From Big Medical Encyclopedia

EKLAMPSYYa (eclampsia; Greek eklampsis flash, sudden emergence) — the severe form of late toxicosis of pregnant women which is characterized by sudden emergence of spasms and a loss of consciousness.

AA. it is known to obstetricians since ancient times. Hippocrates in 4 century BC described the disease of pregnant women similar to attacks of epilepsy. Egyptians e the purpose of prevention of tongue biting during attacks E. inserted a small piece of a tree between jaws of the woman. In 1668 the fr. obstetrician F. Mauriceau for treatment E. offered bloodletting. Big contribution to studying E. domestic scientists A. Ya. Krassov-sky, V. V. Stroganov, etc. brought.

Frequency E. in our country, according to V. N. Vlasov-Denisov who generalized material of 1 020 877 childbirth for 1917 — 1947 made 0,74% of total number of childbirth. In the subsequent frequency E. decreased and in 70 — made the 80th, according to different researchers, 0,05 — 0,1% of total number of childbirth. According to the aggregated statistical data published by I. I. Yakovlev (1953), the eclampsia arose at the time of delivery in 45,2 — 62,8% of cases, in a puerperal period in 22,6 — 30,5% and during pregnancy in 8,5 — 24,2% of cases. In the last 10 — 15 years nearly a half of all cases E. it falls on the period of pregnancy that is connected using effective medicamentous therapy and aneste-ziol. grants in labor at women with late toxicosis of pregnant women. AA. develops more often at primapara, preferential young women (up to 30 years). However dependence of frequency E is noted. from klimatogeografichesky conditions. So, in a temperate climate the disease develops at primapara, in the conditions of hot climate more often — at multipara. Sharp weather changing, especially often observable in northern areas, promote emergence E., therefore in the southern regions of the country the frequency of emergence E. it is less, than in northern.

On time of emergence distinguish an eclampsia of pregnant women, an eclampsia of women in labor and a puerperal eclampsia. Allocate a transitional form of an eclampsia, for a cut developing of attacks is characteristic during pregnancy and their repetition at the time of delivery or developing of attacks at the time of delivery and their repetition after the delivery, and also a recurrent form of an eclampsia, at a cut after the period of the wellbeing lasting several days or weeks there is a resuming of attacks. Depending on preferential disturbance of functions of this or that body allocate cerebral, hepatic and renal (an eclamptic pseudouremia) forms of an eclampsia.

Etiology and pathogeny. Emergence E. it is connected with pregnancy

(see). Leading role in development E. belongs to disturbance of the adaptable mechanisms of an organism connected with change of reactivity of c. N of page, including its vegetative departments. The role of a psychogenic factor in development E. Rol of neurogenic factors in development of late toxicoses does not raise doubts., and in particular E., confirm the following data:

Pris Tupov E. emergence at insufficient anesthesia of obstetric operations at pregnant women and women in labor with late toxicosis of pregnant women, reduction of frequency E. as a result of use of a method of Stroganov (see below) and the modern principles of treatment directed to elimination of nervous and vascular reactions (use of the medical and guarding mode, sedative, anticonvulsant and antispasmodics). It is confirmed also by changes of the electroencephalogram, to-rye appear long before developing of toxicosis of pregnant women and remain at all forms of late toxicosis. The obtained data confirm disturbance of a condition of subcrustal structures, first of all a diencephalon, with the subsequent distribution patol. process on other subcrustal formations and bark of a great brain. Many researchers consider late toxicosis of pregnant women as the corticovisceral disease having lines of neurosis.

