Hypertensive disorders in pregnancy are a leading cause of maternal and fetal morbidity and mortality in India. It is characterized by new onset hypertension and proteinuria after 20 weeks of gestation. The disorder includes gestational hypertension, preeclampsia, and preeclampsia superimposed on chronic hypertension. Symptoms include headaches, visual disturbances, and right upper quadrant pain. Management involves hospitalization, bed rest, blood pressure monitoring, magnesium sulfate administration to prevent seizures, and often early delivery. Untreated hypertensive disorders can lead to serious maternal complications like eclampsia and organ damage as well as fetal growth restriction and death.
ACOG
ACOG 2019 Guidelines
American College of Obstetrics and Gynecology
Practice Bulletin
CVD in pregnancy
Cardiovascular Diseases in pregnancy
Managing heart disease in pregnancy
Managing heart diseases after pregnanacy
post-partum management of heart diseases in pregnancy
ACOG
ACOG 2019 Guidelines
American College of Obstetrics and Gynecology
Practice Bulletin
CVD in pregnancy
Cardiovascular Diseases in pregnancy
Managing heart disease in pregnancy
Managing heart diseases after pregnanacy
post-partum management of heart diseases in pregnancy
The increased cardiac output related to pregnancy can lead to heart failure, and the increased heart rate in the third trimester can lead to ischemic events. The potential obstetrical complications include preeclampsia or other hypertensive related disorders, premature birth, and small-for-gestational-age births.
Preeclampsia is a disorder that is unique to human pregnancy, and the only known cure for this complication is delivery. Preeclampsia affects approximately 4% to 5% of pregnancies . The Preeclampsia Foundation states that: “Globally, preeclampsia and other hypertensive disorders of pregnancy are a leading cause of maternal and infant illness and death. By conservative estimates, these disorders are responsible for 76,000 maternal and 500,000 infant deaths each year.” As is evident from the statement that, preeclampsia is a major contributor to maternal and fetal morbidity and mortality worldwide. In India, the incidence of preeclampsia is reported to be 8-10% among the pregnant women. According to a study, the prevalence of hypertensive disorders of pregnancy was 7.8% with preeclampsia in 5.4% of the study population in India
A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.
The increased cardiac output related to pregnancy can lead to heart failure, and the increased heart rate in the third trimester can lead to ischemic events. The potential obstetrical complications include preeclampsia or other hypertensive related disorders, premature birth, and small-for-gestational-age births.
Preeclampsia is a disorder that is unique to human pregnancy, and the only known cure for this complication is delivery. Preeclampsia affects approximately 4% to 5% of pregnancies . The Preeclampsia Foundation states that: “Globally, preeclampsia and other hypertensive disorders of pregnancy are a leading cause of maternal and infant illness and death. By conservative estimates, these disorders are responsible for 76,000 maternal and 500,000 infant deaths each year.” As is evident from the statement that, preeclampsia is a major contributor to maternal and fetal morbidity and mortality worldwide. In India, the incidence of preeclampsia is reported to be 8-10% among the pregnant women. According to a study, the prevalence of hypertensive disorders of pregnancy was 7.8% with preeclampsia in 5.4% of the study population in India
A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.
Gestetional hypertension, Preeclampsia and Eclampsiasunil kumar daha
Please find the power point on Gestetional hypertension, Preeclampsia and Eclampsia . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Primary Maternal Care: Hypertensive disorders of pregnancySaide OER Africa
Primary Maternal Care addresses the needs of healthcare workers in level 1 district hospitals and clinics who provide antenatal and postnatal care, but do not conduct deliveries. It is adapted from theory chapters and skills workshops from Maternal Care. This book complements the national protocol of antenatal care in South Africa. It covers: booking for antenatal care, assesing fetal growth and wellbeing, hypertensive disorders of pregnancy, antepartum haemorrhage, preterm labour, important medical conditions
The kidneys filter waste and excess fluid from the blood. As kidneys fail, waste builds up.
