Emergency care for an attack of renal eclampsia, treatment, medications

If during an attack of renal eclampsia the patient was not in the hospital, he must be immediately hospitalized (in the case of acute nephritis in the therapeutic or nephrological department, and in the case of nephropathy in pregnant women - in the obstetric department). In this case, it is necessary to prevent tongue bite and retraction (insert a spatula or spoon wrapped in a thick layer of gauze between the teeth, push the lower jaw forward), damage to the head and other parts of the body (support the head, place a pillow or blanket).

Immediately using the venipuncture method (if it fails, then using the venesection method), it is necessary to perform a fairly massive bloodletting (300-500 ml) to lower blood pressure and reduce cerebral edema. At the same time, 40-60 ml of a 40% glucose solution and 10-15 ml of a 25% magnesium sulfate solution are administered intravenously (slowly, over 3-4 minutes). The latter has a vasodilator, anticonvulsant effect, and also, along with hypertonic glucose solutions, reduces cerebral edema. Along with intravenous administration, intramuscular administration of 15-20 ml of a 25% solution of magnesium sulfate is also used.

If an attack of eclampsia does not stop, after 1-2 hours you need to repeat the intravenous infusion of glucose and magnesium sulfate in the same doses. It must be remembered that in large doses, magnesium sulfate can have a depressant effect on the respiratory center. In such cases, a magnesium antagonist, calcium, is administered (10 ml of 10% calcium chloride solution intravenously). Additionally, to relieve frequently recurring convulsive attacks, 1 ml of a 2.5% solution of aminazine is administered intravenously, 1 ml of a 1% solution of morphine hydrochloride is administered subcutaneously, 50 ml of a 3-5% solution of chloral hydrate is administered as an enema, if necessary, up to 7 g of chloral hydrate and 0.025-0 .03 g of morphine hydrochloride per day.

If cerebral edema is combined with general edema and left ventricular failure, 60 mg of furosemide (Lasix) should also be administered slowly intravenously, continuing its intravenous drip administration if necessary. For renal eclampsia, dibazole (3-4 ml of 1% solution or 6-8 ml of 0.5% solution intravenously), aminophylline (10 ml of 2.4% solution intravenously repeatedly) are also used.

In most cases, with the help of the measures listed above, an attack of renal eclampsia is stopped. It is relatively rare to resort to lumbar puncture, which is usually performed in a hospital setting. The release of cerebrospinal fluid should be done slowly and not sharply reduce intracerebral pressure. After a spinal puncture, intracranial pressure decreases and eclamptic seizures stop. After stopping the attack, the patient needs hospital treatment. In the first days, he needs to be prescribed an achloride diet, and then a diet limiting sodium chloride to 3-4 g per day and liquid to 1 liter per day (in the first 1-2 days, classic treatment with hunger and thirst can be carried out). For high blood pressure, antihypertensive drugs (reserpine, dibazole, aldomet or dopegit, clonidine, etc.) are prescribed in appropriate doses. For severe edema, diuretics are indicated; for heart failure, cardiac glycosides are indicated.

Is the most severe complication acute nephritis and is characterized comatose state, clonic and tonic convulsions.

Acute jade observed in children aged 7 to 12 years, less often in children aged 1 to 3 years. It is rare in infancy.

At the core renal eclampsia are changes in the central nervous system- spasm of cerebral vessels and rapidly developing cerebral edema. Therefore, it is more correct to call eclampsia angiospastic encephalopathy.

The tendency to eclampsia in acute nephritis in children is explained by the easier formation of edema or swelling of the brain in childhood. At the same time, their arterial hypertension is less pronounced.

Symptoms: headache, nausea, sometimes vomiting. Blood pressure in children increases slightly, sometimes it remains normal. More often, the pressure is increased only relatively compared to the numbers before the attack. An attack of eclampsia often begins after a cry or deep noisy breath. After 1/2-1 minute, clonic and tonic convulsions of the whole body appear. The child's pallor is replaced by a sharp cyanosis of the face. Breathing becomes rare, sometimes intermittent due to spasms of the respiratory muscles. The pupils are dilated and do not react to light. When examining the fundus, congestion is noted. Consciousness is darkened. The attack lasts several minutes, usually repeating several times on the same day (2-10). Seizure attacks, as their number increases, become less severe and shorter in duration. The symptoms of eclampsia usually end within the first or second day. The pulse is usually slow and tense blood pressure usually higher than before the attack. The amount of residual blood nitrogen is normal or slightly increased, the amount of chlorides is reduced.

