HYPERTENSION INSIDE

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HYPERTENSION Intracranial - increased intracranial pressure. It is manifested by headache, nausea, vomiting, persistent hiccups, drowsiness, oppression of consciousness, doubling (due to unilateral or bilateral compression of the abduction nerve), transient episodes of visual impairment, the appearance of congestive optic discs (in the study of the fundus). In cases of marked increase in intracranial pressure (ICP) systolic blood pressure increases, bradycardia occurs (50-60 beats per minute).

The main causes of intracranial hypertension are volumetric lesions (tumor, hematoma), hydrocephalus , as well as stroke , meningitis , encephalitis, water-electrolyte imbalance (hyponatremia), craniocerebral trauma , eclampsia , acute hypertensive encephalopathy and other diseases that cause cerebral edema. The increase in ICP can also be a consequence of congestive heart failure, chronic obstructive pulmonary disease, hypercapnia, violation of outflow in the jugular veins, pericardial effusion. Normally, the pressure of the cerebrospinal fluid (CSF) in a person lying in the lying position on the side is 100-180 mm of water column.

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

The wedge of the temporal lobe hook occurs when there is a volume formation in the middle cranial fossa. The earliest sign is the dilatation 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 the ICP increases, there are signs of bilateral dysfunction of the brainstem - sopor, then coma , enlargement of the other pupil, disturbances in the rhythm of breathing, decerebral pose (arms uncurled and rotated inward, legs extended).

Central transcendental wedging is due to diffuse edema of the brain, acute hydrocephalus or middle volume formations. Early signs - drowsiness and stunning, frequent deep breaths, yawning, narrowing of pupils, revitalization of tendon reflexes, bilateral Babinsky reflex. Then the pupils dilate, with pain, irritation in the non-paralyzed limbs, a decortication posture appears (arms bent at the elbow joints, legs stretched out), which then changes into a decerebral one, the rhythm of breathing is disrupted.

With volumetric formations located in the posterior cranial fossa, the structure of the cerebellum can be wedged into the incision (from the bottom upwards) or into the large occipital foramen (from top to bottom).

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

For rapid reduction of ICP are shown;

1) osmotic diuretics (mannitol 0.25-1 g / kg intravenously for 10-15 minutes, then in the same dose every 6 hours, or glycerol 30 ml each in a mixture with fruit juice or 250 ml of 10% solution Intravenously for 1-2 hours, then repeatedly every 6 hours for 24-48 hours). The effect of mannitol begins in 10-20 minutes and lasts 4-6 hours. As a result of the increase in the volume of circulating blood, cardiac insufficiency and pulmonary edema may increase, and after stimulation of diuresis, dehydration and hypokalemia occur. Due to the violation of the blood-brain barrier, the drug can accumulate in the brain tissue, which causes a rapid increase in brain edema after its removal. The effectiveness of glycerol is lower, it acts more slowly, but the effect lasts longer;

2)

Loop diuretics - furosemide (lasix) for 20-40 mg intravenously or intramuscularly 3 times a day; Application in Combination with osmotic diuretics;

3)

Corticosteroids are shown mainly in brain tumors, but are ineffective in cases of craniocerebral trauma, stroke. Usually, prescribe dexamethasone at a dose of 8-12 mg intravenously, then 4 mg intravenously or intramuscularly 3 to 4 times a day. The effect manifests itself after about 12 to 24 hours. Simultaneously, antacid agents or blockers of H2 receptors (ranitidine) should be used to protect the gastric mucosa;

4)

In critical situations with the threat of wedging in an intensive care unit, ventilatory ventilation is used in the regime of hyperventilation, the use of barbiturates, and puncture of the ventricles. The method of long-term monitoring of ICP is developed, which allows more effective treatment of patients with severe head injury and stroke.

Benign intracranial hypertension (pseudotumour of the brain) occurs mainly in obese women aged 20 to 45 years. In many of them, a significant increase in body weight occurred not long before the onset of the disease. Provocative factors may also be drugs (oral contraceptives, estrogens and progesterones, thyroxine, tetracyclines, nalidixic acid , nitrofurans, ampicillin , ketamine, amiodarone , phenothiazines), pregnancy , hyperparathyroidism, hypervitaminosis or hypovitaminosis A, and the abolition of corticosteroids, etc. The complaint is a headache , which can be diffuse, bursting or more local (usually retroorbital). The pain increases with tilting, coughing, sneezing. Often there are double vision and episodes of transient blurring of vision, usually when the posture changes. The restriction of movement of one or both eyeballs to the outside due to dysfunction of the abducent nerve is revealed, stagnant discs of the optic nerves are found. As a result of compression of the optic nerves, irreversible loss of vision is possible.

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