Hypertensive (hypertensive) encephalopathy (GE) is a violation of the brain activity against the background of malignant hypertension. According to ICD-10, acute hypertensive encephalopathy is encrypted as I67.4. The term was introduced in 1928 by Oppenheimer in collaboration with Fischberg to describe this particular form of encephalopathy. Although a similar condition can occur with various diseases (with eclampsia, a sudden increase in pressure, existing hypertension, acute nephritis, adrenal tumors, etc.), the greatest danger comes from a hypertensive crisis. It causes acute symptoms with cognitive impairment and tissue necrosis.
How does hypertension affect brain cells?
Even a single jump in pressure for the brain does not pass without a trace. Regulation of the tone of venules and arterioles is impaired. The target is not only the brain, but also the heart and kidneys. With a slight increased pressure, protective spasm of small vessels is first started. This organism does in order to prevent their rupture and pressure.
If the pressure remains elevated for a long time, the muscle layer of the vessels begins to hypertrophy. The result is a narrowing of the lumen of the vessel and a decrease in blood perfusion. There is a varying degree of hypoxia. The brain is most sensitive to hypoxia. Which causes neurological symptoms.
Thus, with HE of any form, the hemodynamics of the brain are disturbed, and brain tissue lesions up to necrosis occur. All this goes against a background of prolonged hypertension, which is poorly controlled.
Acute hypertensive encephalopathy according to the ICD is highlighted as a separate type of encephalopathy that occurs with symptomatic hypertension. Primarily small vessels are affected at first, but pathology quickly begins to be combined with the involvement of other calibers. This form usually manifests itself against the background of a hypertensive crisis. According to ICD-10, acute hypertensive encephalopathy has the following code - I67.4. In this case, the level of pressure may vary in hypo- and hypertensive patients.
For hypertensive patients, dangerous numbers range from 180-190 mmHg. Art., and in hypotensive patients - within 140/90. In any case, we are talking about raising the norm.
Specialists call this condition of hypertensive encephalopathy a peculiar manifestation of hypertensive crisis. A more common chronic form of pathology.
GE in acute form
Acute GE is an emergency condition and immediate help is required. Otherwise, complications in the form of cerebral edema, hemorrhagic stroke, heart attack, and fatal outcome are required.
Acute hypertensive encephalopathy according to ICD-10 has the code I67.4. Discirculatory vascular hypertensive encephalopathy is considered a separate manifestation. It is possible at any age.
Pathology occurs against the background of hypertension - crises. Aggravation against their background in the form of GE is such a chain. Her progression is faster than that of other forms of discirculatory encephalopathy.
The diagnosis of “discirculatory hypertonic encephalopathy” is made in case of chronic damage to brain tissue due to insufficient supply of blood. Its development is gradual and progressive. It is accompanied by morphological changes in brain tissue, impaired functionality and can cause dementia, disability and disability.
Causes of the problem
The leading cause of EH (hypertensive encephalopathy according to the ICD is encrypted I67.4) is the advanced form of hypertension. In this case, it can be primary and secondary, that is, against the background of other diseases accompanied by pressure surges: kidney damage (chronic pyelonephritis, glomerulonephritis, hydronephrosis), hyperthyroidism.
An important point is the pathology of the adrenal gland and pituitary gland - pheochromocytoma, excessive function of the adrenal cortex or in the glomerular zone - aldosterone, aortic atherosclerosis.
Uncontrollable hypertension is dangerous for hypertensive patients, changes are especially rapid when refusing hypotensive drugs. Repeated crises of hypertension, in which the vessels quickly wear out and thin. Their permeability increases and there is a quick hemorrhagic impregnation of brain tissue. Differences aimed at normalizing pressure, hypotension with a slowdown in blood flow also behave. Nighttime hypertension often has a hidden character.
High pulse pressure is another important factor. If the difference between the upper and lower pressures exceeds 40 mm RT. Art. - the course of vascular disease is exacerbated. Such pressure constantly affects the vascular wall and puts a strain on the muscle apparatus of the vascular wall.
Risk factors
Risk factors include:
- Deviations in the functioning of blood vessels and the heart, which are not diagnosed on time.
- Diseases of the kidneys (congenital or acquired) and the brain.
- An unstable state of blood vessels. Overstrain of any type - physical and mental.
- Incorrect or irregular treatment of hypertension.