Protein, red blood cells, and casts are detected in the urine. During an attack of eclampsia, spinal pressure increases to 500 mm of water column (versus 120-200 mm normally).

Sometimes children have only the equivalent of a seizure in the form of small convulsive movements, weakness of one limb or hemiparesis with positive symptom Babinsky, mild blurred vision, severe headache and vomiting.

Differential diagnosis. You should remember about epilepsy, which is also rare in children and is characterized by the appearance of short-term clonic and tonic seizures with loss of consciousness. In this case, foamy saliva is often released from the mouth, tongue biting and involuntary release of urine and feces often occur.

To distinguish epilepsy, anamnesis is essential, since epilepsy is a chronic disease, the anamnesis contains indications of similar phenomena in the past, and most importantly, a clinical examination of the child does not give signs of acute nephritis.

Urgent Care. You should start with bloodletting, administration of glucose and magnesium sulfate. Bloodletting for eclampsia is a reliable emergency measure. It reduces intracranial pressure and should be massive (100-150 ml). Following bloodletting, 10-15 ml of a 40% glucose solution is injected into a vein, which obviously counteracts angiospastic conditions and has a neutralizing effect. Intravenous or intramuscular administration of a solution of magnesium sulfate dilates the vessels of the kidneys, lowers blood pressure, increases diuresis and reduces neuromuscular excitability. A 25% heated solution of 0.25 ml per kilogram of the child’s weight is used intramuscularly; intravenously 1% solution, 5-10 ml per kilogram of child’s weight. If these measures do not produce any effect, only then do they resort to lumbar puncture in order to reduce intracranial pressure. The cerebrospinal fluid should be released until it flows out in rare drops.

In order to reduce the excitability of the central nervous system, enemas with a 2% solution of chloral hydrate are recommended - 20-30 ml, depending on the age of the child. In case of heart failure, intravenous administration of strophanthin with glucose is recommended.

Massive doses of ascorbic acid (200-300 mg), vitamin K (for hematuria), as well as a complex of vitamins B (B1, B2) are recommended. When providing care at home, it is necessary to bleed the sick child and immediately hospitalize him on a stretcher.

Treatment. The basis for the treatment of eclampsia should be the unloading of water-salt metabolism, which is achieved by prescribing hunger and thirst for 1-2 days with a gradual transition to a diet with a restriction of sodium chloride and protein substances (until the edema completely disappears). The diet should correspond to the dietary regimen for acute nephritis, including 2 sugar days per week.

Renal eclampsia is acute condition with a number of characteristic signs, which are based on disorders of the brain (encephalopathy with swelling of brain tissue as a result of a sharp and prolonged spasm of arterioles). This syndrome is different:

• convulsions (clonic and tonic);
• clouding or loss of consciousness (coma);
• an increase in blood pressure to critical levels;
• pronounced metabolic disorders in the body.

Renal eclampsia is a fairly rare but very dangerous disease. As a rule, it manifests itself in pregnant women as a complication in the last trimester, as well as in people with chronic renal pathologies. In early childhood, the pathology practically does not occur; in junior and senior schoolchildren and adolescents it is diagnosed sporadically, that is, only in isolated cases with acute forms jade

Causes

1. Nephropathy in pregnant women (impaired kidney function).
2. Chronic nephritis.

Factors that provoke renal eclampsia include:

• consumption by pregnant women and sick people of significant amounts of salty, spicy, spicy foods or large volumes of liquid;
• disturbances in the functioning of the endocrine system;
• neuropsychic overexcitation, stress;
• changes in the composition of the blood (increase in its viscosity, release large quantity platelets, enhancing their coagulation processes).