Major pathogenetic factors E. the hemodynamic disturbances caused by considerable decrease in volume of the circulating blood, hl are. obr. plasmas, due to increase in permeability of a vascular wall, circulator disturbances in various vascular pools, especially a brain and system of uteroplacental blood circulation. Exit of a liquid fraction of blood from a vascular bed in fabric as a result of increase in permeability of a vascular wall, disturbance of water and electrolytic balance, increase in hydrophily of fabrics, decrease in the oncotic pressure caused by a hypoproteinemia is the leading reason of a hypovolemia. The disturbances of vascular permeability and development of a hypoxemic state characteristic of this pathology are considerably caused by shifts of oxidation-reduction balance in nonprotein thiol - disulfide and the expert-korbatnoy systems of blood, and also dissociation of lipoprotein complexes. In development E. the generalized spasm of arterioles and capillaries of vitals with disturbance of microcirculation (see) and change of the rheological properties of blood (strengthening of aggregation of erythrocytes, decrease in content of antithrombin III, etc.) promoting the disseminated intravascular blood coagulation are of great importance (see. Hemorrhagic diathesis), hypoxias (see) fabrics and to a metabolic acidosis (see). Are a consequence of the listed disturbances decrease disintoxication belkovoobrazovatelny, glikogenoobrazovatelny and a mochevinoobrazovatelny liver of functions, and also the reduction of glomerular filtering in kidneys leading to a delay of sodium and excess liquid, a proteinuria. The hypoxia of tissue of kidneys is followed by emission of a renin that in turn (by means of increase in formation of angiotensin) promotes progressing of a vascular spasm and further increase in the ABP. Functional, and then and morfol. changes develop also in a brain, a myocardium, a placenta. Strengthening of frustration of cerebral circulation at women with late toxicosis of pregnant women against the background of excess fluid accumulation promotes a hypoxia of a brain, development of a convulsive syndrome and mental disturbances, and the wet brain caused by a hypoxia is the leading reason of the coma (eclamptic coma) arising later an attack of spasms.

In recent years many researchers began to attach great value in developing of toxicoses of pregnant women, and in particular E., to changes of immune system. It is supposed that at normal pregnancy the placenta is covered with a layer of the sialomutsin performing protective function (see Mucin). The insufficiency (exhaustion) of a sialomutsin arising at matochnoplatsentarny ischemia leads to receipt in blood of mother of the antigens of a placenta and fruit causing a sensitization of an organism of the pregnant woman, development of antibodies and formation of cell-bound immune complexes antigen — an antibody (see Antigen — an antibody reaction) not only to fabrics of a placenta and fruit, but also to tissues of own vitals — to kidneys and a liver. A certain role in development E. plays a histamine (see) that is confirmed by similarity of attacks of eclamptic spasms to histamine shock, and also falloff of enzyme of diaminoxidase (see) at women with an eclampsia. As a result of difficult immunogematol. shifts in an organism of mother and a fruit corticovisceral, vascular and hormonal relationship is broken, insolvency of an uteroplacental barrier appears.

Thus, pathogeny E. finds strong likeness with a pathogeny of other forms of late toxicosis, and first of all a nephropathy of pregnant women (see). However at E. disadaptation of an organism and disintegration of the vast majority of its functions is more expressed that connect with genetic predisposition.

Pathological anatomy. Characteristic for E. defeat of vascular system and existence of intravascular coagulation is. The segmented spasm and dilatation of small arteries and arterioles, signs of a hyperpermeability of vascular walls (perivascular hypostasis, hemorrhages, subendothelial deposits of fibrin), and also formation of fibrinous blood clots in vessels of a micro circulator bed are noted. Prevalence of thrombosis depends on weight E. At placental detachment, edges it can be observed at E., an intravascular blood coagulation is most expressed and is followed by massive bleedings, to-rye can lead to a lethal outcome. Defeat of vessels and an intravascular blood coagulation are the cornerstone morfol. changes of internals (liver, kidneys, brain, lungs, etc.) *

Changes of a liver at E. are not identical. In typical cases the liver is slightly increased in sizes. Under the glissonovy capsule (a fibrous cover, T.), is more often in the right hepatic lobe, there is a set of krupnopyatnisty (landkartoobrazny) hemorrhages. Sometimes they merge, otslaivat a glissonova the capsule and form a hematoma, edges can be complicated by a hemoperitoneum (see). On a section a liver dim, motley, with hemorrhages and the light yellow centers of a necrosis that causes its motley look. Microscopically the centers of a necrosis are located preferential on the periphery of segments. Proteinaceous and fatty dystrophy of hepatocytes, disturbance of a frame and lobular structure of tissue of liver, a circulatory disturbance, accumulations of hepatocytes in a gleam of hepatic veins are noted. The specified changes can be reversible. In hard cases there is a progressing massive necrosis of a liver (see. Toxic dystrophy of a liver). Cirrhosis (see) can be the result of these disturbances. Sometimes changes in a liver are insignificant { single fibrinous blood clots in sinusoids) or absolutely are absent.

