This page has been robot translated, sorry for typos if any. Original content here.

Intracranial hypertension


Intracranial hypertension - increased intracranial pressure. It manifests itself as 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 nerves (during fundus examination). In cases of a marked increase in intracranial pressure (ICP), systolic blood pressure 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 , disturbance of water-electrolyte balance (hyponatremia), traumatic brain injury , eclampsia , acute hypertensive encephalopathy and other diseases that cause cerebral edema. An increase in ICP can also be a consequence of congestive heart failure, chronic obstructive pulmonary disease, hypercapnia, impaired outflow through the jugular veins, and pericardial effusion. Normally, the pressure of the cerebrospinal fluid (cerebrospinal fluid) in a person who is lying on his side is 100-180 mm of water.

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 ischemia of the brain, as well as wedging - displacement of brain tissue from one cranial compartment to another due to focal increase in ICP. The wedging often occurs in the notch (tentorium) of the cerebellum (transtentorial wedge) or a large occipital fissure. The wedge quickly leads to death due to compression of the brain stem and vital centers located in it.

Wedge hook of the temporal lobe occurs in the presence of volumetric formation in the middle cranial fossa. An early sign is the expansion of the pupil on the affected side with the loss of its reaction to light. Later, hemiparesis develops on the affected side or the opposite side. As ICP increases, signs of bilateral dysfunction of the brain stem appear - stupor, then coma , expansion of the other pupil, respiratory rhythm disturbance, decerebral posture (arms are extended and rotated inward, legs are extended).

Central transtentorial wedging is caused by diffuse cerebral edema, acute hydrocephalus, or median volume formations. Early signs are drowsiness and stunning, frequent deep breaths, yawning, narrowing of the pupils, revitalization of tendon reflexes, a two-way Babinsky reflex. Then the pupils dilate, with pain, irritation in unpaired limbs, a decortication posture appears (hands are bent at the elbow joints, legs are extended), which is then replaced by a decerebration, breathing rhythm is disturbed.

With volume formations located in the posterior cranial fossa, its structures can wedge into the notch of the cerebellum (from bottom to top) or into the large occipital foramen (from top to bottom).

To prevent an increase in ICP in acute brain injuries, it is necessary: ​​1) to restore airway patency, ensure sufficient oxygenation, prevent and treat pulmonary complications in a timely manner; 2) 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) do not introduce solutions containing a lot of "free water" (for example, 5% glucose solution); 5) maintain water-electrolyte balance and acid-base balance; 6) timely stop arterial hypertension, hyperthermia, epileptic seizures, psychomotor agitation; 7) if possible, avoid the use of vasodilators.

To quickly reduce the ICP are shown;

1) osmotic diuretics (mannitol 0.25 - 1 g / kg intravenously, percutaneous 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 10% solution intravenously for 1-2 hours, then again every 6 hours for 24-48 hours). The action of mannitol begins in 10-20 minutes and lasts 4-6 hours. Due to the increase in the volume of circulating blood, heart failure and pulmonary edema may be increased, and after diuresis stimulation, dehydration and hypokalemia are possible. Due to a violation of the blood-brain barrier, the drug can accumulate in the brain tissue, which causes a rapid increase in cerebral edema after its cancellation. 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 combination with osmotic diuretics;


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


in critical situations, with the threat of wedging in the intensive care unit, they resort to mechanical ventilation in hyperventilation, the use of barbiturates, and ventricular puncture. A method for long-term monitoring of ICP has been developed, which allows more effective treatment of patients with severe traumatic brain injury and stroke.

Benign intracranial hypertension (pseudotumor of the brain) occurs mainly in obese women aged 20 to 45 years. In many of them, a significant increase in body weight occurred shortly before the onset of the disease. Drugs (oral contraceptives, estrogens and progesterones, thyroxine, tetracyclines, nalidixic acid , nitrofurans, ampicillin , ketamine, amiodarone , phenothiazines), pregnancy , hyperparathyroidism, hypervitaminosis and hypovitaminosis A, as well as coreosteroids can also be provoking factors. complaint is a headache that may be diffuse, bursting, or more local (usually retroorbital). The pain intensifies with bending, coughing, sneezing. Often there are double vision and episodes of transient blurred vision, usually with a change in posture. There is a restriction of the movement of one or both eyeballs outward due to dysfunction of the abducent nerve, and congestive disks 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 resort to a course of treatment with corticosteroids in small doses. It is important to regularly monitor visual acuity and field of view. With a rapid decrease in vision, methylprednisolone is administered (500-1000 mg intravenously in 200 ml of isotonic sodium chloride solution) and the patient is referred to an ophthalmologist to consider surgical intervention (optic decompression).