Development mechanism

The syndrome develops against the background of vascular spasm and tissue swelling in the brain. This occurs due to sodium retention in the body’s cells, accumulation and long-term retention of water in them. This process triggers mechanisms for raising arterial and intracranial pressure, brain hypoxia, and ischemia of its tissues. Therefore, the work of brain structures (both brain and spinal cord) is disrupted, a significant narrowing of its functions occurs, and everyone suffers greatly internal organs(heart, lungs, liver).

Renal eclampsia is characterized by:

• increased tissue permeability in the body, which is expressed in the formation of internal and external edema;
• metabolic disorders - accumulation harmful substances formed as a result of decomposition reactions (acidosis);
• lack of normal filling of blood vessels, decrease in blood volume in them;
• increased loss of fibrin and its sedimentation in the cells of the body, which changes the normal process of blood clotting;
• hemorrhages (single and multiple petechial) in the brain and (or) internal organs.

Clinic, symptoms of renal eclampsia

In medicine, there is such a thing as preeclampsia (a triad of signs signaling the danger of a crisis) - this is:

• increased blood pressure;
• the appearance of severe swelling;
• protein in urine.

Any doctor who discovers a combination of these symptoms is obliged to “sound the alarm” and immediately begin therapeutic measures. The main thing is to prevent an impending attack or provide emergency assistance in a timely manner (preferably at the very beginning). Delay in this case can lead to the death of the patient, and in pregnant women, the fetus.

Prodromal (preceding) signs of renal eclampsia, in addition to the main ones, include:

• double vision or a white veil in front of them;
• dizziness and migraine-like pain;
• lethargy and confusion;
• the occurrence of delirium, hallucinations, fainting;
• decreased desire to urinate;
• nausea, vomiting, heaviness in the epigastrium.

With chronic pathologies in the renal system, preeclampsia can last up to 4 days, in other cases the attack develops rapidly within several hours. After sharp jump pressure, patients develop convulsions according to a certain “scenario”:

• twitching of individual muscles (1-3 min);
• trismus of the whole body with further loss of consciousness, with pronounced bluish discoloration of the skin (cyanosis), dilated pupils (up to 30 seconds);
• clonic contraction of the entire body muscles, with signs of respiratory and heart failure (up to 2 minutes);
• involuntary urination and bowel movements, return to consciousness; with irreversible changes in the body, patients die during this period from suffocation, cardiac arrest, and extensive hemorrhages in the brain.

The number of convulsive seizures can range from 1 to 10 or more.

In the recovery phase, patients are left with a foggy consciousness, speech and coordination disorders are observed, they do not remember their feelings during attacks, they are disoriented in space and perception of the world.

Objective symptoms of eclampsia are characterized by:

• slow heart rate;
• high tendon reflexes;
• congestion in the fundus;
• When cerebrospinal fluid is taken (puncture), an increase in pressure in it is diagnosed.

Atypical and mild, renal eclampsia can occur in people with chronic nephritis, without pronounced convulsions and “turning off” consciousness (it leaves patients for seconds). Urine tests in such patients do not show a large number of protein fractions, although blood pressure is significantly elevated and there may be edema.

Diagnostics

It is important to distinguish seizures in eclampsia from seizures in epilepsy. The distinctive signs of eclampsia are:

• decreased heart rate;
• swelling on the body;
• increase in blood pressure.

With epilepsy, the pulse is normal or rapid, there is no swelling or hypertension, and visible marks on the tongue from previous attacks may remain.

To differentiate from traumatic coma or stroke, urine analysis is used; in the latter cases, protein is not detected in it, and observations also show the presence of paresis and (or) paralysis in patients. In eclampsia they are not present.

Distinctive feature this state from uremic coma is the absence of organic changes in the kidneys (wrinkling, reduction), as well as dystrophy and hypertrophy of the myocardium.

The main laboratory method for determining the development of renal eclampsia is to study urine (for protein, for creatinine) and blood (biochemistry, for electrolytes, for pH balance, for urea, for platelet levels, etc.).

Instrumental examinations include: ultrasound, CT, X-ray, MRI of the kidneys and other organs.