Kidneys are a little increased. At histologic and electronic microscopic examination increase in the sizes of renal little bodies, hypostasis of capillary loops of balls, narrowing or full closing of their gleam owing to swelling and vacuolation of endothelial cells (a so-called glomerular and capillary endotheliosis), a nek-swarm the thickening of a basal membrane caused by adjournment in a subendothelial layer of electronic and dense material is defined (the last is available as well in endothelial cells). By means of immunohistochemical methods it is established that these deposits contain fibrinogen and its derivatives, immunoglobulins (IgM, IgG), sometimes a complement. These data allowed to assume that at the heart of damage of kidneys at E. either intravascular fibrillation, or immune disturbances can lie. Mezan-gialny cells of a giperplazirovana are also hypertrophied. In an epithelium of renal tubules symptoms of proteinaceous dystrophy constantly come to light (see), obstruction can be observed by derivatives of protein of collective renal tubules, the quantity and volume of cells of a periarterial pad increases. The described changes in most cases are reversible. Seldom at E. there is a bilateral necrosis of cortical substance of kidneys, to-ry is usually combined with thrombosis of branches of renal arteries. Kidneys at the same time are slightly increased, flabby; their capsule is strained. Bark on a section sharply eminates, has yellowish or gray color. The large merging centers of a necrosis are separated from surrounding fabric by a hemorrhagic nimbus. Sometimes also a part of marrow is exposed to a necrosis.

At E. hypostasis, a hyperemia and a focal anemia of tissue of brain are found. In bark of a great brain, basal kernels and the varoliyevy bridge (the bridge of a mesencephalon, T.) often pete-hialny and focal hemorrhages come to light. Microscopically along with hemorrhages, perivascular and pericellular hypostasis widespread thrombosis, fibrinoid swelling and a fibrinoid necrosis of walls of small vessels, dystrophic changes of nervous cells, the small centers of a necrosis of tissue of brain are defined.

In hard cases E. defeat of organs of sight is noted: in patol. process all departments of a choroid (a uveal path), retinas, an optic nerve, a conjunctiva are involved. Microthromboses, hypostasis of walls and perivascular hypostasis of small vessels of eyes are noted a plethora, staz; special value has the spasm of arterioles and hypostasis of a retina promoting dystrophy of nervous cells of a ganglionic layer, a necrosis and amotio of a retina.

In a myocardium dystrophic changes of cardiomyocytes are observed, it is frequent — subendocardial hemorrhages in papillary muscles and an interventricular partition. Hemorrhages in the carrying-out system of heart can become the reason of a decompensation of cordial activity and a lethal outcome.

Changes in lungs at E. are caused by circulator frustration and the aspiration of gastric contents connected with the disturbance of normal function of the lower esophageal sphincter arising during pregnancy — a so-called syndrome of Mendelssohn (see the Anaesthesia). The acid and aspiration syndrome of Mendelssohn is followed by necrotic changes of all departments of a bronchial tree. In lobar bronchi are usually observed focal, and in intra lobular bronchial tubes and bronchioles — total circulator necroses. In lungs hypostasis, hemorrhages, swelling of an endothelium of capillaries, an intravascular blood coagulation, hyaline membranes, sometimes a vascular embolism by cells of a sincytium, a vorsinama of a placenta or hepatocytes, and also signs focal (acinous, lobular, segmented) serous and purulent pneumonia are noted. Further at patients with E. in lungs the perifocal serous and hemorrhagic, purulent or fibrinous inflammation, the extensive centers of a necrosis can develop.

A spleen and limf, nodes several giperplazirovana, are full-blooded.

Cortical substance almost does not contain lipids in adrenal glands; it is possible to find hemorrhagic heart attacks of adrenal glands and necroses of a hypophysis.

Changes in a placenta are similar to changes at other forms of late toxicosis of pregnant women (see the Placenta), however differ in bigger prevalence. White and red heart attacks of a placenta, massive deposits of fibrinoid in the field of a basal deciduous cover and a fetal part of a placenta, fibrinferments of intervillous space are most often observed. Trunk and trailer (secondary) vorsina of chorion contain few blood vessels, are sclerosed. It is followed by reduction of content of RNA, decrease of the activity of oxidation-reduction enzymes, desquamation and death of a sincytium vorsin, emergence in these sites of fibrinoid substance that as a result leads to decrease in trophic function sin-tsitiotrofob a last. In arterioles decidual (deciduous, T.) covers the lipoidosis, plasmatic treatment, fibrinoid changes up to a necrosis, fibrinferments develops. Signs of a delay of maturing of chorion — identification on a surface

vorsin Langkhans's cells are noted (see. A trophoblastic disease), characteristic of early durations of gestation, and in a stroma vorsin — Kashchenko's cells — Hofbauera (see the Placenta). Along with the specified changes increase in quantity well vaskulyarizovan-ny small secondary, or trailer, vorsin is observed, on a surface to-rykh the syncytial small knots of proliferative type testimonial of the expressed compensatory and adaptive reaction are formed. Lymphoid and cellular infiltration in a placenta is described, to-ruyu regard as manifestation of immune disturbances in system mother — a fruit. Quite often at E. there is premature placental detachment (see), the cut is a sign a retroplacental hematoma.

