It is the elevation of the intracranial pressure due to the alteration of the mechanisms regulating the intracranial pressure.
Intracranial hypertension is caused by changes in brain parenchymal, cerebrospinal fluid, and cerebral blood volumes that exceed the compensation capabilities.
Increased intracranial hypertension may cause limiting conditions that induce secondary clinical alterations.
Intracranial hypertension can be classified according to the etiology, the pathogenic mechanisms, and the patterns of increased intracranial pressure in:
Parenchymal endocranial hypertension
A cerebral etiology is known mainly because it causes an alteration in the intracranial volume, and cerebral edema appears, evolving towards an increase in intracranial pressure.
In traumatic cerebral edema, parenchymal intracranial hypertension appears in expansive intracranial processes (tumors, bruises, brain abscesses, etc.). It is generally poisoning with other neuronal toxins (exogenous or endogenous).
The direct parenchymal injury occurs initially due to an intrinsic cerebral etiology and primary alterations in intracranial volume (expansive, compressive, hypoxic, or traumatic cerebral edema).
Often, cerebral edema is sectoral, and often, there are differences between the cerebrospinal compartments.
There is a very rapid or slow increase in intracranial pressure above 20 mm Hg, but the duration of time of pathological endocranial hypertension is short due to decompensation.
Parenchymal intracranial hypertension can evolve into the acute form with brainstem ischemia or cerebral herniation.
Vascular endocranial hypertension
The development of cerebral edema and increased intracranial pressure are determined by cerebral blood volume disorders (excluding the etiology of parenchymal endocranial hypertension).
Cerebral edema occurs due to ” cerebral congestion ” after increased cerebral blood volume, caused by a significant blood flow or a reduction or interruption in cerebral blood flow.
There is also a reduction in the absorption of cerebrospinal fluid involved in decreasing cerebral blood flow.
Vascular endocranial hypertension occurs in cases of:
- Vascular cerebral diseases include cerebral venous thrombosis, superior sagittal sinus thrombosis, and mastoiditis with transverse or sigmoid thrombosis (the “otic hydrocephalus”).
- Extracerebral diseases: hypertensive encephalopathies such as acute hypertensive encephalopathy in cases of malignant hypertension of any cause, in glomerulonephritis, eclampsia, etc.
Vascular etiologies can individualize the vascular types of endocranial hypertension:
- Cerebral venous thrombosis reduces venous flow and determines low cerebrospinal fluid drainage and cerebral edema.
- Hypertensive encephalopathies cause brain swelling, cerebral edema, and congestive brain swelling with elevated intracranial pressure.
- Ischemic strokes increase capillary permeability with an open blood-brain barrier, cerebral edema, and severe elevation in intracranial hypertension.
The causes of intracranial hypertension are classified as acute or chronic:
- Acute causes include brain trauma, ischemic injury, and intracerebral hemorrhage. Infections such as encephalitis or meningitis can also cause endocranial hypertension.
- Chronic causes include intracranial tumors, such as ependymomas, which can gradually affect the cerebrospinal fluid pathways and interfere with the outflow and circulation of the cerebrospinal fluid.
Chronic subdural hematomas can also cause endocranial hypertension.
Intracranial hemorrhage is the result of arterial bleeding directly into brain tissue.
Localized lesions occur at the source of the hemorrhage and can directly damage brain tissue and cause a global injury due to cerebral edema and elevations of intracranial pressure.
Intracerebral hemorrhage can also lead to obstructive hydrocephalus due to compression or occlusion of the cerebrospinal fluid pathways.
The brain tissue becomes distorted as the intracranial pressure increases, resulting in a hernia and additional vascular injury.
In severe cranioencephalic trauma, in addition to localized direct tissue damage and hemorrhage associated with the injury, edema in brain tissue usually occurs, resulting in increased intracranial pressure and brain injury.
Meningitis is an inflammation of the meninges. It can lead to localized or global cerebral ischemia, cerebral edema, and hydrocephalus due to the decrease in the resorption of the cranioencephalic fluid and the increase in its production.
These acute and chronic causes of intracranial hypertension can have devastating consequences if not managed aggressively.
Signs and symptoms
The importance of the onset of intracranial hypertension is not limited to the initial traumatic or hemorrhagic event.
The initial event causes physical distortion, nerve tissue damage, or increased pressure within a single compartment. Additional vascular and tissue damage may occur.
This phenomenon, known as secondary brain injury, occurs for hours or days after the initial brain injury.
The secondary lesion is progressive and often begins shortly after a brain injury.
The primary and secondary lesion can begin a “vicious circle,” leading to multiple progressive neuronal damage stages.
From the point of injury, disruption of cell membranes leads to loss of electrical stability and depolarization.
Through the effects of the inflammatory response, the generation of free radicals, and the damage mediated by calcium, the integrity of the membrane is further degraded, leading to an increase in tissue edema and elevation of intracranial pressure.
