What Is Intracranial Pressure?

Intracranial pressure, which is the pressure of the cerebrospinal fluid in the cranial cavity, is usually 100-150 mm H2O and 10-15 mm Hg. According to the National Physician Qualification Examination Practical Skills Guide p325, the normal cerebrospinal fluid pressure is 0.78 ~ 1.76kpa (80 ~ 180 mm water column) or 40 ~ 50 drops / min in the lying position of normal adults, and the fluctuation in breathing is within 10 mm water column. 0.4 ~ 1.0kpa (40 ~ 100mm water column).

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Intracranial pressure, which is the pressure of the cerebrospinal fluid in the cranial cavity, is usually 100-150 mm H2O and 10-15 mm Hg. According to country

Adult intracranial pressure 70-200mmH2O (0.69-1.96KPa)

Intracranial pressure of children 50-100mmH2O (0.49-0.98KPa)

Intracranial pressure (ICP) refers to the pressure produced by the contents of the cranial cavity on the wall of the cranial cavity, also known as cerebral pressure. Due to being

Causes of intracranial pressure (1)

Common causes are:

Craniocerebral injury, such as cerebral contusion, intracranial hematoma, surgical trauma, extensive skull fracture, craniocerebral firearm injury, traumatic subarachnoid hemorrhage, etc.

Intracranial space-occupying lesions, including various cancers, abscesses, hematomas, granulomas, cysts, and cerebral parasites. This is the most common cause of increased intracranial pressure.

Cerebrovascular diseases, common diseases are cerebral infarction, hypertensive cerebral hemorrhage, subarachnoid hemorrhage, hypertensive encephalopathy and so on.

Intracranial inflammation, such as various encephalitis, meningitis, sepsis and so on.

Brain hypoxia, such as respiratory obstruction, asphyxia, cardiac arrest, carbon monoxide poisoning, and hypoxic encephalopathy caused by various diseases.

poisoning and metabolic disorders, such as hepatic encephalopathy, acidosis, lead poisoning, acute water poisoning and hypoglycemia.

False brain tumor syndrome, also known as benign intracranial pressure.

Congenital abnormalities, such as aqueduct developmental malformations, depression of the skull base, and congenital cerebellar subtonsal hernia deformity, can cause cerebrospinal fluid reflux to be blocked, resulting in secondary hydrocephalus and increased intracranial pressure. , Restricts the normal development of the brain, and often increases in intracranial pressure.

Intracranial pressure (two) pathogenesis

The mechanisms that cause intracranial pressure increase are as follows:

The volume of brain tissue increases due to cerebral edema.

Intracranial blood volume increase, various causes of carbon dioxide accumulation or carbonic acid in the blood, can expand cerebral blood vessels, increase cerebral blood flow sharply; when the hypothalamus, saddle area or brain stem damage, can lead to cerebral vascular regulation center The dysfunction of the brain and the reactive expansion of the cerebral blood vessels cause a sharp increase in cerebral blood flow.

(3) Cerebrospinal fluid is too much, and it is found in various hydrocephalus.

Intracranial space-occupying lesions are additional contents in the cranial cavity. In addition to the lesions occupying a certain volume of the cranial cavity, they can also cause cerebral edema around the lesions or obstruction of the cerebrospinal fluid circulation pathway, leading to increased intracranial pressure.

Pathophysiology of Intracranial Hypertension Syndrome

Systemic vasopressor response: When the autoregulatory function of the cerebral blood vessels is lost, in order to maintain the required cerebral blood flow, the body constricts the blood vessels around the body through the reflex effect of the autonomic nervous system, increases blood pressure, and increases the stroke volume. In order to increase cerebral perfusion pressure, accompanied by slowing of the respiratory rhythm and increased breathing depth. This triad that raises arterial pressure with slowed heart rate, increased stroke volume, and slowed breathing rhythms is called the systemic vasopressor response or the Cushing triad. More common in patients with acute head injury or acute intracranial pressure.

Relationship between intracranial pressure and volume: Langfitt et al. (1965) showed through animal experiments that the presence of external pathological factors does not necessarily cause changes in intracranial pressure due to the compensation of cranial contents. The volume of cranial content and intracranial pressure The increase in the number is not in a linear relationship but in an exponential relationship. This relationship can also be expressed by intracranial plasticity and compliance. Plasticity comes from the plasticity and elasticity of the soft tissue in the cranial cavity. It is the pressure change caused by the change in unit volume, which is expressed by P / V. Compliance represents the volume compensation function in the cranial cavity. It is the volume change caused by the change of unit intracranial pressure, which is expressed by V / P. In the early stage of increasing the volume of cranial content, there is enough room for adjustment, that is, the compliance (compensation) is strong; in the later stage of increasing the volume of cranial content, there is less and less space for adjustment. The resistance is increasing, so intracranial pressure increases sharply. Examination of compliance and plasticity can help determine the severity of increased intracranial pressure. The clinical method is as follows: 1ml of cerebrospinal fluid is released during ventricular drainage or lumbar puncture. If the pressure drops little, it is still in the compensatory period. If the pressure drops more than 0.39kPa (3mmHg), it indicates that the intracranial pressure / volume curve has exceeded the threshold. Point, that is, the compensation function is exhausted.