Clinical picture. In development E. allocate a preeclampsia (eclampsism), edges, as a rule, precedes an eclampsia. The preeclampsia develops against the background of a nephropathy of pregnant women and is caused by disturbance of cerebral circulation and wet brain. Patients to symptoms of a nephropathy of pregnant women have hypostases, hypertensia, a proteinuria (see the Nephropathy of pregnant women) — the painful headache, feeling of weight in the head, dizziness, separate visual hallucinations in the form of spangles, a golden shower, multi-colored circles, the suppressed mood, alarm, internal tension, slackness, an adynamia, impossibility to concentrate, a visual disturbance (flashing of front sights, fog, a veil before eyes, deterioration in sight join up to its short-term loss), motive concern, easing of memory, drowsiness. At patients pains in an anticardium, nausea, vomiting, a diarrhea are observed. There is puffiness of the person, cyanosis of skin and mucous membranes. Duration of a preeclampsia (of several minutes till several o'clock, it is rare — weeks) and expressiveness of symptoms are various. In an attack E. allocate three the following one after another period. The attack usually begins with small fibrillar reductions of face muscles and upper extremities, to-rye proceed to 30 sec. Then there comes the period of tonic spasms, duration to-rogo makes 20 — 25 sec. It is followed by tonic spasms (see) all skeletal muscles and breath holding up to its dead stop, and also strengthening of cyanosis, expansion of pupils and a loss of consciousness. In the final period of an eclamptic attack, to-ry lasts of 40 sec. to

1U2 — 2 min., clonic myotonia of a trunk, top and bottom extremities appear; there is a recovery of breath (irregular, hoarse in the beginning), from a mouth foam is emitted. Spasms gradually weaken and stop. All attack E. 3 min. proceed from 1V2 to 2kh/2, sometimes, quite often is followed by fervescence and bradycardia. After the termination of spasms the patient continues to be in coma (eclamptic coma), a cut can proceed of several seconds and minutes till several o'clock and even days. During an eclamptic coma the diuresis is, as a rule, reduced up to an anury, arterial hypertension remains (see arterial hypertension). After an attack of an eclampsia patients are sleepy, there can be a devocalization of consciousness (see Devocalization) which is replaced on a nek-swarm time by an adynamy (see. Asthenic syndrome). Characteristic for E. amnesia of the period preceding an attack is. Sometimes against the background of unconsciousness the new attack E develops. In some cases E. proceeds without spasms, and the patient falls into coma at once (a convulsiveless form E.). Sometimes attack E. it is limited only to fibrillar twitchings of muscles.

Depending on duration of coma, frequency of attacks and duration of intervals between them, level and ABP loudspeakers, conditions of function of a liver, kidneys, cardiovascular system allocate easy, moderately severe and heavy forms E. Easy form E. it is characterized by bystry recovery of consciousness after an attack, decrease in the ABP, increase in a diuresis and normalization of biochemical indicators of blood (decrease in level of residual nitrogen, urea and creatinine, increase in a clearing coefficient of urea, etc.). At E. moderately severe coma proceeds

no more than 2 — 3 hour. Further single attacks of spasms can repeat. They are usually preceded by increase in the ABP and reduction of a diuresis. The proteinuria does not accrue, renal failures, a liver, cardiovascular system are expressed moderately and are gradually normalized. Under the influence of the carried-out therapy the general condition of the patient improves, biochemical indicators are normalized. Carry E to moderate severity., at a cut after the only attack of spasms the headache, hypertensia, decrease in a diuresis, periodic deterioration in sight remain. At a severe form E. duration of coma after attacks makes several hours (or days), on its background attacks of spasms proceed, the diuresis decreases, the proteinuria accrues and the ABP increases. Bystry decrease in the high ABP against the background of coma is also a sign of a severe form E. also it is, as a rule, observed at a hematencephalon. Carry E to a severe form. with a large number of eclamptic attacks when there is no improvement of the general condition of the patient, increase in a diuresis is not noted and hypertensia, and also a convulsiveless form E remains., at a cut the patient falls into long coma at once.

