Volume 02 Issue 04-2022
1
International Journal of Medical Sciences And Clinical Research
(ISSN
–
2771-2265)
VOLUME
02
I
SSUE
04
Pages:
01-06
SJIF
I
MPACT
FACTOR
(2022:
5.
705
)
OCLC
–
1121105677
METADATA
IF
–
5.654
Publisher:
Oscar Publishing Services
Servi
ABSTRACT
The article under discussion depicts peculiarities of varicose vein disease in pregnancy. Venous disease in women
often complicates pregnancy, childbirth and the postpartum period. Venous insufficiency complicates pregnancy,
delivery and postpartum period and leads to increased maternal morbidity and mortality. The author of the article
considers that correction of placental dysfunction, especially in the early stages, can significantly improve perinatal
outcomes.
KEYWORDS
varicose vein disease, vascular system, pregnancy, anatomic, premature, amniotic fluid, extremities.
INTRODUCTION
Varicose vein disease (VD) is a disease of the vascular
system of the div. In pregnant women the
occurrence of varicose veins disease is associated
with a slowing down of the rate of blood flow during
pregnancy, as well as with the anatomic features of
the venous system of the lower extremities.
DISCUSSION
Research Article
PECULIARITIES OF VARICOSE VEIN DISEASE IN PREGNANCY
Submission Date:
April 10, 2022,
Accepted Date:
April 15, 2022,
Published Date:
April 21, 2022
Crossref doi:
https://doi.org/10.37547/ijmscr/Volume02Issue04-01
Tilyakhodjaeva Gulbakhor Batyrovna
Senior Teacher Of The Department «Anatomy», Ferghana Medical Institute Of Public Health, Ferghana,
Uzbekistan
Journal
Website:
https://theusajournals.c
om/index.php/ijll
Copyright:
Original
content from this work
may be used under the
terms of the creative
commons
attributes
4.0 licence.
Volume 02 Issue 04-2022
2
International Journal of Medical Sciences And Clinical Research
(ISSN
–
2771-2265)
VOLUME
02
I
SSUE
04
Pages:
01-06
SJIF
I
MPACT
FACTOR
(2022:
5.
705
)
OCLC
–
1121105677
METADATA
IF
–
5.654
Publisher:
Oscar Publishing Services
Servi
Increased venous pressure, decreased rate of blood
flow leads to local metabolic disorders with a shift of
pH to the acidic side and activation of the blood
coagulation system. Venous disease in women often
complicates pregnancy, childbirth and the postpartum
period. The incidence of early and late gestosis (10%),
chronic fetal hypoxia (10%), umbilical cord pathology
(24-26%), untimely outflow of amniotic fluid (22-24%) is
rather high due to varicose veins disease of the lower
extremities, weak obstetrical activity (15%), premature
detachment of the normally located placenta (2%),
postpartum and early postpartum hemorrhages (18%),
postpartum endometritis (7%) [1].
In physiological pregnancy there is stimulation and
activation of the fetoplacental complex, which leads
to an increase in the coagulant potential, almost
doubling the content of all clotting factors against a
decrease in fibrinolytic and anticoagulant activity.
Beginning in the second trimester of pregnancy,
endothelial production and secretion of Willebrand
factor, thromboxane, endothelin-1, thrombomodulin,
and fibronectin into the blood increased, suggesting
the formation of an endothelial dysfunction syndrome
in
the
feto-placental
complex
even
during
physiological pregnancy [8].
Hemostasis in pregnant women with varicose veins is
a serious problem, and the effect of drugs improving
microcirculation and regulating angioprotective
effects on its parameters has been little studied. It is
of great scientific and practical interest to study the
effect of drugs affecting endothelial dysfunction
being introduced into clinical practice. Pregnant
women with varicose veins have a generalized
impairment of all endothelial functions accompanied
by the impaired regulation of vascular tone and
permeability
and
increased
procoagulant,
proaggregant, antifibrinolytic and anti-inflammatory
activity of the endothelial layer. Chronic venous
insufficiency and VF are the most common group of
extragenital cardiovascular pathology in pregnant and
postpartum women, according to different authors -
in 30-50% of women. Varicose veins first appear in 50-
96% of women during pregnancy. Venous insufficiency
complicates pregnancy, delivery and postpartum
period and leads to increased maternal morbidity and
mortality [9].
