When the intracranial volume is increased by various pathogenic factors and the cerebrospinal fluid pressure measured by lumbar puncture in the lateral position exceeds 1.92 kpa, it is called increased intracranial pressure syndrome, and when a series of clinical manifestations such as headache, vomiting, visual impairment and optic papilledema occur, it is called increased intracranial pressure syndrome.
Etiology and pathogenesis
According to the Monroe-kellie principle, the cranial cavity (including the spinal cord cavity connected to it) can basically be treated as a non-stretchable container whose total volume is constant, except for the blood vessels connected to the outside of the cranium. There are three kinds of contents in the cranial cavity, namely, brain tissue, blood and cerebrospinal fluid, whose volumes cannot be compressed but can be compensated for each other within a certain range. The contradiction between the total volume of the cranial cavity and the variable volume of the cranial contents under different physiological and pathological conditions is created. A precise physiological regulation is needed to ensure the balance between the two. If the volume of one part of the cranial contents increases, it will inevitably lead to a compensatory reduction of the other part to accommodate. This is the basic principle of maintaining normal intracranial pressure, and disruption of this mechanism beyond a certain limit can lead to an increase in intracranial pressure. Of the three contents, brain tissue is the largest in volume but plays the least role in volume compensation, relying mainly on compression of cerebrospinal fluid and cerebral blood flow to maintain normal intracranial pressure. Generally, a 5% increase in the volume of cranial contents can still be compensated, while a significant increase in intracranial pressure occurs when the volume exceeds 8-10%.
Increased cranial contents can be caused by cerebral edema, increased cerebrospinal fluid volume or cerebral blood flow and intracranial occupying lesions due to various reasons. If the contents of the cranial cavity are normal, but the volume of the cranial cavity is reduced due to narrow cranial deformity, skull base depression, cranial osteoma, deformational osteitis or skull depression fracture, etc., it may also cause increased intracranial pressure.
Cerebral edema
(A) Cerebral edema of vascular origin. Clinically common. It is due to increased permeability of cerebral capillary endothelial cells, disruption of the blood-brain barrier, and intravascular protein.
Intracranial pressure elevation syndrome Causes:The extracellular space is enlarged due to the leakage of mass into the extracellular space, usually due to partial edema of the white matter of the brain. It is commonly seen in the early stage of cerebral edema in lesions such as traumatic brain injury, brain tumor, cerebrovascular accident, encephalitis and meningitis.
(B) Cytotoxic cerebral edema. Mostly due to cerebral ischemia and hypoxia or various kinds of poisoning caused by cerebral edema. Ischemia, hypoxia or poisoning, the sodium pump on the membrane of neurons, glial cells and vascular endothelial cells is impaired, sodium and chloride ions enter the cells to synthesize sodium chloride, the intracellular osmotic pressure increases, and water enters the cells in large quantities and causes intracellular edema. It is commonly seen in cerebral ischemia and hypoxia, carbon monoxide and organophosphorus hydrotoxicity, sepsis, toxemia and water-electrolyte imbalance. Such edema is evident in the gray matter.
(iii) Interstitial cerebral edema. Due to increased pressure in the ventricular system, water and sodium ions enter the cellular spaces around the ventricles, as seen in obstructive hydrocephalus.
(iv) Osmotic cerebral edema. When plasma osmolarity drops sharply, water molecules enter from the extracellular fluid into the cellular intracranial pressure increase syndrome in order to maintain the osmolarity balance, causing cerebral edema. Increased amount of cerebrospinal fluid
Increased cerebrospinal fluid volume can be caused by obstruction of cerebrospinal fluid circulation pathways or excessive cerebrospinal fluid production (e.g., choroidal plexus papilloma, inflammation within the lateral ventricles, etc.) and decreased cerebrospinal fluid absorption (e.g., intracranial venous sinus thrombosis subarachnoid hemorrhage arachnoid adhesions, etc.), resulting in increased intracranial pressure.
Increase in intracranial volume
Cerebral vasodilatation after traumatic brain injury, intracranial occupying lesions, hypertensive encephalopathy, cerebral vasodilatation and cerebral blood volume increase caused by respiratory obstruction and CO2 accumulation in respiratory center failure (hypercapnia) can all cause increased intracranial pressure. Clinical manifestations of increased intracranial pressure are acute and chronic, local and whole brain due to different etiologies, and their clinical symptoms are mild and severe. Symptoms of increased intracranial pressure.