Treatment

Attacks of renal eclampsia can only be stopped in a hospital; if there is any suspicion of them, patients are urgently hospitalized. Therapeutic procedures include:

• application anticonvulsants(Droperidol, Seduxen, Sodium oxybutyrate), antihypertensive drugs(Magnesium sulfate);
• bleeding up to 400 ml.;
• taking diuretics (Furosemide, Lasix).

1. The diet is salt-free in the first weeks, and then with limited sodium chloride intake.
2. Antihypertensive drugs as prescribed by a doctor.
3. Decongestants, including folk ones. You can drink kidney tea (Orthosiphon stamen), the regimen will be prescribed by a specialist.

Romanovskaya Tatyana Vladimirovna

Main syndromes in kidney diseases

- nephrotic syndrome

- nephritic syndrome

- renal arterial hypertension syndrome

- renal eclampsia syndrome

- renal failure syndrome (acute and chronic)

Nephrotic syndrome

This is a clinical and laboratory symptom complex, clinically characterized by peripheral or generalized edema to anasarca, and laboratory- proteinuria more than 3.5 g/day or more than 50 mg/kg/day, hypoproteinemia (below 55 g/l), hypoalbuminemia (below 35 g/l), dysproteinemia, hyperlipidemia and lipiduria.

Etiology

I. Primary NS – in the background primary diseases kidneys (only the kidneys are affected):

1) Glomerulonephritis (chronic). Morphological variants: minimal change disease (small process podocyte disease), focal segmental glomerulosclerosis and membranous nephropathy.

2) Primary amyloidosis.

H) Lipoid nephrosis (more often in children) is a variant of CGN (minimal change disease).

4) Kidney tumor (hypernephroma) - most often manifested by hematuria, sometimes it’s just a finding. However, with any malignant diseases, glomerulonephritis can develop, morphologically - membranous nephropathy.

I I. Secondary NS – secondary kidney damage occurs against the background of other diseases:

1) Infectious group:

Syphilis;

Malaria;

Tuberculosis;

Leishmaniasis;

Septic endocarditis is the cause of glomerulonephritis;

Chronic inflammatory and suppurative diseases of the lungs and bones are the cause of secondary amyloidosis;

Rheumatism;

Periarteritis nodosa;

Goodpasture's syndrome;

Hemorrhagic vasculitis;

Nonspecific ulcerative colitis;

NB! All of the above are accompanied by the development of glomerulonephritis

Diabetes;

Tumors of extrarenal localization;

Thrombosis of the veins and arteries of the kidneys, aorta, inferior vena cava

Periodic illness;

drug disease,

Diffuse toxic goiter.

Pathogenesis.

The main role in pathogenesis is played by immune mechanisms.

Pathogenesis.
A model of acute nephritic syndrome is poststreptococcal glomerulonephritis. The presence of a focus of infection (upper respiratory tract, skin, middle ear) caused by group A vetta-hemolytic streptococcus (strains 1, 4, 12, 29) is necessary. AT are produced against streptococcal Ag (for example, M-protein of the cell wall), Ag-AT complexes are deposited in the walls of the glomerular capillaries, activating the complement system, and leading to immune inflammation and damage to kidney tissue.

Pathomorphology - diffuse proliferative endocapillary glomerulonephritis

Infiltration of glomeruli by neutrophils and monocytes

The walls of the glomerular capillaries are thinned and fragile

Discrete deposits of protein (electron-dense deposits in electron microscopy) protruding from outer surface capillary walls into the capsule lumen and corresponding to electron-dense deposits observed by electron microscopy

Segmental extracapillary proliferation (crescents) is detected in several glomeruli; diffuse formation of crescents is uncharacteristic.

Red blood cell casts are found in the lumens of the distal tubules

Granular deposits of IgG in the peripheral loops of capillaries and in the mesangium, accompanied by deposits of the complement component C3 and properdin and, less commonly, deposits of Clq and C4.

Clinical picture.

The clinical picture of nephritic syndrome can be considered using the example of acute glomerulonephritis and consists of

1 - edematous syndrome

2 - arterial hypertension syndrome

3 - urinary syndrome

4 - pain syndrome

5 - general intoxication syndrome

The disease manifests itself 1-6 weeks after streptococcal infection.

