Increased intracranial pressure is a common symptom of craniocerebral injury, brain tumor, cerebral hemorrhage, hydrocephalus and intracranial inflammation. The increase in volume of cranial cavity contents due to the above-mentioned diseases leads to a sustained intracranial pressure above 2,0 Kpa (200 mmH2O), which causes the corresponding syndrome called increased intracranial pressure. Understanding the regulation of intracranial pressure and the mechanism of the occurrence of intracranial pressure increase is the key to the condition assessment, rescue and surgery of craniocerebral trauma.
(A) Formation and normal value of intracranial pressure
The cranial cavity holds three kinds of contents: brain tissue, cerebrospinal fluid and blood, and when the cranial suture is closed in children or adults, the volume of cranial cavity is fixed, which is about 1400-1500 ml. The above three contents in the cranial cavity keep a certain pressure inside the cranium, which is called intracranial pressure, and since the cerebrospinal fluid inside the cranium is between the cranial cavity wall and brain tissue, the hydrostatic pressure of cerebrospinal fluid generally represents the intracranial pressure, and the pressure is increased by lateral position This pressure value is obtained by lumbar puncture or direct ventricular puncture measurements. The normal intracranial pressure in adults is 0.7-2.0 Kpa (70-200 mmH2O) and in children is 0.5-1.0 Kpa (50-100 mmH2O).
(B) Regulation and compensation of intracranial pressure
The intracranial pressure can have small fluctuations, and it is closely related to blood pressure and respiration. The intracranial pressure increases slightly during systole and decreases slightly during diastole; the pressure increases slightly during expiration and decreases slightly during inspiration. The regulation of intracranial pressure is mainly regulated by the increase or decrease of cerebrospinal fluid volume. When the intracranial pressure is lower than 0.7 Kpa (70 mmH2O), the secretion of cerebrospinal fluid increases, while the absorption decreases, so that the amount of intracranial cerebrospinal fluid increases to maintain the same intracranial pressure. On the contrary, when the intracranial pressure is higher than 0.7 Kpa (70 mmH2O), the secretion of cerebrospinal fluid decreases and the absorption increases, resulting in a decrease in the amount of intracranial cerebrospinal fluid to compensate for the increased intracranial pressure. In addition, when the intracranial pressure increases, some of the cerebrospinal fluid is squeezed into the spinal subarachnoid space, which also plays a role in regulating the intracranial pressure. The total volume of cerebrospinal fluid accounts for 10% of the total volume of the cranial cavity, while blood accounts for about 2%-11% of the total volume depending on the blood flow, and generally the critical volume allowed to increase intracranially is about 5%, beyond which the intracranial pressure begins to increase. When the volume of cranial cavity contents increases or the volume of cranial cavity shrinks more than 8%-10% of the cranial cavity volume, it will produce serious intracranial pressure increase.
(C) Causes of increased intracranial pressure
1.Increased volume of cranial cavity contents such as increased volume of brain tissue (cerebral edema), increased cerebrospinal fluid (hydrocephalus), obstructed intracranial venous reflux or excessive perfusion, increased cerebral blood flow, and increased intracranial blood volume.
2, intracranial occupying lesions make the intracranial space relatively small such as intracranial hematoma, brain tumor, brain abscess, etc.
3, congenital malformation makes the volume of cranial cavity become smaller such as narrow skull, skull base depression, etc.
(D) Pathophysiology of increased intracranial pressure
1.Factors affecting the increase of intracranial pressure
(1) Age The cranial sutures of infants and children are closed or not yet firmly fused, so the increase of intracranial pressure can make the cranial sutures open and increase the volume of cranial cavity accordingly, thus moderating or prolonging the progress of the disease. In the elderly, the course of the disease is also longer because of the increase in intracranial compensatory space due to brain atrophy.