The initial brain injury plus secondary events result in a cumulative process that threatens life.
Finally, the physiological stability is altered, and there is damage to the compromising tissue, advancing the secondary injury cycle.
The resulting change in brain physiology can produce dramatic, potentially catastrophic elevations of intracranial pressure by more than 20 mm Hg.
If significant elevations in intracranial pressure are not treated aggressively, severe and permanent neurological deficits and even death will occur.
Intracranial hypertension may cause additional ischemic injury and highlights the need for early monitoring of intracranial pressure and optimal hemodynamic management to maintain adequate global cerebral perfusion.
Cerebral ischemia is an important secondary event after a brain injury. Cerebral ischemia can occur for two reasons:
- A cerebral blood flow is already compromised near massive lesions caused by the compression of localized blood vessels.
- The presence of vasospasm after a traumatic injury or subarachnoid hemorrhage.
The loss of self-regulation, the ability of the brain to maintain a constant cerebral blood flow despite variations in systemic blood pressure, can also occur after a traumatic brain injury.
The loss of self-regulation increases the risk of secondary brain injuries, such as cerebral ischemia and intracranial hypertension.
There is no consensus on the specific symptoms and signs when intracranial pressure increases. These depend on several factors such as:
- The cause that causes intracranial hypertension.
- The grade: acute, subacute, chronic.
- The volume, the elasticity, the adaptability, and the brain’s anatomy.
- The existence of other pathologies such as hypoxia or ischemia and other factors.
Symptoms such as headache, vomiting, and papilledema have been reported. Also, others like:
- The vertigos .
- The constipation
- The disorders in the function of the encephalon: the memory, the intellect, the will, the behavior, the emotions, among others.
- The convulsions.
- Signs of cerebral herniation.
- False signs of localization: paralysis of the sixth cranial nerve and psychic symptoms.
Patients who experience intracranial hypertension are among the most challenging in intensive care practice.
Rapid treatment onset to protect them from a devastating outcome depends on a thorough clinical evaluation.
It should be borne in mind that a late diagnosis leads to severe sequelae in patients; they can even cause death.
The initial evaluation of patients with possible neurological injury includes a physical examination and an imaging study such as a head CT scan.
This study provides vital information about the state of the brain before invasive monitoring begins.
Continuous monitoring of intracranial and cerebral perfusion pressure is a determining factor for clinical outcomes since it provides a practical guide in managing elevations of intracranial pressure and hemodynamic status.
Currently, the treatment of intracranial hypertension is cause-directed. The treatment is divided into:
- Position of the patient: this must be assessed in each patient individually.
- Mechanical Hyperventilation: guarantees a permeable airway with enough oxygen to achieve a correct diffusion.
- Osmotic diuretics: 3%, 5% or 7.5% Hypertonic saline solution.
- Fluid management: using osmotic diuretics for cerebrospinal fluid drainage through an intraventricular catheter (Ringer-Lactate, Saline Hypertonic Solution, and Dextran).
- Coticoesteroides: la Dexametazona, Alfametilprednisolona y Tirilazad.
- Barbiturates: Thiopental and Pentobarbital.
- Hypothermia: a decrease in body temperature below 30 degrees centigrade.
- Indomethacin: decreased cerebral blood flow associated with increased arteriovenous oxygen difference.
- Hyperbaric oxygen is based on the decrease of cerebral blood flow and the increase of tissue oxygenation.
Two fundamental techniques are known based on decreased cerebral blood flow and increased tissue oxygenation. These surgical measures are bone decompression and removal of brain tissue.
The treatment of intracranial hypertension has been modified since the introduction of neuromonitoring techniques. Using medications or other means is not allowed without being physiopathologically justified in each case.
In treating intracranial hypertension, intracranial pressure monitoring and waveform analysis allow the real-time evaluation of alterations in brain physiology, which facilitates rapid intervention and optimal results.
The Monroe-Kellie doctrine dictates that the three components of the skull (blood, brain tissue, and cerebrospinal fluid) interact for intracranial pressure stability and intracranial physiology.
Treating elevations in intracranial pressure selectively involves manipulating or decreasing the relative volume of one or more of these components.
Treatments for the elevation of intracranial pressure must do more than address the specific disorder in intracranial physiology, such as elevated cerebral blood flow, edema, or hydrocephalus; they must also adapt to specific physiological changes at any given time.
The interactions between the three components of the skull are a dynamic process. How the brain responds to injuries over time is similarly dynamic.
The need for vigilance in monitoring intracranial pressure and evaluating patients is further highlighted by the response of these to treatments.
The optimal evaluation of intracranial compliance is tremendously essential to obtaining favorable results.
Recognizing even subtle changes in intracranial compliance can have far-reaching implications for general management.