Headache
In acute intracranial pressure increase, headache appears suddenly, while in chronic cases, headache develops slowly. It is mostly throbbing pain, distending pain or bursting pain, and exertion, coughing and
Clinical manifestations Headache
Sneezing and defecation may aggravate the headache. Headache can also be aggravated by lying down or lying on the side in a low position and alleviated when sitting. The early headache is obvious in the latter half of the night or in the early morning, and then the headache becomes persistent with paroxysmal intensification. The mechanism of headache may be related to the stimulation or pulling of pain-sensitive tissues in the skull due to the increase of intracranial pressure.
Vomiting
Most often occurs when the headache is severe, often in the form of a jet, unrelated to eating, with or without nausea. It is more common in children. The mechanism may be due to increased intracranial pressure stimulating the vomiting center of the medulla oblongata. Posterior cranial recess tumors, vomiting is common.
Optic nerve papilloedema
Early manifestations of optic nerve papilloedema are dilated retinal veins in the fundus, congested optic papillae, blurred margins, followed by loss of physiological depression, elevated optic papillae (up to 8-10 diopters), interrupted veins, exudate in the retina, and flaky or flaming hemorrhages visible in and near the optic papillae. Early on, it is considered normal or there is a transient black clouding. If the intracranial pressure increases without improvement, visual acuity may be reduced, secondary to neurological atrophy, leading to blindness. The mechanism of optic papillar edema is mainly intracranial arachnoid cavity cerebrospinal fluid pressure and increase, so that the pressure of cerebrospinal fluid in the optic nerve sheath increases, and then the optic nerve is compressed, axial pulp flow is slowed or stopped, and the optic papilla is swollen.
Pulse blood pressure respiration
Changes in pulse rate, blood pressure and respiration
In acute or subacute intracranial pressure increase, the pulse is slow (50-60 beats/min), and can increase faster if the pressure continues to increase. Blood pressure often increases when intracranial pressure increases rapidly. Respiration is mostly frequency change, first deep and slow, followed by tidal breathing, but also shallow and fast, hyperventilation is not uncommon.
Consciousness and mental disorders
When the intracranial pressure increases sharply, it may lead to coma, or different degrees of consciousness disorders, such as blurred consciousness, drowsiness, etc. In chronic intracranial pressure increase, the lighter patients may have memory loss and inattention, and the heavier patients may have progressive dementia, emotional indifference, incontinence. Psychiatric symptoms are more common in elderly and middle-aged patients.
Other
Grand mal seizures, vertigo, one or both sides of abducens nerve palsy, positive bilateral pathological reflex or grasping reflex, etc.
Brain herniation formation
When intracranial pressure increases beyond a certain compensatory capacity or continues to increase, brain tissue is squeezed and moves in the direction of least resistance in the neighborhood, and if it is squeezed into the dura or physiological fissure in the cranial cavity, brain herniation is formed. The herniated brain tissue can compress the surrounding important brain tissue structures and further increase the intracranial pressure when the cerebrospinal fluid circulation is obstructed, endangering life safety. The following two types of brain herniation are common in clinical practice.
Herniation of the cerebellar curtain
Most commonly seen in lesions above the cerebellum. It is a partial herniation of the temporal lobe or/and midline brain structures down through the cerebellar curtain notch. Depending on the herniated brain tissue and the filled brain pool, there are two types of herniations: lateral and central. When the temporal lobe is squeezed downward, the hippocampal hook initially herniates downward through the cerebellar curtain notch (filling
Herniation of the cerebellar curtain notch
When the lesion continues to develop, the hippocampal hook on the lesion side and the hippocampal gyrus herniate downward through the cerebellar vena cava pool, which is the total herniation of the temporal lobe, the following three temporal lobe tissues herniate the lateral type of the cerebellar vena cava herniation. If the important midline structures such as the third ventricle and the lower thalamus move downward, causing the upper midbrain to herniate below the cerebellar curtain notch, this is the central type. In addition to the general symptoms of increased intracranial pressure, the following clinical manifestations are also seen in cerebellar herniation.
1. Disorders of consciousness. From wakefulness to drowsiness or even coma, or from shallow coma to sudden development of moderate or deep coma. It is caused by the pressure on the brainstem, reduced cerebral blood flow, and impaired function of the ascending activation system of the reticular formation.