Symptoms develop slowly and aren't specific to the disease. Some people have no symptoms at all and are diagnosed by a lab test.
Medication helps manage symptoms. In later stages, filtering the blood with a machine (dialysis) or a transplant may be required.
Although the most important causes of kidney injury in late pregnancy are preeclampsia and the associated disorders eclampsia and HELLP (hemolysis, elevated liver enzyme levels, low platelet count) syndrome, they will be discussed with the hypertensive disorders of pregnancy.
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
What is greenhouse gasses and how many gasses are there to affect the Earth.moosaasad1975
What are greenhouse gasses how they affect the earth and its environment what is the future of the environment and earth how the weather and the climate effects.
Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
holes and slow-speed, highly variable, streams whose source regions are
under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
solar wind sources and understand what drives the complexity seen in the
heliosphere. By combining magnetic feld modelling and spectroscopic
techniques with high-resolution observations and measurements, we show
that the solar wind variability detected in situ by Solar Orbiter in March
2022 is driven by spatio-temporal changes in the magnetic connectivity to
multiple sources in the solar atmosphere. The magnetic feld footpoints
connected to the spacecraft moved from the boundaries of a coronal hole
to one active region (12961) and then across to another region (12957). This
is refected in the in situ measurements, which show the transition from fast
to highly Alfvénic then to slow solar wind that is disrupted by the arrival of
a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
This pdf is about the Schizophrenia.
For more details visit on YouTube; @SELF-EXPLANATORY;
https://www.youtube.com/channel/UCAiarMZDNhe1A3Rnpr_WkzA/videos
Thanks...!
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
Deep Behavioral Phenotyping in Systems Neuroscience for Functional Atlasing a...Ana Luísa Pinho
Functional Magnetic Resonance Imaging (fMRI) provides means to characterize brain activations in response to behavior. However, cognitive neuroscience has been limited to group-level effects referring to the performance of specific tasks. To obtain the functional profile of elementary cognitive mechanisms, the combination of brain responses to many tasks is required. Yet, to date, both structural atlases and parcellation-based activations do not fully account for cognitive function and still present several limitations. Further, they do not adapt overall to individual characteristics. In this talk, I will give an account of deep-behavioral phenotyping strategies, namely data-driven methods in large task-fMRI datasets, to optimize functional brain-data collection and improve inference of effects-of-interest related to mental processes. Key to this approach is the employment of fast multi-functional paradigms rich on features that can be well parametrized and, consequently, facilitate the creation of psycho-physiological constructs to be modelled with imaging data. Particular emphasis will be given to music stimuli when studying high-order cognitive mechanisms, due to their ecological nature and quality to enable complex behavior compounded by discrete entities. I will also discuss how deep-behavioral phenotyping and individualized models applied to neuroimaging data can better account for the subject-specific organization of domain-general cognitive systems in the human brain. Finally, the accumulation of functional brain signatures brings the possibility to clarify relationships among tasks and create a univocal link between brain systems and mental functions through: (1) the development of ontologies proposing an organization of cognitive processes; and (2) brain-network taxonomies describing functional specialization. To this end, tools to improve commensurability in cognitive science are necessary, such as public repositories, ontology-based platforms and automated meta-analysis tools. I will thus discuss some brain-atlasing resources currently under development, and their applicability in cognitive as well as clinical neuroscience.
3. Also known as “Toxaemia of pregnancy”
Major cause of maternal mortality in India.
Asso with poor outcome of pregnancy if
uncared for.
It affects 7 – 15 % of all pregnancies.
4. • Decreases during the first trimester,
• Reaching its lowest point at 20 weeks,
• Returns to pre-pregnancy levels
during the third trimester.
7. CLASSIFICATION OF HYPERTENSION IN PREGNANCY
1) Chronic HTN : HTN present before the 20th week
of pregnancy or that present before pregnancy.
2) Chronic HTN with superimposed Preeclampsia :
defined as proteinuria developing for first time during
pregnancy in a woman with known chronic HTN.