(2) Expansion rate of the lesion Langfitt placed a small balloon outside the intracranial dura in monkeys in 1966 and injected 1 ml of fluid into the balloon every hour to make it gradually expand. At first, the changes in intracranial pressure were small or insignificant due to the presence of the intracranial pressure regulating function described above; as the balloon continued to expand and the regulating function was gradually depleted, the increase in intracranial pressure gradually became obvious. When the intracranial fluid finally reaches a critical point when it is injected to 4ml, at this time, as long as a very small amount of fluid is injected into the balloon, the intracranial pressure will have a substantial increase, and the intracranial pressure will drop significantly when a small amount of fluid is released. This relationship between the volume of the cranial cavity contents and the intracranial pressure is called the volume/pressure relationship. The relationship between intracranial pressure and volume is not linear but similar to exponential relationship, this relationship can explain some clinical phenomena, such as when intracranial occupying lesions, with the slow growth of the lesion, can be a long time without symptoms of intracranial pressure increase, once due to intracranial pressure compensatory dysfunction, the disease will develop rapidly, often in a short period of time that the intracranial hypertension crisis or brain herniation; on the contrary, if the original intracranial pressure If the increase in intracranial pressure is within the compensatory range (below the critical point), the release of a small amount of cerebrospinal fluid will only cause a small pressure drop, a phenomenon known as volumetric pressure response.
(3) Lesion site Occupational lesions in the midline or posterior cranial fossa can cause obstructive hydrocephalus because the lesion can easily block the cerebrospinal fluid circulation pathway, so the symptoms of increased intracranial pressure can appear early and be severe. Occupational lesions near the large intracranial venous sinuses can compress the venous sinuses at an early stage, causing the return of intracranial venous blood or the absorption of cerebrospinal fluid, so that the symptoms of increased intracranial pressure can also appear at an early stage.
(5) The degree of concomitant cerebral edema Brain parasitic disease, brain abscess, tuberculoma, brain granuloma, etc. can be accompanied by more obvious cerebral edema due to inflammatory reaction, so the symptoms of increased intracranial pressure can appear at an early stage.
(6) Systemic diseases such as uremia, hepatic coma, toxemia, pulmonary infection and acid-base imbalance can cause secondary cerebral edema and increase intracranial pressure. Hyperthermia often aggravates the degree of increased intracranial pressure.
2.Consequences of increased intracranial pressure
Continuous increase of intracranial pressure can cause a series of central nervous system functional disorders and pathological changes. The main pathological changes include the following six points.
(1) Reduced cerebral blood flow, cerebral ischemia and even brain death: about 1200ml of blood per minute enters the skull in normal adults, which is regulated through the automatic regulation function of cerebral blood vessels. The formula is.
Mean arterial pressure (MAP) – intracranial pressure (ICP)
Cerebral blood flow (CBF) = ——— ——–
Cerebrovascular resistance (CVR)
The numerator part of the formula (mean arterial pressure – intracranial pressure) is also known as the perfusion pressure of the brain (CPP), and therefore the formula can be rewritten as
Perfusion pressure of the brain (CPP)
Cerebral blood flow = ——— –
Cerebrovascular resistance (CVR)
Normal cerebral perfusion pressure is 9,3 to 12 Kpa (70 to 90 mmHg), and cerebrovascular resistance is 0,16 to 0,33 Kpa (1,2 to 2,5 mmHg), when the cerebral vascular autoregulation is good. If the cerebral perfusion pressure decreases due to the increase of intracranial pressure, the ratio of the above formula can be made constant by vasodilation to reduce the autoregulatory response of vascular resistance. Thus, the stability of cerebral blood flow is ensured. If the intracranial pressure increases continuously so that the cerebral perfusion pressure is lower than 5,3 Kpa (40 mmHg), the cerebrovascular autoregulation function fails, then the cerebral vessels can no longer make the corresponding further expansion to reduce the vascular resistance. The ratio of the formula becomes smaller, and cerebral blood flow then drops sharply, which will cause cerebral ischemia. When the intracranial pressure rises to a level close to the mean arterial pressure, the intracranial blood flow stops almost completely and the patient is in a state of severe cerebral ischemia, or even brain death.
(2) Brain displacement and brain herniation Pressure is transmitted from high to low in the closed capacitance cavity, brain tissue is displaced to some orifices, and brain herniation is formed.