For assessment of severity of an eclampsia use Vittlin-ger's scale, with the help consider a cut and estimate in points expressiveness of hypostases, an increase of body weight, degree of a proteinuria, level of arterial hypertension, a diuresis, and also subjective feelings.

Especially hard E. proceeds at the accompanying somatopathies, such as idiopathic hypertensia, chronic glomerulonephritis and pyelonephritis, diabetes mellitus, and also at the women who had encephalitis, meningitis, hepatitis, a rheumatic carditis.

In process of progressing E. disorder of functions of vitals accrues that can lead to life-threatening complications — to a hematencephalon, amotio of a retina (see) and loss of sight, premature placental detachment, an acute renal failure (see), a liver failure (see), respiratory insufficiency (see). At women with E. there can be bleedings at the time of delivery and in an early puerperal period, and also pneumonia and septic complications. Rather seldom (approximately in 2 — 4% of cases) at E. psychoses develop. Their emergence is connected with intoxication, disturbances of a hemodynamics and lpkvorodinamika, a hypoxia of a brain. As a rule, psychoses are observed at primapara and usually arise after several attacks E. or during the period between attacks, is more rare — in the absence of attacks, being shown by disorders of consciousness. Most often twilight stupefaction meets (see), a cut differs from similar psychosis at epilepsy in lack of spiteful affect, aggression, impulsiveness. At the beginning of psychosis there can be plentiful visual hallucinations of stsenopodobny character, to-rye unlike hallucinations at epilepsy have no ecstatic character, have no religious contents. Twilight stupefaction is replaced, as a rule, by devocalization. Psychosis proceeds 2 — 12 days, is more rare — several weeks and comes to an end usually with recovery, Krom is preceded by the an adynamy (see. Asthenic syndrome) accompanied with easing of memory on current events. Permanent loss of memory on events of the period of psychosis, on childbirth, the previous circumstances is characteristic. Recovery of mental activity happens slowly. Heavy and permanent mental disturbances in the form of amnesia (see) or paramnesias (see), aphasias (see), alexias (disorder of reading), agraphias (disturbance of ability to write), affective frustration are observed rather seldom.

The diagnosis is made on the basis by a wedge, pictures, existence in the anamnesis of the previous stages of late toxicosis of pregnant women (E. can be not only end of a heavy nephropathy of pregnant women, but also to develop against the background of it is long the current nephropathy of the I—II degree), results Ophthalmolum. and lab. researches.

At Ophthalmolum. a research hypostasis, an inflammation of a retina, hemorrhage in an eyeground, in hard cases — amotio of a retina is defined. At biochemical researches increase in activity of enzymes of glycolysis — zymohexase, phosphohexaisomerases, a lactate dehydrogenase and enzymes of interamination — asparaginic and alanine transaminases, decrease in the general protein content, increase in content in blood of a histamine, serotonin is noted. For definition of severity E. use indicators of EEG, results of functional trials of a liver and kidneys.

Differential diagnosis is carried out with epileptic seizures (see Epilepsy), an uremic, diabetic and hepatic coma (see), hysteria (see). At differentiation E. with epilepsy it is necessary to consider data of the anamnesis (existence of attacks before pregnancy) and emergence of harbingers of epileptic seizures, absence patol. changes in urine, results Ophthalmolum. and lab. researches. Epileptic seizures can be observed during all pregnancy unlike attacks E., to-rye are observed at the end of pregnancy, in time and after the delivery; after epileptic seizures there occurs rather bystry improvement of a condition of the patient. Diagnosis becomes complicated if the epileptic seizure for the first time arises against the background of late toxicosis of pregnant women.

Differential diagnosis E. with the uraemia (see) proceeding with spasms and a coma is more difficult because at these two states hypostasis of a brain is the cornerstone of development of spasms (see Hypostasis and swelling of a brain). Uraemia develops at the persons who transferred an acute diffusion glomerulonephritis (see) has a long current with aggravations, proceeds with headaches, nasal bleedings, anemia and a skin itch. Emergence of attacks of spasms at uraemia is preceded by the expressed deterioration in the general condition of the patient. The stomacace and an ulitis, formation of ulcers on a mucous membrane of a stomach, small and large intestine are characteristic of uraemia a smell of urine from a mouth.

