Hypertensive (hypertensive) encephalopathy (HE) is a violation of brain activity against the background of malignant hypertension. According to the ICD-10, acute hypertensive encephalopathy is coded as I67.4. The term was introduced in 1928 by Oppenheimer in collaboration with Fishberg to describe this particular form of encephalopathy. Although such a condition can occur in 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 one-time jump in pressure for the brain does not pass without a trace. The regulation of the tone of venules and arterioles is impaired. The target is not onlybrain, but also the heart and kidneys. With a slight increase in pressure, protective spasm of small vessels first starts. This is done by the body in order to prevent their rupture and pressure.
If the pressure remains elevated for a long time, the muscular layer of the vessels begins to hypertrophy. The result is a narrowing of the lumen of the vessel and a decrease in blood perfusion. Hypoxia occurs to varying degrees. The most sensitive to hypoxia is the brain. Which causes neurological symptoms.
Thus, with HE of any form, the hemodynamics of the brain is disturbed, and brain tissue is damaged up to necrosis. All this comes against the backdrop of long-term hypertension, which is difficult to control.
Acute hypertensive encephalopathy according to the ICD is distinguished as a separate type of encephalopathy that occurs with symptomatic hypertension. At first, predominantly small vessels are affected, but the 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 the ICD-10, acute hypertensive encephalopathy has the following code - I67.4. At the same time, the level of pressure may differ in hypo- and hypertensive patients.
For hypertensive patients, dangerous numbers range from 180-190 mm Hg. Art., and in hypotensive patients - within 140/90. In any case, we are talking about raising the norm.
Specialists call this state of hypertensive encephalopathy a kind of manifestation of a hypertensive crisis. The chronic form of pathology is more common.
GE in acute form
Acute GE is an emergency condition and immediate assistance is required. Otherwise, complications are required in the form of cerebral edema, hemorrhagic stroke, heart attack, death.
Acute hypertensive encephalopathy according to ICD-10 has 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. An exacerbation against their background in the form of GE is such a chain. Her progression is faster than other forms of dyscirculatory encephalopathy.
The diagnosis of "dyscirculatory hypertensive encephalopathy" is made with chronic damage to brain tissues due to insufficient blood supply. Its development is gradual and progressive. Accompanied by morphological changes in brain tissue, impaired functionality and can cause dementia, incapacity and disability.
Causes of the problem
The leading cause of HE (hypertensive encephalopathy according to the ICD is coded I67.4) is a neglected 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.
Pathologies of the adrenal and pituitary glands - pheochromocytoma, excessive function of the adrenal cortex or in the glomerular zone - aldosterone, aorticatherosclerosis.
For hypertensive patients, uncontrolled hypertension is dangerous, changes develop especially rapidly when antihypertensive drugs are abandoned. Repeated crises of hypertension, in which the vessels quickly wear out and become thinner. Their permeability increases and there is a rapid hemorrhagic impregnation of brain tissues. There are also fluctuations aimed at normalizing pressure, hypotension with slowing blood flow. Nocturnal hypertension is more often latent.
High pulse pressure is another important factor. If the difference between the upper and lower pressures exceeds 40 mm Hg. Art. - the course of vascular diseases is exacerbated. Such pressure constantly affects the vascular wall and puts a load on the muscular apparatus of the vascular wall.
Risk factors
Risk factors include:
- Deviations in the work of blood vessels and the heart that are not diagnosed in time.
- Diseases of the kidneys (congenital or acquired) and the brain.
- Unstable state of blood vessels. Overexertion of any type - physical and mental.
- Incorrect or irregular treatment of hypertension.
- Eating disorders and physical inactivity, bad habits.
Hypertensive encephalopathy (hypertensive encephalopathy according to ICD-10 code I67.4) can also be provoked by:
- obesity, old age, diabetes;
- refusing or switching to another antihypertensive drug without consulting a doctor;
- eclampsia with edema,high blood pressure and proteinuria;
- adrenal tumors;
- addiction to some drugs - steroids, caffeine, sports doping;
- stress against the background of existing problems with blood vessels;
- bad ecology can also do a disservice to vessels;
- systematic hypothermia of the body.
Under certain conditions, the diagnosis of hypertensive encephalopathy (ICD code I67.4) can be made to anyone.
Pathogenesis
When there is a shortage of nutrition delivered to the vessels, changes occur in their walls in the form of a decrease in their tone. Next comes the thickening of the muscles of the walls of the vessels and their lumen narrows. Hypoxia gets worse. This, in turn, worsens the condition of the nerve fibers.
Spasm of cerebral arterioles leads to hypoxia and nutritional deficiency for brain cells, chronic cerebral ischemia develops. Further, degenerative changes occur in the cerebral structures. If there is atherosclerosis, it only aggravates the situation.
The white medulla 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 - they spread periventricularly.
Of direct importance in the development of OGE is the excessive spasm of small arterioles that pass into the capillaries, their permeability increases and paralysis andacute form of GE.
Sharp shape
Hypertensive crisis with blood pressure over 180-190 mm Hg. Art. causes, as a rule, serious changes in the tissues of the vessels. Which? When there are obstacles to its movement, namely: a narrowed lumen of the vessel or plaques on the walls, the blood reacts to this by the appearance of hemorrhages along the walls of the vessels. The tone of the veins of the soft meninges changes and intracranial pressure increases. It causes the appearance of neurological symptoms. Acute hypertensive encephalopathy - a consequence of a hypertensive crisis; but it also becomes a harbinger of strokes with the subsequent development of disability and death. 16% of the complications of the crisis are precisely the OGE.
Symptomatics
The clinic of acute hypertensive encephalopathy includes:
- Expanding unbearable headaches.