(3) Cerebral edema Increased intracranial pressure can directly affect brain metabolism and blood flow thus producing cerebral edema, which increases the volume of the brain and thus aggravates the increased intracranial pressure. The accumulation of fluid in cerebral edema can be in the extracellular space or in the cell membrane. The former is called vasogenic cerebral edema and the latter is called cytotoxic cerebral edema. Vascular-derived cerebral edema is most often seen in the early stages of lesions such as brain injury and brain tumors, and is mainly due to increased capillary permeability, which leads to water retention in the interstitial spaces of nerve cells and glial cells, contributing to an increase in brain volume. Cytotoxic cerebral edema may be caused by metabolic dysfunction due to the direct action of certain toxins on brain cells, resulting in the retention of sodium ions and water molecules in nerve cells and glial cells, but without changes in vascular permeability, and is commonly seen in the early stages of cerebral ischemia and cerebral hypoxia. In the case of increased intracranial pressure, since the above two factors can exist simultaneously or sequentially, most of the cerebral edema is mixed, or vasogenic cerebral edema is first transformed into cytotoxic cerebral edema later.
(4) Cushing reaction In 1900, Cushing used isotonic saline to instill into the subarachnoid space of dogs to cause an increase in intracranial pressure. When the increase in intracranial pressure approached the arterial diastolic pressure, the blood pressure increased, the pulse slowed down, and the pulse pressure increased, followed by tidal breathing, a drop in blood pressure, a weak pulse, and eventually respiratory arrest and cardiac arrest leading to death. This experimental result is very similar to the clinical situation seen in acute craniocerebral injury, when the intracranial pressure increases sharply, the patient has high blood pressure (systemic vasopressure response), slow heartbeat and pulse rate, respiratory rhythm disturbance and body temperature rise and other changes in vital signs, this change is called Cushing’s reaction. This crisis is mostly seen in acute cases of increased intracranial pressure, but is not obvious in chronic cases.
(5) Gastrointestinal motility disorders and gastrointestinal bleeding Some patients with increased intracranial pressure may first develop gastrointestinal disorders, vomiting, gastric and duodenal bleeding, ulcers and perforations. This is related to the dysfunction of the hypothalamic vegetative nerve center due to ischemia caused by increased intracranial pressure. It is also believed that when intracranial pressure increases, the mucosal vasoconstriction of the gastrointestinal tract causes ischemia, resulting in extensive peptic ulcers.
(6) Neurogenic pulmonary edema occurs in up to 5-10% of cases of acute intracranial pressure increase. This is due to increased a-adrenergic neural activity due to hypothalamic and medullary compression, increased blood pressure reactivity, left ventricular overload, increased left atrial and pulmonary venous pressure, increased pulmonary capillary pressure, and fluid extravasation, causing pulmonary edema, with patients exhibiting shortness of breath, sputum, and large amounts of foamy, bloody sputum.
(E) Classification of increased intracranial pressure
Increased intracranial pressure is the most common problem of craniocerebral trauma, especially combined with intracranial hematoma, which often presents symptoms and signs of increased intracranial pressure. Increased intracranial pressure can trigger brain herniation crisis, which can cause death of patients due to respiratory and circulatory failure, so it is very important to diagnose and correctly deal with increased intracranial pressure in time.
1.According to the different etiologies, increased intracranial pressure can be divided into two categories.
(1) Diffuse intracranial pressure increase caused by narrow cranial cavity or volume increase of brain parenchyma, which is characterized by uniform pressure increase in various parts of the cranial cavity and among the subcavities, without obvious pressure difference, so there is no obvious displacement of brain tissue. The increased intracranial pressure caused by diffuse meningoencephalitis, diffuse hydrocephalus, and transmissible hydrocephalus seen clinically are all of this type.
(2) Focal intracranial pressure increase Because of the limited dilated lesion in the skull, the pressure at the lesion site increases first, causing the nearby brain tissue to be squeezed and displaced, and the pressure is transmitted to the distant area, resulting in pressure difference between the cranial spaces, and this pressure difference leads to the displacement of the ventricles, brainstem and midline structures. The patient’s tolerance to this increased intracranial pressure is low, and the recovery of neurological function is slow and incomplete after the pressure is relieved, which may be related to cerebral ischemia and cerebrovascular autoregulation damage caused by brain displacement and local pressure on the brain.
2, the different speed of lesion development, intracranial pressure increase can be divided into three categories: acute, subacute and chronic.
(1) Acute intracranial pressure increase is seen in acute intracranial hematoma caused by cranial injury, hypertensive cerebral hemorrhage and so on. The symptoms and signs caused by the increased intracranial pressure are severe, and the vital signs (blood pressure, respiration, pulse rate, body temperature) change drastically.