2. Pupillary changes. In the early stage, the pupil on the side of the lesion may narrow briefly, then the pupil on the affected side gradually dilates and the light reflex is blunted or disappears. At the end of brain herniation, the pupil is obviously dilated, the response to light disappears, and the eye is immobilized (damage to the motoneural nerve).
3. Paralysis. Paralysis of the limb contralateral to the lesion is caused by damage to the pedunculopontine tract of the brain. In the late stage, it may also present as decerebral tonicity, which is caused by severe compression of the midbrain, ischemia, and damage to the reticular hypoglossal inhibitory system.
4. Change of vital signs. In the early stage, breathing is deep and slow, followed by tidal breathing, hyperventilation or double inspiration; in the late stage, breathing is irregular, shallow, fast and weak until respiratory arrest. The pulse rate is slow and then fast, and the blood pressure rises and then falls, which is a sign of central failure of the medulla oblongata.
Occipital foramen magnum hernia
It is most often seen in posterior cranial sulcus occupying lesions and also in the late stage of cerebellar curtain herniation. Increased intracranial pressure herniates the cerebellar tonsils downward into the greater occipital foramen.
The herniation of the foramen magnum is divided into chronic and acute types according to the speed of development.
1. Chronic type. In the early stage, there is occipital pain, cervical tonicity, mild damage to the linguopharyngeal, vagus, paracentral and hypoglossal nerves, and the patient is conscious. Occasionally, tonicity of the limbs, mild respiratory depression, rapid deterioration of vital signs and coma may occur after the disease has progressed beyond the compensatory capacity.
2. Acute type. It can occur suddenly or due to lumbar puncture, exertion, etc., which can cause acute aggravation of the original chronic type of foramen magnum hernia. Due to the compression of the vital center of the medulla oblongata, the blood supply to the cerebellum is impaired, and the intracranial pressure increases rapidly (obstruction of the fourth brain to the foramen magnum), severe suboccipital pain and cervical ankylosis, vertigo, dysphagia, decreased muscle tone, bradykinesia of the extremities, and respiratory and circulatory failure occur clinically. Sudden coma, respiratory arrest, and later cardiac arrest may also occur.
Diagnosis
Determination of increased intracranial pressure
Determine the presence or absence of increased intracranial pressure
There are acute, subacute and chronic intracranial pressure increases. Generally, slow-onset diseases have more symptoms such as headache, vomiting, optic papillar edema, etc. Initial
Intracranial hypertension syndrome CT manifestation. It is not difficult to diagnose intracranial hypertension at a step-by-step basis. In acute and subacute brain diseases, due to the short course and rapid development of the disease, most of them are accompanied by different degrees of consciousness impairment and no obvious optic papilledema, so it is often difficult to confirm the diagnosis of intracranial hypertension, and the following examinations are needed to determine it.
(a) Fundus examination. Prior to the appearance of typical optic papilledema, there are often changes such as filling and dilatation of the fundic veins, loss of pulsation, microvascular hemorrhage in the fundus, and gray-white radiating lines on the upper and lower margins of the optic papilla.
(B) Increased intracranial pressure in infants and young children can be found early with increased tension of fontanelle, separation of cranial sutures, and percussion like the sound of a broken water jug.
(C) dehydration test treatment. 20% mannitol 250 ml rapid intravenous drip or tachyphylaxis 40 mg intravenous push, if the headache, vomiting and other symptoms are reduced, then the possibility of increased intracranial pressure is greater.
(iv) Imaging examination. Cranial plain film may reveal signs of increased pressure traces in the inner plate of the skull or/and saddleback absorption of certain primary pathologies. Cerebral angiography has considerable diagnostic value for cerebrovascular disease and most intracranial occupying lesions. CT scan and MRI (magnetic resonance imaging) of the head is a safe and reliable way to detect acute and subacute intracranial pressure increase without significant optic papilledema.
For patients with suspected severe intracranial pressure increase, especially those with acute or subacute onset with limited brain damage symptoms, blind lumbar puncture should not be performed. Lumbar puncture should only be performed after adequate preparation if the diagnosis is encephalitis or meningitis and subarachnoid hemorrhage without restrictive brain damage.