- Eating disorders and lack of exercise, bad habits.
Hypertensive encephalopathy (hypertensive encephalopathy according to ICD-10 code I67.4) can also provoke:
- obesity, old age, diabetes;
- refusal or transition to another antihypertensive drug without consulting a doctor;
- eclampsia with edema, high blood pressure and proteinuria;
- adrenal tumors;
- hobby for some drugs - steroids, caffeine, sports doping;
- stresses against the background of existing problems with blood vessels;
- poor ecology can also do poor service to vessels;
- systematic hypothermia of the body.
Under certain conditions, the diagnosis of hypertensive encephalopathy (ICD code I67.4) can be made to any person.
Pathogenesis
With a deficiency of the delivered food to the vessels in their walls, changes occur in the form of a decrease in their tone. Next is a thickening of the muscles of the walls of the vessels and their lumen is narrowed. Hypoxia is aggravated. This, in turn, worsens the condition of nerve fibers.
Cramping of cerebral arterioles leads to hypoxia and nutritional deficiency for brain cells; chronic cerebral ischemia develops. Next, degenerative changes in cerebral structures occur. If there is atherosclerosis, it only exacerbates the situation.
White brain matter is affected earlier than others, lacunar infarcts develop here and demyelination of nerve fibers occurs.
These changes are diffuse and affect both hemispheres symmetrically. Lesions first occur along the ventricles, then they expand their space - spread periventricularly.
An excessive spasm of small arterioles passing into the capillaries acquires direct importance in the development of OGE, their permeability increases and paralysis and acute form of HE can develop.
Acute form
Hypertensive crisis with blood pressure above 180-190 mm RT. Art. causes, as a rule, serious changes in the tissues of blood vessels. What kind? When there are obstacles to their movement, namely: a narrowed lumen of a vessel or plaque on the walls, the blood reacts to this with the appearance of hemorrhages along the walls of the vessels. The tone of the veins of the soft meninges changes and intracranial pressure rises. It causes the appearance of neurological symptoms. Acute hypertensive encephalopathy - a consequence of hypertensive crisis; but she also becomes a harbinger of strokes with the subsequent development of disability and death. 16% of complications of the crisis are occupied by OGE.
Symptomatology
The clinic of acute hypertensive encephalopathy includes:
- Bursting intolerable headaches.
- First they are localized in the back of the head, then they become spilled, i.e. are growing.
- Analgesics do not relieve pain. Often this is accompanied by nausea and vomiting without relief. Acute hypertensive encephalopathy occurs most often at the time of the course of a hypertensive crisis.
- Vision suddenly deteriorates due to swelling of the optic disc, dark flies and spots appear in front of the eyes.
- Severe dizziness. With coughing and sneezing and other tension in the neck muscles, the condition becomes even worse.
- Hearing worsens - ringing and tinnitus appear.
- Convulsions and meningeal symptoms occur without inflammatory changes (meningism).
- The threshold of surface sensitivity rises.
In general, these are symptoms of a hypertensive crisis, but involving brain dysfunction. In the absence of proper treatment, mass death of neurons and the appearance of new ischemic foci occur.
The main symptoms of the clinic of acute hypertensive encephalopathy also include:
- the state of stunning, which is preceded by excitement, passing into paresis;
- slow heartbeat;
- numbness of the tip of the tongue, fingers, orientation in space is broken;
- gait becomes shaky.
Body temperature may increase. An attack can take several hours or last up to 2 days. Further, hemorrhagic stroke develops, cerebral edema and a fatal outcome with failure to provide assistance are guaranteed.
Acute hypertonic encephalopathy thus occupies an intermediate position between crisis and strokes.
The determining factor is the pressure figures: during an attack it is up to 250-300, the lower one - up to 130-170. But the vessels are dilated. They no longer narrow, and their permeability increases. In the tissues of the brain, blood flow is disturbed, with a deficiency of plasma, protein, oxygen, its edema is developing. Small foci of necrosis develop.
Acute hypertonic encephalopathy is also one of the early signs of a stroke, so first of all, the patient should be at rest and call an ambulance.
Diagnostics
The diagnostic algorithm includes:
- Mandatory examination by a neurologist. In the initial stage, the status may not be violated, but anisoreflexia occurs earlier than others. Special cognitive testing identifies mnestic, practical, and gnostic disorders of varying degrees.