(2) Subacute intracranial pressure increase The disease develops faster, but it is not as urgent as acute intracranial pressure increase, and the response of intracranial pressure increase is mild or not obvious. Subacute intracranial pressure increase is mostly seen in fast developing intracranial malignant tumors, metastases and various intracranial inflammatory diseases, etc.
(3) Chronic intracranial pressure increase The development of the disease is slow, and there may be no symptoms and signs of intracranial pressure increase for a long time, and the development of the disease is sometimes good and sometimes bad. It is mostly seen in slow-growing benign intracranial tumors, chronic subdural hematoma, etc.
Intracranial hematoma due to intracranial vascular injury caused by cranial trauma; cerebral edema associated with cerebral contusion is a common cause of traumatic intracranial pressure increase; traumatic subarachnoid hemorrhage, impaired cerebrospinal fluid circulation caused by blood clots deposited in the brain pool at the base of the skull, and impaired cerebrospinal fluid absorption caused by red blood cells obstructing the arachnoid granules are also common causes of intracranial pressure increase; other causes such as venous sinus thrombosis or fat embolism Other causes, such as venous sinus thrombosis or fat embolism, can also lead to increased intracranial pressure, but are less common. Acute or chronic intracranial pressure increase can lead to brain herniation. After brain herniation, displaced brain tissue is squeezed into the cerebellar fissure, dural fissure, or occipital foramen, compressing the brainstem and producing a series of critical symptoms. Brain herniation can aggravate the cerebrospinal fluid and blood circulation disorder, which further increases the intracranial pressure, thus making brain herniation more serious.
(F) Clinical manifestations of increased intracranial pressure
1.Headache One of the most common symptoms of increased intracranial pressure, the degree of headache increases progressively with the increase of intracranial pressure. The headache is often aggravated when exerting, coughing, bending or head-down activities. The nature of the headache is mostly distending pain and tearing pain.
2. Vomiting When the headache is severe, it may be accompanied by nausea and vomiting. Vomiting is jet-like, and it is easy to occur after meals. Sometimes it can lead to water-electrolyte disorders and weight loss.
Optic nerve papilla edema is one of the important objective signs of increased intracranial pressure. It shows that the optic nerve papilla is filled with blood, the edge is blurred, the central depression disappears, the optic disc is elevated, and the veins are angered. If the optic nerve papilla edema persists for a long time, the optic disc will be pale, the visual acuity will be diminished, and the visual field will shrink centripetally, which is called secondary optic nerve atrophy. At this time, if the increased intracranial pressure is lifted, the recovery of vision is often not satisfactory, and even continues to deteriorate and blindness.
The above three are typical manifestations of increased intracranial pressure, which are called the “three main signs” of increased intracranial pressure. Each of the three main signs of increased intracranial pressure does not appear at the same time, and one of them may be the first symptom. Increased intracranial pressure can also cause one or bilateral abductor nerve palsy and diplopia.
4. Disorders of consciousness and changes in vital signs The early stage of disorders of consciousness may include drowsiness and unresponsiveness. In severe cases, drowsiness, coma, dilated pupils, loss of response to light, brain herniation and cerebral tonicity may occur. Vital signs change to elevated blood pressure, bradycardia, irregular respiration, elevated body temperature, and other critical states, and even respiratory arrest, and eventually death due to respiratory and circulatory failure.
5. Other symptoms and signs Dizziness, sudden collapse, and scalp venous rage. In pediatric patients, there may be cranial enlargement, widening of cranial sutures, and full bulging of fontanelle. The cranial percussion shows the sound of broken cans and dilated superficial veins in the scalp and frontal orbit.
(vii) Treatment: The treatment of intracranial hypertension depends on the cause, the degree and duration of intracranial hypertension, and the degree of intracranial hypertension is closely related to the location and extent of intracranial lesions. Therefore, the etiology should be clarified as soon as possible to solve the problem of intracranial hypertension at its root.
The treatment goals of intracranial hypertension are: intracranial pressure should be controlled at least below 250-300 mmH2O; cerebral perfusion pressure should reach above 60 mmHg by maintaining appropriate mean arterial pressure to ensure normal functional activities of the brain; and all unfavorable factors that can aggravate or promote intracranial hypertension should be avoided.