At a diabetic coma the hyperemia of the person, a smell of acetone from a mouth, hypotonia of eyeglobes, frequent small pulse, falling of the ABP, deep and frequent breath, a hyperglycemia, in urine — sugar, acetone and ketone bodies, and also rather bystry improvement of a condition of the patient against the background of the corresponding therapy are observed.

The hepatic coma develops against the background of a heavy liver failure at women with diseases of a liver. At patients jaundice is noted, dispeptic frustration, a hemorrhagic syndrome, changes in urine are absent.

At hysteria consciousness between attacks of spasms is kept, the general condition of the patient satisfactory, patol. there are no changes in urine.

Treatment. For treatment of an eclampsia a number of methods and schemes which basis actions for reduction of hypostases, decrease in the ABP, reduction of excitability of a nervous system are was offered. In 1897

V. Stroganov offered the method of treatment including a complex of the actions directed to elimination of any irritation and pains, stopping and the prevention of attacks, improvement of function of the major bodies, careful delivery. Patients were placed in the separate darkened well aired chamber, eliminated light, sound and tactile irritants, made anesthesia of all manipulations (injections, catheterizations, vaginal examonations, etc.) by means of an easy inhalation chloroformic anesthesia. In 1928 V. Stroganov improved a method:

for the purpose of the prevention and stopping of spasms applied morphine, Chlorali hydras, and also the magnesium sulfate having sedative, somnolent, hypotensive, diuretic effect. Also other methods were offered (Brovkina, Salgannik, the Dublin method), to-rye in a crust, time are not applied.

In a crust, time treatment of an eclampsia is spent taking into account the major pathogenetic factors and is defined by disease severity and possible complications. All actions are directed to elimination of a generalized vasospasm, hypovolemia, decrease in the ABP, fight against intoxication, improvement of microcirculation, on correction of water and electrolytic disturbances and acid-base equilibrium and are held taking into account associated diseases. The principles of the medical and guarding mode developed by V. V. Stroganov directed to decrease in excitability of c are observed. N of page. The patient is placed in intensive care unit, exclude external (light, sound) irritants and carry out constant overseeing by a condition of mother and a fruit. Make control of a diuresis, breath, sight, function of cardiovascular system and c. N of page. All manipulations (injections, vaginal examonation, etc.) are carried out under anesthetic (nitrous oxide with oxygen) or against the background of neuroleptics. In a complex of the anesthetizing actions the patient with severe forms of late toxicosis, including and an eclampsia, include a long peridural analgesia Trimecainum or lidocaine, edges it can be continued at the time of delivery and after operation of Cesarean section. Stopping of a convulsive attack E. also 2 ml of 0,5% of solution of diazepam or 1 ml of 2,5% of solution of isopromethazine are reached by immediate intravenous administration of 1 ml of 2% of solution of Promedolum. Necessary sedation is gained from intravenous administration

2 — 4 ml of 0,25% of solution of Droperidolum and 2 ml

of 0,5% of solution of diazepam. The last can be replaced with Suprastinum, Seduxenum, isopromethazine or Dimedrol. The specified drugs eliminate convulsive readiness, cause the general block, reduce the ABP and reaction to external irritants, kill a headache, improve sight. For strengthening of hypotensive effect along with Droperidolum and diazepam appoint an Euphyllinum, Dibazolum, a papaverine, gan-glioblokator (Pentaminum, benzogek-sony, gigrony, etc.), and also enter glyukozonovokainovy mix. Dehydrational therapy includes purpose of furosemide (lasixum), Euphyllinum, diuretic action to-rykh amplifies against the background of Droperidolum. For elimination of acidosis enter 4 — 5% solution of hydrosodium carbonate. For the purpose of cerebral decompression after elimination of acidosis include intravenous administration of a mannitol (30 — 60 g) in a complex of dehydrational therapy, however it is necessary to appoint it only after elimination of acidosis; use of a mannitol is contraindicated at an anury.