Edema syndrome

Edema(85%). Swelling of the face (especially the eyelids) is most common in the first half of the day. Swelling is usually located on the face, appears in the morning, and decreases in the evening. Before visible edema develops, about 2-3 liters of fluid can be retained in the muscles and subcutaneous tissue. Hidden edema is detected using the McClure-Aldrich test (carried out to identify hiddenswelling and a tendency to edema due to the accelerated resorption of papules formed with intradermal administration of an isotonic solution sodium chloride. Normally, the papule resolves within 60 minutes. If the patient’s body is prone to edema, the papule disappears in less than 40 minutes. due to increased tissue hydrophilicity due to increased capillary pressure.).

Edema is caused by:

increased capillary tissue permeability due to increased hyaluronidase activity leading to depolymerization hyaluronic acid main substance connective tissue And decreased glomerular filtration(as a consequence immune inflammation and affects the capillaries of the whole body) is a trigger for the formation of edema, which in turn triggers other pathogenetic mechanisms of fluid retention:

ü increased tubular reabsorption of sodium and water,

ü increased secretion of aldosterone and antidiuretic hormone,

Oligoanuria(52%) in combination with thirsty– are caused by fluid retention in the body and the development of hypovolemia, are possible more often in the first days of the disease and usually last 2-3 days. However, hypovolemia is not a characteristic feature of nephritic syndrome, because the mechanism of edema differs from nephrotic edema: as a rule, it is not massive and the blood volume does not fall.

Arterial hypertension syndrome (symptomatic, parenchymal)

Arterial hypertension(82%). Blood pressure is usually moderately elevated (160/100 mmHg) in 60–70% of patients. Long-term persistent increase in blood pressure is prognostically unfavorable. Leading importance in the pathogenesis of hypertension in nephritic syndrome is given to the retention of sodium and water, an increase in the volume of circulating blood and stroke volume of the heart, and activation of the renin-angiotensin-aldosterone system. Clinically manifested by headache and other symptoms characterizing damage to the brain and heart against the background of high blood pressure.

Urinary syndrome

Urine turns the color of meat slop, which is related to g ematuria(100%). Macrohematuria occurs in 30% of cases (urine the color of meat slop). The pathogenesis of hematuria in these patients is mainly associated with damage to the glomerular basement membranes and an increase in their permeability. With glomerular hematuria, more than 80% are altered red blood cells. The volume of urine decreases (oliguria, possibly anuria, but this is already evidence of the development of acute renal failure).

Pain syndrome . Pain in the lumbar region has varying degrees of severity, often symmetrical, depending on the swelling of the kidneys and stretching of their capsule, and urodynamic disturbances. The pain is dull, constant, intensifies when standing and moving, decreases when lying on your back.

Other signs

Increased body temperature (weight gain is associated with edema).

Weakness.

When studying other organs and systems:

Signs of infectious diseases of the respiratory tract (including acute tonsillitis, pharyngitis)

Signs of scarlet fever

Signs of impetigo (pustular skin disease caused by streptococci and staphylococci). In the anamnesis.

General inspection.

The condition is severe, consciousness is often depressed, especially with the development of acute renal failure.

Pallor of the face and pasty eyelids (facies nefritica) are noted.

Edema is one of the components of nephritic syndrome. The loose fatty tissue of the eye sockets and eyelids swells the most.

The skin is pale, a hemorrhagic rash may appear as a manifestation of an active autoimmune process.

Kidneys: When examining the lumbar region, there are no changes; upon palpation, sharp pain in the kidneys is noted and their size may increase, but not always.

Positive Pasternatsky symptom.

The cardiovascular system. A characteristic feature OGN (with its classic version) is bradycardia, which is combined with hypertension. It is detected already in the first days of the disease, especially in persons young, lasts for 1-2 weeks, sometimes longer.

On palpation, the apical impulse in acute nephritic syndrome is strong, high; in chronic nephritic syndrome - strong, high, diffuse, resistant.

The combination of bradycardia, hypertension, and edema serves as an important differential diagnostic sign for distinguishing between edema caused by glomerulonephritis and many heart diseases, in which edema is usually combined with tachycardia.
On auscultation: the rhythm is regular, in the presence of electrolyte disturbances there may be disturbances heart rate, the rhythm is rare, often detected weakening of the first tone, accent of the second tone on the aorta ( as a manifestation of arterial hypertension in nephritic syndrome).