1 General measures: timely and appropriate dehydration treatment to effectively reduce intracranial pressure and enable patients to pass the acute phase smoothly is the key to successful rescue of acute intracranial hypertension.
Patients with acute intracranial hypertension should absolutely rest in bed, and elevating the head position can reduce cerebral venous pressure and cerebral blood volume, which is a simple method to reduce cranial pressure. The ideal head position angle should be based on the individual response of the patient’s intracranial pressure monitoring, and a head elevation of 15-30° is safer to keep intracranial pressure down. Keep the intracranial venous return flow smoothly, avoid overhead or tight neck sash, improper head position and patient agitation to prevent the increase of intracranial pressure. Keep the environment quiet and comfortable for those with unstable vital signs, and closely observe the changes in condition. Keep the patient’s head and neck in a lateral position during vomiting to prevent accidental aspiration; keep the airway open to prevent airway obstruction, hypoxemia and hypercapnia, and ensure real-time monitoring of blood oxygen saturation and timely oxygenation. In addition to immediate artificial respiration, patients with respiratory arrest should be rapidly intubated through the mouth with endotracheal pressure and oxygen, and be given dehydrating agents and respiratory stimulants at the same time. In addition to immediate tracheal compression oxygenation and intracardiac injection of epinephrine hydrochloride, external cardiac compressions should be performed immediately in patients with simultaneous cardiac and respiratory arrest. The amount of daily fluid intake should not be too much, generally controlled at about 2000ml, and intravenous rehydration should be low-sodium glucose saline mixed with 5% glucose and 0.45% sodium chloride, and the daily amount of sodium rehydration should be controlled at 5.6g. Pay attention to monitoring water, electrolytes and acid-base balance, and properly deal with dilute hyponatremia syndrome. Combined with stress hyperglycemia can cause non-ketotic hypertonic hyperglycemic encephalopathy.
Severe hypertension, hyponatremia, anemia and seizures can all cause increased intracranial pressure and should be treated accordingly.
Intracranial pressure monitoring should be considered for patients with severe brain injury to dynamically observe intracranial pressure changes, select appropriate treatment according to the latter’s specific conditions, and monitor the treatment effect
2 Reduce cerebral edema: Injecting hypertonic drugs intravenously within a short period of time to increase the osmotic pressure of blood and make use of the pressure difference between blood and brain cells, so that water inside and outside the swollen brain cells can rapidly enter the blood and be excreted through urine, thus reducing the volume of brain tissue and achieving the purpose of reducing intracranial pressure.
(1) Preferred hypertonic dehydrating agent 20% mannitol is commonly used clinically, which is the most widely used osmotic dehydrating agent with positive clinical efficacy at home and abroad; mainly through intravenous injection, it causes osmotic dehydration and reduces brain volume to lower intracranial pressure. Mannitol can expand plasma volume, reduce erythrocyte volume and blood viscosity, and increase cerebral blood flow and cerebral oxygen release after input into the body. The effect of mannitol on blood rheology depends on the state of the brain’s own pressure regulation. When the latter state is intact, mannitol input induces cerebral vasoconstriction and maintains constant cerebral blood flow, resulting in a significant decrease in intracranial pressure; however, when the brain’s own pressure mediation function is lost, mannitol input instead increases cerebral blood flow and reduces intracranial pressure very slightly. Mannitol also improves the blood rheology of the brain microcirculation and has the function of scavenging free radicals. Mannitol should be given intravenously by rapid drip, requiring 250 ml of solution to be dripped within 30-60 min, too slow to achieve the purpose of hyperosmolarity in the blood. A single dose of mannitol takes effect in 1-5min, with a peak effect in 20-60min, and can last 1,5-6h, depending on the clinical condition of the brain. In order to continuously reduce cranial hypertension, the drip should be repeated for 4-6h, or it can be supplemented with other cranial hypotensive drugs or diuretics between drips. The general dosage is calculated as 0.25-1g/kg, and a high dose of 1.4g/kg can be given in emergency situations. The water and electrolyte balance should be paid close attention to during the medication period, and fluid and electrolytes such as potassium and sodium should be replenished in time. Once a decrease in urine volume is detected, it is indicated that the drug should be reduced or discontinued, and should not be used for a long time.