Pregnancy is often the triggering factor that
manifests or causes symptoms of venous insufficiency
and IBD. This association (venous insufficiency and
pregnancy) is characterized by a rapid onset of
symptoms and their partial regression after delivery.
Treatment during pregnancy is aimed at elimination of
symptoms and prevention of complications. The
development of chronic venous insufficiency and VD
during pregnancy is usually explained by the pressure
of the pregnant uterus on the inferior vena cava and
iliac vein. Persistent venous dysfunction in the weeks
after delivery suggests that changes in venous
function in pregnancy are influenced not only by
venous compression by the pregnant uterus, but also
by other factors. Some authors have studied the
effects of sex hormones on the venous wall, but did
not find a relationship between the development of
chronic venous insufficiency and the plasma
concentrations of estradiol, estriol or progesterone.
However, 17% of women with normal pregnancy
developed pathological venous insufficiency and VF.
At the same time, outside of pregnancy we found
almost no or very insignificant concentrations of
estrogen receptors and significant concentrations of
progesterone receptors in the great saphenous vein
wall taken after venectomy for varicose veins.
Consequently, sex hormones can directly affect the
vein wall through the classical receptor pathway [7].
Volume 02 Issue 04-2022
3
International Journal of Medical Sciences And Clinical Research
(ISSN
–
2771-2265)
VOLUME
02
I
SSUE
04
Pages:
01-06
SJIF
I
MPACT
FACTOR
(2022:
5.
705
)
OCLC
–
1121105677
METADATA
IF
–
5.654
Publisher:
Oscar Publishing Services
Servi
Endothelial dysfunction and changes in hemostasis, in
particular, hypercoagulation, play a significant role in
the development of chronic venous insufficiency.
Endothelial dysfunction leads to changes in vascular
reactivity, activation of intravascular coagulation
cascade and disruption of vascular integrity. The main
markers of endothelial dysfunction are decreased
production of prostacyclin and N0, a relative increase
in thromboxane, and a significant increase in
endothelin-1. Nitric oxide is the "face" of the
endothelium, as it provides in the maintenance of
vascular homeostasis: regulation of vascular tone;
inhibition of adhesion, platelet aggregation and
thrombosis; regulation of proliferation and apoptosis;
regulation of oxidative processes; inhibition of
leukocyte adhesion. Moreover, it regulates all these
processes with "+" sign, i.e., it is one of the most
demanded substances in pathological conditions.
Under the influence of various damaging factors, the
ability of endothelial cells to synthesize N0 decreases,
while the formation of vasoconstrictors is preserved
or increases, i.e., a condition defined as endothelial
dysfunction (ED) is formed [2].
The above changes create a "favorable" environment
for the formation of predominantly chronic placental
dysfunction (PD). In 16-25% of patients with PD there
are manifestations of CHD, chronic venous
insufficiency and pelvic varicose veins. The treatment
of this category of patients presents significant
difficulties, as it can lead to the most severe
complications
in
obstetrics,
thrombosis
and
thromboembolism of the pulmonary artery [4].
Placental dysfunction is the most important problem
of modern perinatology. The frequency of its
detection varies from 3-4 to 45%, the perinatal
morbidity reaches 70%. Despite the intensive use of
the latest methods of diagnosis and treatment,
insufficient placental function remains the leading
cause of high morbidity and mortality of children not
only in the perinatal period, but also at the stages of
subsequent development. At the present stage PD is
considered as a clinical syndrome caused by
morphofunctional changes in the placenta and
disorders of compensatory-adaptive mechanisms that
ensure the functional fullness of the organ. It is the
result of a complex response of the fetus and
placenta to various pathological conditions of the
maternal div and is manifested in a complex of
disorders of transport, trophic, endocrine and
metabolic functions of the placenta, underlying the
pathology of the fetus and the newborn [5].