Changes in the level of consciousness are the most important measure of brain stability. Consciousness reflects physiological stability and coordination among multiple brain areas.
Consequently, any change in consciousness, cognition, or responsiveness level, even if it is subtle, can have great significance.
Decreases in the level of consciousness can be caused by brain compression due to hemorrhage, edema, hematoma formation, and expanding solid tumors.
The control of consciousness and excitement through the Glasgow coma scale is vital.
Among the monitoring treatments for the control of intracranial hypertension are currently the following:
Ventriculostomy or intraventricular catheter
Ventriculostomy is the most accurate, cost-effective, and reliable method to control intracranial pressure.
It is the standard for its measurement. The ventriculostomy catheter is part of a system that includes an external drainage system and a transducer.
The drainage system and the transducer are primed at the insert with preservative-free saline solution. The transducer can be easily calibrated or zeroed against a known pressure.
This calibration guarantees the consistency and accuracy of the pressure measurements obtained.
A ventriculostomy is often placed in the non-dominant lateral ventricle through a torsion hole in the skull.
An incision or puncture is made in the dura, and the catheter passes through the brain tissue to the ventricle.
Then, the catheter is usually placed under the scalp and sutured to the skin’s surface a few centimeters from the initial insertion site.
The advantages of using a permanent ventricular catheter include allowing the drainage of cerebrospinal fluid to effectively decrease intracranial pressure and using the catheter to instill medication.
Access to cerebrospinal fluid drainage allows serial laboratory tests and determination of volume-pressure ratios.
The disadvantages of ventriculostomy include the risk of infection, which is higher than that associated with other techniques of monitoring intracranial pressure.
In addition, the catheter can be occluded with blood or tissue debris, which interferes with cerebrospinal fluid drainage or intracranial pressure monitoring.
In addition, if there is significant cerebral edema, the location of the lateral ventricle for insertion of the ventriculostomy catheter may be difficult.
Finally, bleeding or ventricular collapse may occur if the cerebrospinal fluid drains too quickly.
The subarachnoid screw is inserted through a rotary drilling hole at the level of the subarachnoid space over the non-dominant cerebral hemisphere.
The dura is then opened, and the device (filled with preservative-free saline) is placed in contact with the subarachnoid space.
The pin is then secured to a pressure tube, and a transducer system is prepared with preservative-free saline solution.
This technique of monitoring intracranial pressure is more accessible to start than a ventriculostomy, which is an advantage.
It is unnecessary to locate the ventricles, which facilitates intracranial insertion and monitoring of intracranial pressure, even in massive or cerebral edema patients.
Because the brain tissue is not violated, the infection rate for the procedure is lower than the rates of other intracranial pressure monitoring methods that penetrate brain tissue.
The disadvantages of a subarachnoid screw include the following:
The screw can be occluded by debris, blood clots, or brain tissue in the device.
This blockage can dampen the intracranial pressure waveform and make inaccurate pressure measurements.
As with any invasive monitoring technique, cerebrospinal fluid leakage and infection may still occur.
Finally, bleeding and intracranial hematoma formation may occur, possibly causing more brain damage.
Subdural or epidural catheter
A subdural or epidural catheter with a fiber optic transducer tip is placed through a small hole drilled through the skull.
This monitoring technique does not require the penetration of brain tissue, and the risk of infection is lower than that associated with other intracranial pressure monitoring techniques that penetrate brain tissue.
The insertion of the catheter and the start of monitoring are also more straightforward, and it is not necessary to calibrate the system.
The disadvantages of this technique are multiple. First, access to the cerebrospinal fluid is not possible.
Second, a wedge effect can be caused by the pressure between the tip of the catheter and the adjacent dura mater. This effect may compromise the accuracy of intracranial pressure measurements and the quality of the waveform.
Third, volume-pressure relationships can not be determined to indicate intracranial compliance.
Finally, the waveforms of intracranial pressure may be of poor quality, limiting the amount of helpful information obtained with this monitoring technique.
Because epidural or subdural monitoring tends to be less accurate than other monitoring techniques, it is used much less frequently.
Intraparenchymal sensors are typically placed through a small torsion hole and passed through a pin device in contact with the subarachnoid space.
The fiber optic transducer tip catheter is placed through the screw into the brain tissue.
This intracranial pressure monitoring device is easy to insert and maintains excellent waveforms even in patients with cerebral edema.
One advantage of using this technique is the minimal risk of tissue hernia and the precision of intracranial pressure measurements despite variations in head positioning.
Because the positioning of the head has a minimal influence on the accuracy of the measurements of intracranial pressure, its monitoring can also be maintained during the transport of patients.
Disadvantages of this technique include lack of access to cerebrospinal fluid for drainage or laboratory tests and the inability to assess intracranial compliance by determining volume-pressure relationships.