The secondary effect of mannitol drip is that the clearance by the kidneys results in a large loss of free water, an increase in serum osmolality, and the transfer of intracellular water to the extracellular space, causing a longer-lasting intracellular dehydration. The large amount of water entering the blood reduces blood viscosity and transiently increases cerebrospinal fluid, which in turn can cause reflex vasoconstriction and a decrease in cerebral blood volume. With the prolongation of intracranial hypertension, the blood-brain barrier in the lesioned area may gradually become dysfunctional and increase in permeability under the action of various factors. On the other hand, because of the small molecular weight of mannitol, it can easily cross the damaged blood-brain barrier into the edematous area, and repeated use may accumulate locally and aggravate local vasogenic edema. after Kaufmann et al. gave animals five consecutive intravenous drips of mannitol, they found that mannitol accumulated in the brain tissue, especially in the edematous part, and an osmotic pressure gradient in the opposite direction appeared between the edematous brain tissue and plasma. Excessive use of dehydrating agents can cause dehydration and atrophy of brain cells, further aggravating neurological impairment and aggravating the disease. Repeated use of the drug can cause mannitol to accumulate in the brain causing rebound increase in intracranial pressure, and prolonged use of the drug has poor effect in lowering cranial pressure, especially when the serum osmolality is >320 mOsm/kg, and can also aggravate congestive heart failure, circulating blood insufficiency, hypokalemia, hypertonic state and acute renal tubular necrosis after long-term use.
If mannitol is used repeatedly in large doses, it can worsen cerebral edema and cause significant intracranial hypertension rebound due to the escape of small molecules of mannitol outside the blood vessels. Acute intracranial pressure rebound can lead to decreased cerebral perfusion pressure, insufficient cerebral blood flow, cerebral metabolic disorders, and brain herniation formation if not detected and controlled early. Paying attention to the presence of rebound phenomenon after drug discontinuation at any time can not only guide the medication, but also facilitate the judgment of patient’s prognosis and take corresponding measures in time. Under the supervision of intracranial pressure, the administration of mannitol should be changed to irregular and variable use, and the primary dosage, interval time and drip rate of mannitol should be adjusted at any time.
Mannitol is also an effective anti-cranial pressure drug, without the side effects of mannitol, but the effect is relatively slow and should not be used in an emergency. Those with cardiac, renal and pulmonary insufficiency should use 10% glycerol fructose injection, but the effect of dehydration on lowering cranial pressure is less than that of mannitol.
(2) medullary collaterals diuretics These drugs promote renal urination and sodium excretion, inhibit cerebrospinal fluid production, reduce glial cell swelling, reduce the concentration of potassium ions in the extracellular fluid, and enhance the hypertensive effect of hypertonic drugs. The commonly used drug is furosemide (tachyphylaxis), 20-40mg each time, intravenously, with milder effects. It has a synergistic effect with mannitol, which can reduce the dosage of the latter and prolong the interval between doses. It can also reduce cerebrospinal fluid production by 40% to 70%. Furosemide is the drug of choice for intracranial hypertension with cardiac, pulmonary and renal dysfunction, and mannitol or albumin will be used after the increase in urine volume to prevent the latter two from increasing blood volume and overloading the heart. It can also be used in combination with glycerol fructose injection for patients with intracranial hypertension with cardiac, renal and pulmonary insufficiency.
(3) Colloidal dehydrating agents such as human albumin, lyophilized plasma, and vegetable protein preparation β-heptaosaponin sodium can be used alone or in combination with other dehydrating agents.
The combination of albumin and tachyzoate, each application of tachyzoate 0, 5 to 1 mg/kg, 2 to 6 times a day, keeps the patient in a mildly dehydrated state, which can absorb water into the blood vessels leading to brain tissue dehydration and diuresis, better than tachyzoate or mannitol alone.
In recent years, it has been proposed to use albumin and/or low molecular dextrose intravenously to dilute the blood, reduce the blood viscosity and lower the red blood cell pressure product to normal, which is best for the blood and oxygen supply to the brain tissue. Albumin can also combine with metal ions in the blood to reduce the effect of oxygen free radicals on brain damage.