Additional Research

Laboratory

UAC: hypochromic anemia, leukocytosis, accelerated ESR

Blood test: dysproteinemia, hypergammaglobulinemia. In some cases, the appearance of C-reactive protein, sialic acids, credits antistreptococcal antibodies – ASL-O, ASC, ASG.

OAM: oliguria, “meat slop” color, hypersthenuria, gross hematuria, cylindruria (due to hyaline casts), erythrocytes (red blood cells, both fresh and leached), leukocyturia, proteinuria from 0.5 to 2 g/m2/day (weak (up to 1 g/day) or moderate proteinuria (up to 2 g/day)) these changes are included in the urinary syndrome.

Kidney function test: Rehberg–Tareev test decreased glomerular filtration. Appearing in the first hours and days from the onset of the disease and disappearing later than other clinical and laboratory signs OGN, proteinuria and hematuria most clearly reflect the dynamics of the disease, its activity, course, and recovery processes. Zimnitsky test, used: creatinine, urea, potassium ( functional tests are not changed in uncomplicated nephritic syndrome).

Immunological blood test reveals increased levels of JgG, Jg M, rarely JgA, circulating immune complexes, high titers of antibodies to streptococcal antigens. Hypocomplementemia (SZ content) - 83% of cases.

Also characteristic blood coagulation disorders hypercoagulation is observed (shortening thromboplastin time, increasing prothrombin time, inhibition of fibrinolytic activity of the blood).

Instrumental

Kidney ultrasound: the size of the kidneys is increased or unchanged, echogenicity is reduced.

Kidney biopsy: Biopsy with subsequent examination of the nephrobiopsy allows a nosological diagnosis to be made. It is carried out according to strict indications: differential diagnosis With chronic nephritis, including systemic connective tissue diseases, rapidly progressive glomerulonephritis. Acute glomerulonephritis is characterized by the following morphological data: a picture of diffuse proliferative endocapillary glomerulonephritis, infiltration of the renal glomeruli with netrophils and monocytes, electron-dense deposits of immune complexes, etc. etc.

Kidney scan: Decreased isotope absorption.

ECG : changes are varied and are determined by the severity of hemodynamic and electrolyte changes. Low voltage, elongation is often observed P-Q interval, biphasicity and flattening of the T wave, shift of the S–T interval, overload
left ventricle and possibly rhythm disturbances.
Ocular fundus: narrowing of the arteries, dilation of the veins, signs of swelling of the optic nerve nipple.

ECHO-KG: signs of arterial hypertension.

Renal hypertension syndrome

This is a condition in which systolic pressure exceeds 140 and diastolic pressure exceeds 90 mmHg. Art., arising as a result of various pathological processes in the kidneys and urinary tract.

Kinds:

Vasorenal (or renovascular)

Atherosclerosis of the renal artery

Fibromuscular dysplasia of the renal artery

· Structural anomalies renal arteries

Vasculitis with damage to the renal arteries

Renal artery thrombosis

Compression of the renal arteries

Renoparenchymatous

Glomerulonephritis

· Pyelonephritis

Amyloidosis of the kidneys

Nephropathy of pregnancy

· Diabetic nephropathy

· Other kidney diseases

SAH associated with urodynamic abnormalities (outflow of urine), the so-called " urological hypertension"(urolithiasis, congenital kidney defects, hydronephrosis, prostate adenoma, reflux nephropathy, etc.);

Mixed hypertension.

Their occurrence is associated both with the defeat of the renal tissue, and with impaired patency of the kidney vessels (nephroptosis, kidney tumors and cysts, a combination of congenital anomalies of the kidneys and their vessels, etc.).

Main pathogenetic mechanisms:

І activation of RAAS pressor systems

Increased production of renin by the UGA of the kidneys during ischemia

Activation of the RAAS

Peripheral arteriolospasm

Increased production of aldosterone

Sodium and water retention

II water retention and accumulationNa(accumulation of Na in the walls of blood vessels leads to swelling of the wall, increased sensitivity vascular wall to KA and increase in OPSS)

ІІІ inhibition of depressor systems; decrease in the synthesis of peripheral vasodilators (kinins, prostaglandins) in the kidneys.