Along with dehydrational therapy make compensation of volume of the circulating liquid. For this purpose, and also for the purpose of elimination of a hypoproteinemia after stopping of spasms and under control of residual nitrogen enter solutions of albumine, a protein, solution of plasma, and also the polyionic solution containing potassium, sodium, calcium, magnesium, glucose and insulin. Normalization of microcirculation and rheological properties of blood reach introduction of a reopoliglyukin, Polydesum, Haemodesum, glyukozonovokainovy mix with insulin, Dibazolum, a papaverine, an Euphyllinum, Nospanum. For maintenance of function of a liver use Essentiale, chloride of sincaline, sorbite, legalonum, LIV-52, methionine, and also appoint fermental drugs — Pancreatinum, festal, panzinorm, etc. Disintoxication therapy along with introduction of Haemodesum, Polydesum, Neocompensanum, etc. includes hemosorption (see Hemosorption, t. 10, additional materials). Normalization of oxidation-reduction processes and desintoxication is promoted by introduction of 5% of solution of Unithiolum (1 ml on 10 kg of body weight) and ascorbic to - you. The patient with a severe form E. at not stopped attacks of spasms, a long eclamptic coma, acute respiratory and cardiovascular insufficiency the intubation of a trachea and artificial ventilation of the lungs is shown (see. Artificial respiration).

Magnesium sulfate, despite about-tivos at road, the spasmolytic, hypotensive, somnolent, cholagogue effect, most of clinical physicians at the time of delivery do not use in connection with the oppressing action this drug on sokratitelny function of a uterus.

Tactics of conducting childbirth at an eclampsia has paramount importance. For elimination of a hypoxia of a fruit use Sygethinum, glucose, ascorbic to - that, Unithiolum, cytochrome C, etc., and also hyperbaric oxygenation. At the same time spontaneous delivery, obstetricians usually aim at Krom, is not always the best escaping of the situation. The long course of childbirth which is quite often observed at E., aggravates hemodynamic and metabolic frustration and dysfunctions of bodies of mother and a fruit, increases danger of developing of bleeding in afterbirth and early puerperal the periods, and also renal, renal and hepatic and respiratory failure. Therefore at inefficiency of an intensive care it is necessary to resort to Cesarean section (see). Absolute indications to its carrying out are ongoing attacks, coma, hemorrhage in an eyeground, an inflammation and amotio of a retina, an anury or an oliguria with a cylindruria and a proteinuria. The issue of time of operation is resolved individually taking into account weight of a condition of the patient and results of treatment. An optimum way of anesthesia is the endotracheal anesthesia with artificial ventilation of the lungs.

In the puerperal (postoperative) period the intensive care proceeds taking into account change in a condition of the patient and data a lab. researches. For prevention of complications, including acute renal and a renal liver failure, and also inflammatory and septic processes the paramount importance has timely and adequate compensation of blood loss with use of the stabilized blood in labor, an early puerperal period and during Cesarean section.

Attentive overseeing of the patient and timely correction of disturbances allow to prevent possible complications, to reduce the frequency of lethal outcomes and to improve recovery of function of vitals.

The forecast for mother and a fruit is defined by degree morfol. and functional disturbances of vitals — a liver, kidneys, a brain, adrenal glands and a placenta. For the forecast duration of coma after attacks of spasms matters. If the coma proceeds several hours and the more so days that testifies to Glouxsideways disturbance of cerebral circulation, wet brain and possible hemorrhage, forecast adverse. A certain predictive value has also quantity of attacks E. Adverse predictive signs are the high level of diastolic pressure, and also the expressed and long hypotension after attacks. Existence of the accompanying somatopathies worsens the forecast.

Prevention consists in timely and intensive treatment of the accompanying extragenital diseases, and also late toxicoses of the pregnant women previous E. If the nephropathy of pregnant women does not respond to treatment, early delivery is shown.

See also Toxicoses of pregnant women. Bibliography: Bekkers. M. Patologiya of pregnancy, JI., 1975; B r about in to and D. P's N. Eclampsia, M., 1948; B e with about S. G.'s N, etc. Maintaining pregnant women with is increased

by ny risk and an intensive care of the newborn, the lane with English, page 263, M., 1979; Grishchenko V. M. Modern diagnostic methods and treatments of late toxicosis of pregnant women, M., 1977;

Zarudin V. V., etc. Morphological changes in a placenta at late toxicoses of pregnant women, Arkh. patol., t. 38, «N» I, page 33, 1976; Ledenevao. A. Morphological changes of lungs at terminal states in cases of death from an eclampsia, in the same place, t. 42, No. 1, page 33, 1980; Leushs. Page and Tymoshenko L. V. Severe forms of late toxicoses of pregnant women, Akush. and ginek., No. 8, page 56, 1981;

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