Cerebral hernia formation: When intracranial lesions, especially intracranial masses and injuries, cause uneven increase in intracranial pressure, the brain tissue is often compressed and displaced, and some brain tissue is displaced to pressure through certain anatomical fissures. In the lower part, it is a brain herniation. This is the deadliest emergency of increased intracranial pressure.

Common symptoms and signs of intracranial pressure

Intracranial hypertension syndrome is a gradual process with different clinical manifestations. The typical manifestations of intracranial hypertension syndrome include clinical manifestations caused by increased intracranial pressure itself, and neurological defects caused by the etiology that causes increased intracranial pressure.

Common symptoms and signs:

The location of the headache is uncertain and progressive.

Vomiting can be jet vomiting.

Optic disc edema can be accompanied by flame-like bleeding and exudation.

Sacral nerve palsy with diplopia, because the abductor nerve travels the longest at the base of the skull, and it is susceptible to compression when high intracranial pressure occurs, resulting in unilateral or bilateral paralysis and diplopia, which has no localization significance.

Localized or generalized seizures may occur in the later stages of high intracranial pressure and coma during epileptic seizures.

Changes in vital signs

Pulse pulse: Slow pulse can be produced in acute high intracranial pressure. The faster the intracranial pressure increases, the more obvious the slow pulse.

Respiration: When acute intracranial pressure is high, the initial breathing is deep and slow, and when bulbar failure occurs, it becomes shallow, slow and irregular breathing or sigh-like breathing, and finally it can stop suddenly.

(3) Blood pressure: The faster the high intracranial pressure increases, the higher the blood pressure increases reflexively, and the blood pressure drops to the end of advanced bulbar failure, and cerebral shock occurs.

Consciousness: Due to high intracranial pressure and cerebral edema, ischemia and hypoxia in the cerebral cortex and brain stem reticular structure can cause varying degrees of consciousness disturbance. Chronic high intracranial pressure may first appear restless, and then drowsiness to coma. High intracranial pressure is not necessarily proportional to the disturbance of consciousness, depending on the site, such as a tumor in the lower thalamus or a contusion of the brain stem can be severe, and the intracranial pressure may not be very high.

Pupil: It may become smaller or smaller in the early stage. If one side is enlarged and the light reaction disappears, it indicates the formation of temporomandibular hernia.

Tinnitus, dizziness, and high intracranial pressure can cause labyrinth, vestibular irritation, and congestion of the inner ear. Tinnitus and dizziness may occur in some patients.

The main clinical manifestations are the "three main signs": headache; nausea and vomiting; retinal disc edema. Other common manifestations are disturbance of consciousness, vision loss, diplopia, convulsions, and decortical rigidity. Some can manifest as emotional instability, irritability or crying, or mental symptoms such as apathy, slow response, slow movements and thinking.

In infants and young children, headache symptoms are often not obvious, often scalp vein bulging, enlarged skull, enlarged cardia, separated bone sutures, increased anterior condylar tension or bulging. Percussion on the head showed a "broken pot sound" (Macewn sign).

For chronic intracranial hypertension syndrome, plain radiographs of the skull can reveal sphenoid saddles, especially the destruction or absorption of the bones on the back of the saddle and the anterior and posterior beds. Widening and separation of cranial sutures can be seen in children older than one year of age. Caused by intracranial occupancy, normal calcification points such as the pineal gland shift, pathological calcification, local hyperplasia or destruction of the skull, and abnormal changes in the inner ear canal and other neural nerve holes can also be seen.

Electronic computed tomography (CT) or magnetic resonance imaging (MRI) can detect intracranial space-occupying lesions and make a clear diagnosis. These two tests are safe, simple, accurate and reliable. For those patients who have objective signs of increased intracranial pressure or positive findings of neurological examination or clinically suspected of increased intracranial pressure, early CT or MRI should be performed.

For patients with increased intracranial pressure, lumbar puncture may promote the risk of cerebral hernia, and lumbar puncture should be prohibited or carefully performed. If necessary, a lumbar puncture pressure measurement should be performed after the dehydrating agent is given. After lumbar puncture, dehydration and close observation should be strengthened.

Typical intracranial hypertension syndrome has symptoms such as headache, vomiting, and optic disc edema, among which optic disc edema is the most objective. Based on this sign, diagnosis is not difficult. However, in the early stage of acute intracranial pressure increase or chronic intracranial pressure increase, disc edema is often ignored, and the patient may only have headache and / or vomiting. Easily misdiagnosed as a functional disease with severe consequences. Therefore, every patient with headache and / or vomiting should be treated with caution and the possibility of increased intracranial pressure should be watched.