Clinical picture.

Symptoms of increased blood pressure are nonspecific. The most typical complaints of patients with hypertension are:

- from the side of the heart:

pain in the heart area, palpitations, a feeling of interruptions in the functioning of the heart. Angina pectoris may occur due to the accelerated development of atherosclerosis, sharp chest pain during aortic dissection, shortness of breath and other signs of acute and chronic heart failure;

- from the side of the brain:

headaches of various types and origins; dizziness, memory impairment, noise in the head, irritability, fatigue, periodic weakness, depressed mood; flashing “fly spots” before the eyes and other signs of visual impairment, decreased performance;

- from the kidneys:

swelling of the face in the morning, hematuria and nocturia, symptoms associated with the development of chronic renal failure;

Complaints related to the underlying disease in cases of symptomatic renal arterial hypertension include:

swelling on the face, pain in the lumbar region, hematuria, nocturia, renal colic – for kidney diseases and urinary tract infections.

sharp muscle weakness, polydipsia, polyuria, paresteria and convulsions with primary hyperaldosteronism – with pathology of the adrenal glands;

episodes of paroxysmal sweating, headaches, anxiety, palpitations ( pheochromocytoma) – with pathology of the adrenal glands;

General inspection.

Patient position in most patients active.

In a relatively small proportion of patients, usually in the later stages of the disease, orthopnea position, which, along with rapid breathing (tachypnea) or suffocation, moist rales in the lungs, indicates the occurrence of left ventricular failure. More often it develops after an MI or during a complicated hypertensive crisis with an unusually high rise in blood pressure and LV overload.

Color of the skin pale, with chronic renal failure with a yellowish tint due to the accumulation of urochromes in the skin

Facies nephritica- - round, puffy, swollen face and eyelids, narrow palpebral fissures

Peripheral edema, pale, soft, mobile.

Inspection, palpation and percussion of the heart

The apex beat and the boundaries of the heart are not changed, the formation concentric myocardial hypertrophy The LV leads to an increase in the force of the apical impulse. Its localization, as well as the left border of the relative dullness of the heart, long time may remain almost unchanged until LV dilatation occurs ( eccentric LV hypertrophy)

A progressive decrease in the contractility of the LV myocardium is accompanied by significant (myogenic) dilation of L G. Reinforced the apex beat shifts to the left and becomes diffuse. The left border of the relative dullness of the heart also shifts to the left.

Percussion sometimes reveals extension vascular bundle in the second intercostal space, conditioned expansion of the aorta, its lengthening and reversal, characteristic of many patients with hypertension.

Auscultation of the heart

I heart sound. In the initial stages of the disease, characterized by quite high speed contractions of the LV myocardium, and its hypertrophy is moderately expressed, as a rule, detected loud 1st heart sound. With a progressive increase in the mass of the LV myocardium, the development of LV dilatation and the occurrence of relative failure mitral valve there is a noticeable decrease in the volume of the first tone, due to a decrease in the rate of isovolumic contraction of the LV. Low-frequency components begin to predominate in tone I, and it acquires the character of a “dull” tone.

II heart sound is accentuated on the aorta, What primarily due to high blood pressure.

Additional tones. Myocardial hypertrophy LV is naturally accompanied by more or less pronounced diastolic dysfunction. The latter, as is known, is accompanied by a significant slowdown in early ventricular filling (during the rapid filling phase) and an increase in the atrial filling fraction (atrial systole). As a result, in the initial stages of the disease, sounds are often heard at the apex. pathological IV heart sound.

Subsequently, when there is a decrease in LV contractility, it develops systolic dysfunction and severe LV dilatation, at the top is determined pathological III heart sound associated with volume overload of the ventricle, characteristic of late stages diseases.

Noise. Functional systolic murmur on the aorta(II intercostal space to the right of the sternum) - a fairly common finding in patients with hypertension . The murmur is associated with the expansion of the aorta and the presence of atherosclerotic changes in its wall, which is accompanied by turbulent blood flow.