- A consultation with a cardiologist will identify and confirm the presence of hypertension.
- Mental status is assessed by a psychiatrist through conversation, observation and testing.
- Diagnosis may be difficult due to the similarity of symptoms of cerebral catastrophes, therefore, CT and MRI of the brain vessels should be performed. In this case, focal changes - cerebral edema - are revealed in the brain. It also makes it possible to identify diffuse degenerative changes, foci of transferred lacunar infarcts in patients with stage II-III HE, and to exclude other organic brain pathologies. The picture of a blood test is uninformative, but the presence of hypercholesterolemia is important.
- At the consultation of an ophthalmologist - swelling of the optic discs. There is an increase in pressure inside the cranium.
- EEG - disorganization of the basic rhythms, especially in the occipital region. ECG - left ventricular wall hypertrophy, dystrophic changes in the myocardium.
- The study of cerebral hemodynamics: ultrasound of the cervical and cranial vessels. In this study, the degree of narrowing of the arterioles, their localization and prevalence are revealed.
Complications
OGE - an urgent condition, which in the absence of treatment leads to:
- coma;
- cerebral infarction;
- a stroke;
- THEM;
- cerebral edema,
- intracranial bleeding and death.
Treatment
The patient is subject to mandatory hospitalization in the intensive care unit and the observation of a whole team of doctors: resuscitator, neurologist, neurosurgeon, ophthalmologist, etc.
Diagnosed OGE requires the use of drugs of prolonged action.
Mandatory is the appointment of diuretics that relieve cerebral tissue edema - "Furosemide", ethacrylic acid, "Lasix" and others. Also important is the control of blood electrolytes to prevent total brain ischemia.
It is impossible to quickly reduce the available pressure, the process should be gradual. During the first hour, the decrease should not exceed 20% for systolic, and 15% for diastolic, and in the next 24 hours, the pressure should already be optimal for this subject. Diastolic pressure should not fall below 90 mm Hg.
With a strong sharp imbalance of cerebral blood flow, a decrease in systolic pressure should be even slower: the upper one is not more than 15%, the lower one - 10% of the usual level.
To accelerate the initial decrease in blood pressure, sodium nitroprusside (0.3-0.5 μg / kg per 1 min.) Is administered intravenously - it allows you to control the decrease in blood pressure.
Also, the main action drugs ("Clonidine" and "Clonidine") are used intravenously in the form of a dropper on saline or in a jet of 1-2 ml.
The hypotensive agent Hypostat gives good results, it normalizes blood pressure within a few minutes.
Further, it is possible to switch to tablets - adrenergic blockers, calcium ion antagonists (Nifedipine - improve cerebral blood flow), ACE inhibitors (Enalapril, Captopril - optimize vascular tone), diuretics, and other drugs.
To prevent new edema and reduce existing prescribe "Prednisolone", "Dexamethasone."
In the treatment of acute hypertensive encephalopathy in the presence of convulsive syndrome, "Relanium" is prescribed.
A soothing and sedative effect will be provided by Magnesia and Eufillin. In view of the violation of lipid oxidation processes, antioxidants are prescribed:
- droppers with Mexidol 400 mg;
- "Ceraxon" at 1000 mg;
- "Cytoflavin" 10 ml intravenously.
It is very good to combine them with activators of gluconeogenesis: Mildronate 10-20 ml intravenously in the form of a dropper.
Preventive drugs are Cavinton and Vinpocetine for 3 months. Hirudotherapy has a good effect.
Preventative measures
Based on the reasons, we can formulate a clear list of adequate measures:
- regularity and timely treatment of hypertension;
- treatment of chronic concomitant provoking pathologies of diabetes - atherosclerosis, obesity;
- quitting smoking and alcohol;
- properly balanced nutrition;
- preventive methods of antioxidants and angioprotectors.
The main measure is optimal pressure control. This will help prevent the development of encephalopathy.
Since the development of GB goes through its 3 stages, at 3 stages encephalopathy is present in almost every patient. Therefore, it is important to prevent the transition of hypertension to stage 3. It is important to achieve the exclusion of nightly pressure surges and sharp fluctuations in the background during the day. It should be remembered that only the initial stage of violations is reversible. In the future, even proper treatment does not give an effect in terms of reducing the violation of mental and motor functions.