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DOMESTIC HYPERTENSION - increased intracranial pressure. It is manifested by headache, nausea, vomiting, persistent hiccups, drowsiness, depression of consciousness, double vision (due to unilateral or bilateral compression of the abducent nerve), transient episodes of visual impairment, the appearance of congestive optic discs (in the study of the fundus of the eye). In cases of marked increase in intracranial pressure (ICP), systolic BP increases, bradycardia appears (50–60 beats / min).

The main causes of intracranial hypertension are volume lesions (tumor, hematoma), hydrocephalus , as well as stroke , meningitis , encephalitis , impaired water-electrolyte balance (hyponatremia), traumatic brain injury , eclampsia , acute hypertensive encephalopathy, and other diseases that cause the brain. Increased ICP may also be due to congestive heart failure, chronic obstructive pulmonary disease, hypercapnia, impaired outflow disturbances in the jugular veins, pericardial effusion. Normally, the pressure of cerebrospinal fluid (cerebrospinal fluid) in a person who is lying on the side is 100-180 mm of water column.

The danger of intracranial hypertension is the possibility of compression of the brain substance in a limited space of the skull, which leads to diffuse brain ischemia, as well as penetration - displacement of brain tissue from one cranial compartment to another due to a focal increase in ICP. Occlusion often occurs in the cutout of the tentorium of the cerebellum (transientory insertion) or the large occipital foramen. A wedge in quickly leads to a lethal outcome due to compression of the brainstem and vital centers in it.

The hooking of the hook of the temporal lobe occurs in the presence of volume formation in the middle cranial fossa. An early sign is the expansion of the pupil on the side of the lesion with the loss of its reaction to light. Later on the side of the lesion or the opposite side, hemiparesis develops. As ICP increases, there are signs of bilateral brain stem dysfunction - stupor, then coma , expansion of another pupil, respiratory rhythm disturbances, decerebration posture (arms outstretched and rotated inwards, legs extended).

The central transtentorial inclination is due to diffuse cerebral edema, acute hydrocephalus or mid-mass lesions. Early signs are drowsiness and stunning, frequent deep breaths, yawning, constriction of the pupils, revitalization of tendon reflexes, Babinsky bilateral reflex. Then the pupils dilate, with pain, irritation in the non-paralyzed limbs, a decortication pose appears (arms bent at the elbows, legs extended), which is then replaced by decerebration, the breathing rhythm is disturbed.

In the case of volume lesions located in the posterior cranial fossa, its structures may be wedged into the necklace of the cerebellum (from bottom to top) or into the large occipital opening (from top to bottom).

To prevent an increase in ICP in acute brain damage, it is necessary: ​​1) to restore the airway, to ensure adequate oxygenation, to prevent and to treat pulmonary complications in a timely manner; 2) to raise the head of the bed by 15 - 30 ° to facilitate venous outflow from the cranial cavity; 3) limit fluid intake to 1.5 l / day; 4) not to introduce solutions containing a lot of "free water" (for example, 5% glucose solution); 5) maintain water-electrolyte balance and acid-base balance; 6) to stop arterial hypertension, hyperthermia, epileptic seizures, psychomotor agitation in a timely manner; 7) to the extent possible avoid the use of vasodilators.

For a quick reduction in ICP shown;

1) osmotic diuretics (mannitol at 0.25 - 1 g / kg intravenously as a whole for 10 - 15 minutes, then at the same dose every 6 hours, or glycerol, 30 ml orally mixed with fruit juice or 250 ml of a 10% solution intravenously for 1-2 hours, then again every 6 hours for 24-48 hours). The effect of mannitol begins after 10–20 minutes and lasts 4–6 hours. Due to an increase in circulating blood volume, heart failure and pulmonary edema are possible, and after stimulation of diuresis - dehydration and hypokalemia. Due to a violation of the blood-brain barrier, the drug can accumulate in the brain tissue, which causes a rapid increase in swelling of the brain after it is canceled. The effectiveness of glycerol is lower, it acts more slowly, but the effect lasts longer;


loop diuretics - furosemide (lasix) 20-40 mg intravenously or intramuscularly 3 times a day; possible application in combinations with osmotic diuretics;


Corticosteroids are indicated mainly for brain tumors, but are ineffective in cases of traumatic brain injury or stroke. Dexamethasone is usually prescribed in a dose of 8-12 mg intravenously, then 4 mg intravenously or intramuscularly 3 to 4 times a day. The effect appears after about 12 to 24 hours. At the same time, antacid agents or H2-receptor blockers (ranitidine) should be used to protect the gastric mucosa;


in critical situations with the risk of penetration in the conditions of the intensive care unit, artificial ventilation is used in the hyperventilation mode, the use of barbiturates, and ventricular puncture. A method of long-term monitoring of ICP has been developed, which makes it possible to more effectively treat patients with severe traumatic brain injury and stroke.

Benign intracranial hypertension (brain pseudotumor) occurs mainly in obese women aged 20 to 45 years. Many of them have a significant increase in body weight shortly before the onset of the disease. Aggravating factors may also be drugs (oral contraceptives, estrogen and progesterone, thyroxine, tetracyclines, nalidixic acid, nitrofurans, ampicillin, ketamine, amiodarone, phenothiazines), pregnancy , hyperparathyroidism, hypervitaminosis A or Vitamin A deficiency, as well as cancellation of corticosteroids and others. Summary A complaint is a headache that may be diffuse, arching, or more local (usually retroorbital). The pain is aggravated by stooping, coughing, sneezing. Doubling and episodes of transient blurring of vision are often noted, usually with a change in posture. A limitation of movement of one or both eyeballs outwards due to dysfunction of the abducent nerve is detected, congestive discs of the optic nerves are detected. As a result of compression of the optic nerves, irreversible loss of vision is possible.

The main goal of treatment is to prevent irreversible damage to the optic nerve. It includes weight loss, taking diacarb or other diuretics, repeated lumbar punctures. Sometimes resorted to treatment with corticosteroids in small doses. It is important to regularly monitor visual acuity and visual field. With a rapid decrease in vision, methylprednisolone is injected (500-1000 mg intravenously drip per 200 ml of isotonic sodium chloride solution) and refer the patient to an ophthalmologist to consider the issue of surgical intervention (decompression of the optic nerve).