Intracranial hypertension/PGS
Intracranial hypertension
Intracranial hypertension syndrome is a life-threatening condition. Intracranial hypertension is the main mechanism of secondary cerebral damage. The intracranial space is a tightly bounded and closed compartment by the calva, which consists of brain tissue (80%), the cerebrospinal fluid compartment (10%) and the filling of blood vessels (10%). This content remains constant and any change in one of these compartments must be associated with a compensatory change in another. Compensation mechanisms are limited. Processes that increase intracranial pressure are referred to as 'expansive intracranial processes. English abbreviation intracranial SOL (space-occupying lesion).
Clinical symptoms of intracranial hypertension syndrome:
- headache - often worse lying down (especially in the morning after waking up) and when using an abdominal press, unresponsive to common analgesics
- pain behind the eyes or when moving the bulbs
- vomiting - sudden, sometimes without nausea (projectile vomiting)
- vertigo states
- visual problems - blurred vision, diplopia, loss of vision
- focal symptoms according to the location of the pathology
- meningeal symptoms
- rise in blood pressure and slowing of heart rate
- disorder of consciousness (quantitative or qualitative)
As the condition progresses, the compensatory mechanisms are exhausted, the brain is pushed into the physiological openings and 'cone symptoms appear. Cerebral cones (herniations) have typical locations due to their anatomical arrangement.
Brain herniation
Brain herniation/PGS/diagnosis
Examination for suspected intracranial hypertension
- CT brain event. MRI of the brain' - sovereign method; changes in the size of the ventricular system, disappearance of subarachnoid spaces, displacement of midline structures, focal expansion.
- Ocular fundus examination - congestive papilla event. even with hemorrhages on the eye background.
- EEG - non-specific diffuse abnormalities (mostly slowing of activity).
The most common causes of intracranial hypertension syndrome
- intracranial tumors − primary, metastatic
- hematomas - spontaneous or traumatic
- extensive ischemia
- hydrocephalus - non-communicating, communicating (normotensive hydrocephalus - clinically Hakim's triad: spastic walking disorder, urinary incontinence, organic psychosyndrome)
- pseudotumor cerebri
- diffuse brain edema various etiologies − CNS inflammation, toxic, drug-induced, hypoxic, hypoosmolar, metabolic − metabolic ketoacidosis, hepatic encephalopathy, uremia
- brain abscess
- brain trauma
Treatment
In addition to targeted therapy, a mandatory part of the treatment of a patient with intracranial hypertension is monitoring and control of heart rate, BP, respiration, SpO< sub>2, ECG, temperatures and central venous pressure, it is also appropriate to monitor ' "Intracranial pressure" (ICP sensors, ultrasound) - within the general intensive care of patients.
The main strategy of targeted treatment is the effort to suppress especially the vasogenic component of brain edema by short-term increasing blood osmolality and creating an osmotic gradient between the vascular compartment and the interstitium (mannitol and other osmotically active substances) , in indicated cases corticoid treatment'', mandatory hyperventilation, neuroprotective barbiturate coma or neurosurgery - see diagram. It is also important to prevent the development of secondary cerebral damage as a result of tissue hypoperfusion (hypoxia), i.e. the effort to maintain sufficient brain perfusion.