Determine the cause of the disease:
Based on the history and the urgency of the onset of the disease, the findings of the medical system and neurological examination, and the necessary laboratory tests, it is entirely possible to initially identify the lesion and the cause of the increased intracranial pressure. The common etiologies are as follows.
(i) Cranio-cerebral trauma. Intracerebral hematoma and cerebral contusions, etc. Cerebral encephalopathy
(ii) Intracranial tumors and intracranial metastases, etc.
(iii) Cerebrovascular disease. Cerebral hemorrhage, subarachnoid hemorrhage and cerebral infarction, etc.
(iv) Intracranial inflammation and cerebral parasitic diseases. Various encephalitis, meningitis, brain abscess, cerebral ragweed cysticercosis, cerebral pulmonary schistosomiasis, cerebral encysticercosis, etc.
(E) cranial malformation. Such as skull base depression, narrow craniosynostosis, conduction duct developmental malformation, congenital submicrocephalic tonsillar herniation malformation, etc.
(F) Benign intracranial pressure increase.
(vii) Cerebral hypoxia. Cardiac arrest, pulmonary encephalopathy, continuous status epilepticus, etc.
(viii) Others. Liver, renal failure, hematologic disease, hypertensive encephalopathy, various toxicities, anaphylaxis, etc.
Treatment
I. Etiological treatment
Second, symptomatic treatment
Mainly in reducing intracranial pressure. Maintain effective blood circulation and respiratory function, and enhance the tolerance of brain cells to the disease damage.
Cranial pressure lowering drugs
1. Dehydration therapy. Dehydration therapy is the key to lowering intracranial pressure, reducing brain tissue edema and preventing brain herniation formation. Adults commonly use 20% mannitol to lower cranial pressure dehydration therapy. Alcohol 250 ml, rapid sedation, once every 4-6 hours. The main point is that the hypertonic solution creates an osmotic pressure difference between the blood and brain, transferring the water in the brain into the circulation as soon as possible, not simply through the diuretic effect. Mannitol can not only lower intracranial pressure and reduce cerebral edema, but also improve brain and body circulation, prevent the production of free radicals, enhance the ability of nerve cells to tolerate hypoxia, and promote the recovery of brain function. 500 ml of 10% glycerol glucose solution or 10% glycerol saline solution should be administered intravenously within 2 to 3 hours. 1～2 times/day, or measured at 1 g/kg per day, mixed with equal amount of saline or orange juice, and given orally or nasally in three divided doses. Glycerol intravenous drip or oral is mostly used for patients with chronic intracranial pressure increase. The dose of hypertonic dehydrating agents should be properly controlled, not the greater the better, the general blood osmolality rise 31 mosm, such as with high doses of mannitol, so that the blood osmolality > 310 mosm, that may cause acidosis, renal failure and hypertonic coma.
2.Diuretics. Mainly inhibit the reabsorption of sodium, chloride and potassium by the renal tubules, thus producing diuretic effect. Due to the large amount of diuresis to dehydrate the body and thus reduce intracranial pressure. Tachyphylaxis 40-60 mg intravenous or 50% glucose 40 mg + tachyphylaxis 40-60 mg static push 1 to 3 times / day, can also be added to mannitol in the rapid static drip; oral dose once 20-40 mg, 3 / day. Sodium diuretic, adults a dose of 25-50 mg added to 10% glucose 20 ml slowly sedated. Acetazolamide, 0.25-0.5 g for adults, 2-3/day, orally, can also be applied for patients with chronic increased intracranial pressure. Application of diuretics and dehydrating agents should be paid attention to potassium supplementation due to excessive potassium excretion.
3. Adrenocorticotropic hormone. Adrenocorticotropic hormone can improve the blood-brain barrier, reduce its permeability, strengthen the regulatory function of water and electrolyte metabolism, stabilize cell membrane function and reduce cell membrane damage; improve local cerebral blood flow and reduce edema around the lesion area; reduce cerebrospinal fluid production; enhance non-specific anti-inflammatory and detoxification effects. When applying adrenocorticotropic hormone, attention should be paid to any contraindications, such as ulcer disease, diabetes mellitus, etc., because of its suppression of immune function, and caution when combined with infection. Commonly used drugs are dexamethasone 20-40 mg added to 5-10% glucose solution 250-500 ml intravenous drip 1/day, or hydrocodone 200-300 mg added to 5-10% glucose 250-500 ml intravenous drip 1/day, after short-term application, change to oral, and gradually reduce the amount of drug discontinuation.