Hypertonic dehydration is contraindicated in cardiac insufficiency; dehydration therapy should not be applied in renal failure; in shock, blood pressure should be raised before dehydration; in hypoproteinemia, albumin or plasma concentrate should be given first, then dehydration should be used as appropriate. Osmotherapy can cause heart failure or shock due to sudden drop in blood volume as a result of diuresis; it can cause electrolyte disorders; in a few cases, it can cause hematuria and hemolysis. In addition, repeated use of hypertonic dehydrating agents can produce systemic hyperosmolarity.
(4) Hypertonic saline is not yet popularly used in China. Hypertonic saline of 3% to 23,4% can also produce osmotic effect and bring water in the interstitial space of brain parenchyma into the vascular cavity through the blood-brain barrier to achieve the effect of reducing intracranial pressure. It is more beneficial for patients with intracranial hypertension with hypovolemia and hypotension. Side effects can cause hemorrhage, hypokalemia and hyperchloremic acidosis.
(5) Carbonic anhydrase inhibitors For chronic intracranial pressure increase, acetazolamide can be considered for oral treatment, but should be combined with sodium bicarbonate tablets for long-term application.
3.Cooling and antispasmodic: Patients with fever should be given antipyretic drugs or ice blankets to cool down the fever, and those with fever caused by infection should be treated with antibiotics reasonably selected according to the causative agent.
Hypothermia can reduce cerebral oxygen consumption, reduce cerebral blood flow, lower intracranial pressure and reduce cerebral edema. Therefore, effective hypothermia and antispasmodic (e.g., artificial hibernation) are also important. With the development of monitoring technology, the side effects of hypothermia on the heart are also decreasing. Systemic hypothermia is more effective than local head hypothermia in lowering brain temperature, and hypothermia has become one of the most important tools in the treatment of severe intracranial hypertension.
The method currently available for clinical use is local physical cooling of the head combined with artificial hibernation therapy, which can reduce cerebral blood flow and brain volume, not only to reduce high cranial pressure, but also to reduce the cerebral metabolic rate and increase the tolerance of brain tissue to hypoxia. Hibernation drugs are prone to induce hypotension when injected intravenously, and once a drop in blood pressure occurs, the drug should be stopped immediately, and if necessary, use antihypertensive drugs.
4, barbiturates anesthesia: only for patients with refractory intracranial hypertension, the possible mechanism of action is related to the reduction of cerebral blood flow and cerebral oxygen metabolism. In addition to lowering the cerebral metabolic rate and reducing brain volume, this class of drugs can also be used as free radical scavengers. Pentobarbital or sodium thiopental can be used clinically. The loading dose of pentobarbital is 3-10 mg/kg, and the maintenance dose is 1-4 mg/kg/h. It is advisable to monitor the intracranial pressure during the drug administration, and the drug should be gradually reduced when the situation improves. It should not be used in patients with cardiovascular disease. Side effects include hypotension, hypokalemia, respiratory complications, infection, abnormal liver and kidney function.
5, hormones: adrenocorticotropic hormone and dexamethasone also have the effect of reducing intracranial pressure, the former is more effective in vasogenic cerebral edema, but should not be used as a routine drug for the treatment of intracranial hypertension. Dexamethasone reduces intracranial pressure mainly by reducing the permeability of the blood-brain barrier, decreasing cerebrospinal fluid production, stabilizing lysosomal membranes, antioxidant free radicals and calcium channel blocking. The effect occurs 12-24h after intravenous injection and lasts for 3 d or more. In recent years, it is advocated to start applying shock dose, 0,5~1mg/kg/dose, intravenous injection every 6h, and after 2~4 times of improvement, it can be rapidly reduced to 0,1~0,5mg/kg/dose. It should be noted that the effect of hormones in lowering intracranial pressure is slower and weaker than that of hypertonic dehydrating agents, and hormones should be used with caution when the etiology of the primary infection is unknown or not easily controlled. The CRASH, a multicenter, randomized, controlled, large-scale clinical trial completed in 2005, enrolled tens of thousands of patients with TBI and showed that methylprednisolone treatment within 48 h after traumatic brain injury increased the risk of death (22.3%-25.7%), suggesting that patients with TBI should not be treated with hormonal agents. It is recommended that hormone therapy should not be routinely administered to patients with TBI. There is also no convincing evidence for the use of hormones to control cerebral edema in patients with acute cerebrovascular disease.