- First they are localized in the back of the head, then they become spilled, i.e. growing.
- Pain is not relieved by analgesics. Often this is accompanied by nausea and vomiting without relief. Acute hypertensive encephalopathy manifests itself most often during a hypertensive crisis.
- Vision suddenly deteriorates due to swelling of the optic disc, dark flies and spots appear before the eyes.
- Severe dizziness. Coughing and sneezing and other tension of the neck muscles make the condition worse.
- Hearing worsens - ringing and tinnitus appear.
- Convulsions and meningeal symptoms occur without inflammation (meningismus).
- Surface sensitivity thresholdrising.
In general, these are symptoms of a hypertensive crisis, but with the involvement of 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:
- stupefaction state preceded by excitation passing into paresis;
- slow heart rate;
- numbness of the tip of the tongue, fingers, orientation in space is disturbed;
- gait becomes unsteady.
Body temperature may rise. An attack can take several hours or last up to 2 days. Further, a hemorrhagic stroke develops, cerebral edema and death if no assistance is provided.
Acute hypertensive encephalopathy thus occupies an intermediate position between a crisis and strokes.
The determining factor is the numbers of pressure: during an attack it is up to 250-300, the lower one is up to 130-170. But the blood vessels dilate. They no longer narrow, and their permeability increases. In the tissues of the brain, blood flow is disturbed, with a deficiency of plasma, protein, and oxygen, its edema develops. Small foci of necrosis develop.
Acute hypertensive encephalopathy is also one of the early signs of a stroke, so the patient should first of all be kept calm and call an ambulance.
Diagnosis
The diagnostic algorithm includes:
- Mandatory examination by a neurologist. In the initial stage, the status may notdisturbed, but anisoreflexia occurs earlier than others. Special cognitive testing determines mnestic, praxic and gnostic impairments 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 can be difficult due to the similarity of the symptoms of cerebral accidents, so CT and MRI of the brain vessels should be performed. In this case, focal changes are detected in the brain - cerebral edema. It also allows to identify diffuse degenerative changes, foci of past lacunar infarcts in patients with II-III stage of HE, to exclude other organic pathology of the brain. The picture of the blood test is not informative, but the presence of hypercholesterolemia is important.
- At an ophthalmologist's consultation - swelling of the optic discs. There is an increase in pressure inside the skull.
- EEG - disorganization of the main rhythms, especially in the occipital region. ECG - left ventricular wall hypertrophy, dystrophic changes in the myocardium.
- Research of cerebral hemodynamics: ultrasound of the cervical and cranial vessels. This study reveals the degree of narrowing of the arterioles, their localization and prevalence.
Complications
OGE is an urgent condition that, if left untreated, leads to:
- come;
- brain infarction;
- stroke;
- IM;
- cerebral edema,
- intracranial hemorrhage andfatalities.
Treatment
The patient is subject to mandatory hospitalization in the intensive care unit and observation of a whole team of doctors: resuscitator, neurologist, neurosurgeon, ophthalmologist, etc.
Diagnosed OGE requires the use of long-acting drugs.
It is mandatory to prescribe diuretics that relieve swelling of brain tissues - Furosemide, ethacrynic acid, Lasix, etc. It is also important to control blood electrolytes to prevent total brain ischemia.
You can not quickly reduce the existing pressure, the process must 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 become optimal for this subject. Diastolic pressure should not fall below 90 mmHg
With a strong sharp imbalance of cerebral blood flow, the decrease in systolic pressure should be even slower: the upper one is not more than 15%, the lower one is 10% of the normal level.
To accelerate the initial decrease in blood pressure, sodium nitroprusside is administered intravenously (0.3-0.5 mcg / kg in 1 min.) - it allows you to control the decrease in blood pressure.
Also, drugs of the main action ("Clonidine" and "Clonidine") are used intravenously in the form of a dropper in saline or in a stream of 1-2 ml.
Good results are given by an antihypertensive agent - "Hypostat", it normalizes pressure within a few minutes.
Next, you can switch totablets - adrenoblockers, calcium ion antagonists ("Nifedipine" - improve cerebral blood flow), ACE inhibitors ("Enalapril", "Captopril" - optimize vascular tone), diuretics and other drugs.
Prednisolone, Dexamethasone are prescribed to prevent new edema and reduce the existing one.
In the treatment of acute hypertensive encephalopathy in the presence of a convulsive syndrome, Relanium is prescribed.
"Magnesia", "Eufillin" will also have a calming and sedative effect. In view of the violation of lipid oxidation processes, antioxidants are prescribed:
- droppers with "Mexidol" 400 mg;
- "Ceraxon" 1000 mg each;
- "Cytoflavin" 10 ml intravenously.
It is very good to combine them with activators of gluconeogenesis: mildronate 10-20 ml intravenously as a dropper.
Prophylactic drugs are "Cavinton" and "Vinpocetine" for 3 months. Hirudotherapy has a good effect.
Preventive measures
Based on the reasons, we can formulate a clear list of adequate measures:
- regularity and timely treatment of hypertension;
- treatment of chronic concomitant provocative pathologies of diabetes - atherosclerosis, obesity;
- quitting smoking and drinking;
- properly balanced nutrition;
- antioxidant and angioprotective preventive measures.
The main measure is to control the pressure at the optimumlevel. This will help prevent the development of encephalopathy.
Since the development of GB goes through its 3 stages, at stage 3 encephalopathy is present in almost every patient. Therefore, it is important to prevent the transition of hypertension to stage 3. It is important to exclude night pressure jumps and sharp background fluctuations during the day. It should be remembered that only the initial stage of violations is reversible. In the future, even the right treatment does not give an effect in terms of reducing the impairment of mental and motor functions.
