intracranial hypertension
Intracranial hypertension – increased intracranial pressure. Characterized 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 blurred vision, the appearance of congestive optic disc (the study of the fundus). In cases of severe increased intracranial pressure increased systolic blood pressure, there is bradycardia (50 – 60 beats / min). Key causes of intracranial hypertension – large lesions (tumor, hematoma), hydrocephalus, and stroke, meningitis, encephalitis, disruption of water and electrolyte balance (hyponatremia), brain injury, eclampsia, acute hypertensive encephalopathy and other diseases that trigger brain edema. Increased intracranial pressure can also result from congestive heart failure, chronic obstructive pulmonary disease, hypercapnia, violations of the outflow of jugular veins, pericardial effusion. The normal pressure of the cerebrospinal fluid in man, which is located in the supine position on the side, is 100-180 mm of water column.
Risk of intracranial hypertension is probably compressing the substance of the brain in the skull of a confined space, which leads to diffuse cerebral ischemia, as well as penetration – the displacement of brain tissue from one department to another cranial due to focal increased intracranial pressure. Penetration often occurs in the cutting gallop (tentorium) of the cerebellum (transtentorialnoe wedging) or foramen magnum. Wedging quickly leads to death due to compression of the brain stem and located in its vital centers.
The penetration of the hook of the temporal lobe occurs in the presence of a large formation in the middle cranial fossa. Early sign – extension of the pupil on the side of his injury with loss of response to light. Later on the affected side or opposite side of hemiparesis developed. With increasing intracranial pressure, there are signs of bilateral brain stem dysfunction – sopor, then coma, the expansion of another pupil, rhythm disturbances of breathing, decerebrate posture (arms straightened and rotated inward, legs extended).
Central transtentorialnoe penetration is defined by diffuse cerebral edema, acute hydrocephalus or median space-occupying lesions. Early effects – drowsiness and torpor, frequent deep breaths, yawning, pupillary constriction, the recovery of tendon reflexes, bilateral Babinski. Then the pupils dilate, with pain, excitation nonparalysed limbs appears dekortikatsionnaya posture (arms bent at the elbows, feet – stretch), which is then followed by decerebrate, disrupted the rhythm of breathing.
For large entities, lying in the posterior fossa, may be infiltration of its structures in cutting gallop cerebellum (bottom up) or in the foramen magnum (from top to bottom).
For the prevention of increased intracranial pressure in acute traumatic brain injury you must: 1) restore the airway, ensure full oxygenation, prevent and treat pulmonary complications in time, and 2) raise the head of the bed by 15 – 30 ° to the weakening of the venous outflow from the cranial cavity, and 3) restrict fluid intake to 1.5 L / day, 4) not to introduce solutions that have a lot of “free water” (eg, 5% glucose solution), 5) to maintain water and electrolyte balance and acid-base balance, 6) in a timely manner to arrest arterial hypertension, hyperthermia, seizures, psychomotor agitation, and 7) as far as possible avoid the use of vasodilators.