6. Application of sedative and analgesic drugs: Appropriate application of sedative and analgesic drugs is an important adjunct to the treatment of intracranial hypertension. Sedative drugs as a key factor in controlling intracranial pressure is often overlooked. Patients with decreased compensatory function of intracranial pressure can increase intracranial pressure by holding their breath, and anxiety and fear can increase intracranial pressure by increasing cerebral metabolic rate. Benzodiazepines can reduce cerebral oxygen metabolism and cerebral blood flow, but have little effect on intracranial pressure. Sedative drugs with minimal effect on blood pressure should be selected, and attention should also be paid to the correction of hypovolemia to prevent excessive lowering of blood pressure. Isoproterenol (propofol) is an ideal intravenous sedative, its short duration of action, does not affect the patient’s neurological examination, there are also anti-seizure, scavenging the role of free radicals.
7, appropriate control of blood pressure: quiet state, lowering blood pressure can cause a parallel decrease in intracranial pressure. If the cerebral perfusion pressure is lower than 150 mmHg and the intracranial pressure is greater than 280 mmH2O, short-acting antihypertensive drugs can be used to lower the cerebral perfusion pressure to 100 mmHg. Care should be taken not to lower the cerebral perfusion pressure below 50 mmHg and induce cerebrovascular reflex dilatation and increase in intracranial pressure. Sodium nitroprusside is contraindicated because it directly dilates the cerebral vasculature and increases intracranial pressure. Labetalol and nicardipine are beneficial in controlling blood pressure in patients with increased intracranial pressure. If the cerebral perfusion pressure is lower than 50 mmHg, vasopressors such as dopamine can be used to reduce intracranial pressure by reducing cerebral vasodilation and lowering cerebral blood volume.
8. Hyperventilation: rapidly lowering PCO2 to 25-30 mmHg can lower intracranial pressure within minutes. Increase the number of ventilation (16-20 times/min) with mechanical assisted respiration or non-intubated patients with emergency mask can achieve hyperventilation and cause respiratory alkalosis, which can reduce intracranial pressure by vasoconstriction and reduction of cerebral blood volume. After the intracranial pressure is stabilized, hyperventilation should be slowly stopped within 6~12h, and sudden termination may cause vasodilation and rebound increase of intracranial pressure. This method is not suitable for adult patients with respiratory distress syndrome and restrictive pulmonary ventilation.
9.Surgical treatment: CT or MRI should be done to determine the pathological volume of blood, cerebrospinal fluid and edematous tissue for acute intracranial pressure increase. Surgical treatment methods include removal of intracranial occupying lesions, cerebrospinal fluid drainage and cranial open flap decompression surgery. Ventricular drainage is important to restore normal circulation of cerebrospinal fluid. The simplest procedure is continuous ventricular drainage, which allows direct release of cerebrospinal fluid and shrinks the ventricles for the purpose of lowering cranial pressure. It is important to prevent infection and avoid blockage of the drainage tube. Ventricular drainage or cerebrospinal fluid shunt is an important tool to relieve severe intracranial hypertension. If brain herniation occurs, decompression can be performed as appropriate. It is important to make full use of decompression surgery with decranial flap, which is one of the best means to lower cranial pressure in case of failure of conservative medical treatment.
In conclusion, for the treatment of intracranial hypertension, pharmacological treatment should be considered first, supplemented by other treatments if necessary, and surgical treatment is only the last resort. The treatment of patients with acute intracranial hypertension should be individualized, the appropriate method should be chosen for different conditions, the course of treatment should not be too long, and attention should be paid to the toxicity and side effects of drugs. During the treatment of intracranial hypertension, it is advisable to keep the body in a mildly dehydrated state, and if the vital signs are stable and conscious, the dosage of dehydrating agents should be gradually reduced or discontinued. In addition to the use of dehydrating agents, attention should be paid to the systemic comprehensive treatment, especially the control of other complications or concomitant diseases. Plasma osmolality, plasma viscosity, hemoglobin content, hematocrit, etc. should also be monitored during dehydration agent treatment. If the osmolarity is too high, blood concentration and viscosity increase, it will aggravate ischemic brain injury, worsen the prognosis, and even induce damage to other important organ functions and produce multi-organ dysfunction, etc.