertension syndrome in children

diagnosis

History

There is a history of cerebral edema or increased intracranial pressure.

2. Clinical manifestations

Children with symptoms and signs of high blood pressure, children often have a lack of complaints and specific manifestations of cranial hypertension, and when the intracranial pressure increases, can be compensated by anterior sacral bulging, fracture of the suture, so that the clinical symptoms are not typical, therefore, must A comprehensive analysis of the condition and comprehensive judgment can make a timely diagnosis. Pei Pelan proposed five main indicators and secondary indicators for the clinical diagnosis of acute cerebral edema in children. When there are 1 main indicator and 2 secondary indicators, diagnosis.

(1) The main indicators are: 1 irregular breathing; 2 pupils are not equal or enlarged; 3 optic disc edema; 4 anterior iliac elevation or tension; 5 hypertension without other causes (blood pressure is greater than age × 0.027 + 13.3.3 kPa).

(2) Secondary indicators: 1 dizziness or coma; 2 convulsions and / or limb muscle tension increased significantly; 3 vomiting; 4 headache; 5 mannitol 1g / kg intravenous injection 4h, blood pressure decreased significantly, symptoms, signs with It is getting better.

This diagnostic standard has certain reference value in clinical work.

3. Clinical diagnosis of cerebral palsy

(1) Cerebellar incision: Based on the clinical manifestations of intracranial hypertension, there are a series of central respiratory failures with different pupil sizes and/or respiratory rhythm.

(2) Occipital macroporous sputum: On the basis of the clinical manifestations of intracranial hypertension, the presence or absence of cerebellar incision sputum, the pupil first shrinks and then dilated, the eyeball is fixed, central respiratory failure develops rapidly, short-term resuscitation stop.

4. Laboratory and auxiliary examinations: Diagnosis is made in conjunction with laboratory and auxiliary examination results.

Differential diagnosis

Different from the various causes of cerebral edema, mainly rely on medical history, clinical manifestations and laboratory, auxiliary examination for differential diagnosis.

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