If the systolic murmur is heard at the apex, is carried to the left axillary region and is combined with a weakening of the first tone and an increase in the size of the left atrium, we are talking about relative mitral valve insufficiency.

Arterial pulse

The arterial pulse with SPAH is rare, regular, full, intense, large.

Tachycardia and arrhythmias are often detected (during the stage of LV decompensation, as well as due to the development of electrolyte disturbances).

Arterial pressure

Blood pressure measurement is key in the diagnosis of SPAH. Hypertension is diagnosed when blood pressure is above 140/90 mm. Hg Art. Characterized by a persistent increase in diastolic pressure, a malignant course of hypertension with high blood pressure numbers.

Kidney examination necessary, first of all, to exclude some symptomatic (renal) hypertension. The method of palpation of the kidneys in some cases makes it possible to detect kidney enlargement (polycystic disease, pyelonephritis, urolithiasis complicated by hydronephrosis, etc.).

Auscultation of renal vessels makes it possible to detect systolic noise in the projection of the renal arteries to the anterior abdominal wall , caused by their stenosis, which gives rise to a more in-depth study of the patient for renovascular hypertension.

Neurological research. When conducting a general examination of a patient with hypertension, one should always remember the need to identify focal neurological symptoms (paresis, paralysis, smoothness of the nasolabial fold, deviation of the tongue, pathological reflexes, nystagmus, etc.).

Data from additional research methods.

ECG:

ECHO-KG: signs of LV hypertrophy

X-ray of the OGK: signs of left ventricular hypertrophy

Daily blood pressure monitoring: Blood pressure≥140 mm Hg. art., blood pressure≥90 mm Hg. Art.

Duplex study of the renal arteries:

Angiography of the renal arteries: signs of renal artery stenosis

Fundus examination: hypertensive retinopathy (narrowing of arteries, dilation of veins)

Additional methods allowing us to clarify the genesis of symptomatic arterial hypertension. If symptomatic renal hypertension is suspected, it is necessary to conduct additional research methods aimed at identifying renal pathology.

Renal eclampsia syndrome

This (eclampsia - Greek outbreak, sudden occurrence) is a convulsive syndrome.

Risk factors

· Edema syndrome

Symptomatic renal arterial hypertension

Contribute to development:

Hypervolemic cerebral edema

Increased intracranial pressure

Causes:

Glomerulonephritis

Nephropathy of pregnancy

Clinical picture.

Preeclampsia: characterized by cerebral syndrome caused by cerebral edema, its characteristic manifestations: headache, nausea vomit, fog before the eyes, decreased or impaired vision. P increased muscle and mental excitability, motor restlessness: decreased hearing loss, insomnia, drowsiness, lethargy.

Extreme manifestation of cerebral syndrome – angiospastic encephalopathy ( eclampsia). An attack of eclampsia is provoked loud sound, bright light and other external influences.

The main symptoms of eclampsia: after a scream or a noisy deep breath, first tonic and then clonic convulsions of the muscles of the limbs, respiratory muscles and diaphragm appear; total loss consciousness; cyanosis of the face and neck; swelling of the neck veins, pupils are wide, foam flows from the mouth, breathing is noisy, pulse is rare, blood pressure is high.

Objective data:

Consciousness in preeclampsia is inhibited,

with eclampsia there is no consciousness, the position is passive

Pale skin

Swelling of the face, limbs, torso

Tonic and clinical seizures

Tongue bitten

Foaming at the mouth

Swelling of the jugular veins

Hard eyeballs

Pupils are dilated and do not respond to light

Noisy, rare breathing, Kussmaul breathing (as a result of high ICP and cerebral edema)

High blood pressure

Bradycardia (as a consequence of high ICP and cerebral edema)

Data from additional research methods

UAC: within normal limits or hypochromic anemia associated with the underlying disease, accelerated ESR

OAM: proteinuria, high density urine, hyaline casts

Blood pressure measurement: high blood pressure

ECG: signs of LV overload and bradycardia

Fundus examination: papilledema, papilledema

Spinal tap: high blood pressure