The amount of fluid intake should be appropriately limited during dehydration treatment, and the daily input for adults generally does not exceed 2,000 ml. For patients with hot and sweaty days, fever or frequent vomiting and diarrhea, the amount can be increased as appropriate, and the infusion rate should not be too fast.
Decompression surgery
Decompression surgery is applied after the application of dehydrating agents and diuretics is ineffective, or when brain crisis occurs in the early stage of increased intracranial pressure, sub-temporal muscle decompression and suboccipital decompression can be used. Ventricular puncture and drainage or ventricular shunt can also be performed.
Other therapeutic effects
Hypothermia, low heat can reduce brain metabolism, reduce brain oxygen consumption and lower intracranial pressure. Local cerebral hypothermia is often used, with ice caps or ice packs. Ice tank head cooling.
Intracranial pressure increase syndrome care
(1) Dynamic observation of increased intracranial pressure: avoid various stimulating factors (emotional excitement, tension, large amounts of water, excessive and rapid rehydration, etc.). Patients with symptoms of cranial hypertension (severe headache, jet vomiting) should be treated promptly.
(2) Observe vital signs and changes in consciousness, pupils and limb movements: change in consciousness is one of the most common signs in patients with cranio-cerebral disorders. It often reflects the functional status of the cerebral cortex and brainstem reticular formation. The presence of agitation, drowsiness, and hazy consciousness in patients with episodic tumors is a precursor symptom of brain herniation. Patients with craniocerebral injury have a coma-awake – coma process, i.e., having an intermediate waking period and then coma is strong evidence of epidural hematoma. Pupil regulation and sensitivity to light response are related to the motor nerve. Pupillary observation has special localization significance in neurosurgery. Patients with supratentorial tumors presenting with small and then large pupils on the diseased side and delayed and absent responses to light are alerted to the development of temporal lobe herniation. In temporal lobe herniation, the impairment of consciousness, pupil and limb movement appears first, and the impairment of respiratory and circulatory system appears at a later stage. In occipital foramen herniation, respiratory and circulatory disturbances appear suddenly, followed by changes in consciousness and pupils. Patients with increased intracranial pressure should be treated at an early stage, and resuscitation after brain herniation may leave irreparable sequelae.
(3) Cooperation of resuscitation: the resuscitation of brain herniation requires concerted efforts and time. In case of temporal lobe herniation, a rapid intravenous drip of 20% mannitol 250ml + dexamethasone 5mg is required within 20 minutes (it can rapidly increase the plasma crystal osmolarity, lower the intracranial pressure quickly and maintain it for a long time). The drip can be repeated every 4~6 hours depending on the condition. In patients with sudden respiratory arrest due to occipital foramen ovale herniation, orbital ventriculotomy can be performed immediately to save the patient’s life, while tracheal intubation, artificial respirator assisted breathing and intravenous infusion of 20% mannitol 250ml and application of stimulants can be performed. Patients with ventricular drains can have their drains cut first and then be connected to a ventricular drainage bottle.
(4) Ventricular drainage care.
① drainage bottle hanging in 10~15cm above the patient’s head (the distance between the patient’s frontal bone and the drainage hoist bottle drip tube), too high can not play the purpose of drainage. Too low drainage too fast can make the ventricle collapse cause cortical and intraventricular hemorrhage.
②The drainage tube should be kept open and not twisted or crumpled.
③ Observe the color and amount of cerebrospinal fluid dripping out. Hemorrhagic cerebrospinal fluid drip proves that there is active bleeding, and cloudy cerebrospinal fluid drip proves that there is infection.
④ Pay attention to keep the wound dressing and the dressing at each articulation dry. Find the reason when the dressing is wet.
⑤Extraventricular drainage should not be left for a long time, and should be treated within 1 week.
(6) Before considering extubation for stable condition, hold the drainage bottle high to 20~25cm and observe for 2 days, pay attention to any symptoms of increased cranial pressure, if there is no discomfort, the tube can be clamped for 2 days, after 2 days, no discomfort reaction can be considered for extubation.
(7) If headache, vomiting and other symptoms of cranial hypertension still appear after hanging high, consider doing cerebrospinal fluid shunt surgery (ventriculo-abdominal drainage or ventriculo-atrial drainage).