Primary and secondary PD are distinguished. Primary
PD develops during the formation of the placenta (up
to 16 weeks of gestation) and is most common in
women suffering from habitual miscarriage, as well as
in pregnant women with a history of infertility.
Secondary PD usually occurs after the completion of
placental formation processes and is caused by
exogenous influences, primarily diseases suffered
during pregnancy.
Chronic placental dysfunction (CPD) is a more
frequent pathology, observed in about one in three
pregnant women of the high risk perinatal pathology
group. Perinatal mortality in this group reaches 60%.
Chronic PD is a long-term placental dysfunction, often
with
compensatory
increase
in
its
weight,
pathological immaturity of the villi, focal or diffuse
sclerosis of their stroma, hemorrhages and extensive
infarcts. Depending on the extent of the lesion,
intrauterine hypotrophy develops or fetal death
occurs. Changes occurring in the placenta in CPD,
primarily due to thrombosis of the vessels of the villi
and chorionic villi with subsequent ischemia, fibrin
deposition and the development of infarction, which
Volume 02 Issue 04-2022
4
International Journal of Medical Sciences And Clinical Research
(ISSN
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2771-2265)
VOLUME
02
I
SSUE
04
Pages:
01-06
SJIF
I
MPACT
FACTOR
(2022:
5.
705
)
OCLC
–
1121105677
METADATA
IF
–
5.654
Publisher:
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leads to a violation of placental perfusion and
interaction of the trophoblast with the uterine vessels
of the placental site, making them insensitive to most
medications.
Preclinical diagnosis of fetal abnormalities is an
important task. This is important because early
detection of fetoplacental insufficiency in a number of
cases allows timely corrective therapy. The
development of methods for studying the feto-
placental complex in dynamics allows timely diagnosis
of the main clinical forms of fetal distress - delayed
intrauterine development of the fetus and/or its
chronic hypoxia. Prenatal diagnosis of these
conditions
traditionally
includes
ultrasound
(ultrasound),
ultrasound
Dopplerometry,
also
conducted cardiotocography (CTG), the study of
placental proteins and hormones. Less frequently, a
cervical cytological examination with determination of
the type of smear is performed. The study of the
hemostasis system and markers of endothelial
dysfunction is also relevant in PD.
The action of any pathological factors on the fetus is
mediated through structural and functional disorders
of the placenta, so of great interest is the study of
placental and endometrial proteins, the so-called
"pregnancy zone proteins" that act as hormones,
enzymes, enzymes, receptors, growth factors and
immunoregulatory agents. The study of placental
proteins synthesized by different parts of the placenta
(maternal and fetal) provides a new clinical
perspective on their function and role in the
development of pregnancy. Of the proteins produced
by the placenta, of particular importance are placental
hormones, in particular: progesterone (PG) and its
analogue 17-hydroxyprogesterone (17-OP), chorionic
gonadotropin (CG), placental lactogen (PL), estriol
(E3), cortisol (C), (a)-fetoprotein (AFP).
The definition of the "biophysical profile" of the fetus,
which includes a comprehensive assessment at
ultrasound of 5 parameters: fetal respiratory
movements, motor activity, fetal muscle tone, the
amount of amniotic fluid, non-stress test at
cardiotocography (CTG), has become widespread. Of
great
importance
is
the
identification
and
interpretation of indirect criteria for placental
insufficiency, as well as the search for prognostic
markers of gestational homeostasis disorders, on the
basis of which we could allocate risk groups for the
development of PD and conduct preventive courses
of therapy in these groups. Among them, there are
markers of primary placental insufficiency - placenta
previa and low location of the placenta, placenta
surrounded by a ridge, double lobe or extra placenta,
marginal or sheath attachment of the umbilical cord.
Markers of secondary PD include a placental or
membranous placenta, placental thickening (more
than 5 cm) or thinning (less than 2 cm), dilation of the
intervillous space, placental infarction, abundant or
small fluid flow.
Another method of diagnosing PD, although largely
historical, but no less informative, is the study of
cervical smear types - cytology. Several pathological
types of smears are distinguished. Cornificatory -
hormonal disorders in pregnancy - threat of
termination of pregnancy - mixed vaginal flora,
epithelium of different layers, eosinophilic and
karyopycnotic index (CI) > 50%. Estrogenic - PD,
gestosis, rhesus conflict, threat of termination of
pregnancy significant reduction in cellular elements,
shift towards superficial cells, their isolated location,
CI up to 30-40%, palmar cells reduced or absent. Type
with predominance of deep intermediate cells with
large nuclei - severe gestosis, AP in threatening,
perinatitis - these cells are arranged in groups, the
palatial cells are few or absent. Regressive - PD,
Volume 02 Issue 04-2022
5
International Journal of Medical Sciences And Clinical Research
(ISSN
–
2771-2265)
VOLUME
02
I
SSUE
04
Pages:
01-06
SJIF
I
MPACT
FACTOR
(2022:
5.
705
)
OCLC
–
1121105677
METADATA
IF
–
5.654
Publisher:
Oscar Publishing Services
Servi
perenaturation - isolated cells of all epithelial layers,
the presence of basal and parabasal cells [10].
In recent years, various methods of treating placental
dysfunction have been developed and continue to
improve, but the problem is far from being resolved.
Correction of placental dysfunction, especially in the
early stages, can significantly improve perinatal
outcomes. PD therapy gives a sufficiently positive
effect only at the compensated and subcompensated
stages of the process. PD treatment in the third
trimester has no significant effect on fetal
development, but can improve fetal condition,
increase resistance to hypoxia and prepare the fetus
for delivery. With signs of decompensated fetal PD,
treatment is not considered and early delivery is
considered. One of the indicators of critical fetal
status is zero or diastolic blood flow recorded in the
umbilical artery or fetal aorta by Doppler. The
detection of critical blood flow, as well as changes in
the cardiotocogram ("mute" curve type, areactive
nonstress test) indicate the need for urgent delivery.
Therapy should begin with the treatment of the
underlying disease and the elimination of the
influence of adverse factors. If placental insufficiency
is confirmed and any infectious foci are identified,
specific treatment according to generally accepted
schemes to prevent intrauterine infection against a
broken placental barrier is mandatory [11-15]. Therapy
of the placental barrier must be comprehensive, i.e., it
must include a set of treatment methods. These are
physical
methods
of
influence
(uterine
electrorelaxation, thermal procedures on the peri-
renal area - diathermy, inductothermy), reflexively
relaxing myometrium and expanding vessels;
abdominal
decompression,
which
improves
uteroplacental blood flow; hyperbaric oxygenation,
which provides preservation of respiratory enzyme
activity; medicinal agents. The general directions of
pharmacotherapy for PD are the correction of
endothelial dysfunction, disorders of uteroplacental
blood flow and microcirculation; normalization of gas
exchange in the "mother-placenta-fetus" system;
improvement of placental metabolism; restoration of
impaired cell membrane function. Therapy should be
prolonged, at least four weeks, of which 10-14 days
are spent in hospital.
CONCLUSION
Delivery of pregnant women with IBD, regardless of
the presence of PD, is carried out at no more than 40
weeks, and pregnancy management is carried out
with timely prevention or treatment of PD. The course
and outcomes of amniotomy-induced labor do not
differ from those of self-induced labor. Pregnant
women with IU should be included in the risk group
for the development of PD and timely prevention of
PD should be carried out. All pregnant women with
VD, in addition to a general clinical examination and
routine ultrasound and CTG, should be examined with
fibronectin, placental proteins and homocysteine, as
well as with the hemostasis system and IAS in AF to
predict the development and course of VD.
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–
2771-2265)
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02
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04
Pages:
01-06
SJIF
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MPACT
FACTOR
(2022:
5.
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OCLC
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1121105677
METADATA
IF
–
5.654
Publisher:
Oscar Publishing Services
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