3) Gestational HTN : HTN without proteinuria
developing after 20wks of gestation during labor or
the peurperium in previously normotensive non
proteinuric woman.
8. 4) Preeclampsia : Gestational HTN asso
with and oedema.
5) Eclampsia : Convulsions occuring in a pt
with preeclampsia.
* HELLP Syndrome : Severe form of
preeclampsia characrised by hemolysis ,
thrombocytopenia (platelets<1lakh/mm3)
and elavated liver enzymes (AST>7)
10. • Blood pressure ≥
140/90 before 20
weeks of gestation.
OR
• persistence of
hypertension beyond
12 weeks after
delivery.
11. Pregnancy-induced hypertension (PIH):-
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gestational hypertension:- Hypertension that
develops after 20 weeks of gestation in the
ab-sence of proteinuria and returns to
normal postpartum is termed gestational
hypertension. Gestational hypertension
devel-ops in 5% to 10% of pregnancies that
proceed beyond the first trimester, with a
30% incidence in multiple gesta-tions,
regardless of parity. Maternal morbidity is
directly related to the severity and duration
of hypertension.
13. CRITERIA FOR MILD GESTATIONAL
HYPERTENSION
Blood Pressure > 140 /90 mm of Hg
Proteinuria < 300 mg per 24-hr
collection
Platelet
count
> 100,000/mm3
Liver enzymes Normal
Maternal symptoms Absent
14. • It is Multisystem disorder of unknown etiology
characterised by as hypertension of at least
140/90mm Hg recorded on two separate occasions at
least 4 hours apart and with proteinuria( presence of
at least 300mg protein in a 24 hour collection of urine),
and oedema arising after the 20th week of gestation in
a previously normotensive and non proteinuric
woman .
23. • HTN patients with
hemolysis (H), elevated
liver enzymes (EL), low
platelet count (LP)
• 4-12% of pt. with severe
preeclampsia and
eclampsia develop
HELLP syndrome
24. • new onset of seizures or unexplained
coma during pregnancy in patients with pre-
existing preeclampsia and without pre-
existing neurological disorder.
25. • addition of convulsions in a woman with
preeclampsia• occurs in 0.5-4% of deliveries
Eclampsia Preeclampsia
Seizure/
Convulsion/
Coma
26. Same as Prereecblraampsia
Cerebral vasospasm , ischemia
and edema
Generalized tonic-clonic
SEIZURES
RISK FACTORS
PATHO - PYSIOLOGY
SYMPTOMS
27. MANAGEMENT
IV MgSO4 – To prevent convulsions
( continue 24 hrs post-partum )
LOWER B.P ( hydralazine or labetalol)
INDUCE LABOR (IV oxytocin and amniotomy )
29. • New-onset proteinuria > 300 mg/24 hrs in
hypertensive women but no proteinuria before 20
wks gestation.
• A sudden increase in proteinuria or blood pressure
or platelet count < 100,000/ cu mm in women
with hypertension and proteinuria before 20 wks
gestation.
31. • Predisposing factors
a.Primigravidae more than multigravidae.
b.Pre-existing hypertension.
c. Previous pre-eclampsia.
d.Family history of pre-eclampsia.
e.Hyperplacentosis i.e. excessive chorionic
tissue as in hydatidiform mole, multiple
pregnancy, uncontrolled diabetes mellitus
and foetal haemolytic diseases.
f. Obesity.
g.Climatic variations.
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• The uteroplacental bed
• Immunological factor
• Genetic factor
• Renin- angiotensin system
• Atrial natriuretic peptide
(ANP)
• Prostaglandins
• Neutrophils
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• In early pregnancy, the cytotrophoblasts
invade the decidual arteries making their
musculature more flaccid and dilated.
During the second trimester of normal
pregnancy, a second wave of invasion
occurs into the myometrial segments of the
spiral arteries. If the second invasion does
not occur pre- eclampsia develops.
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• Stimulation of the maternal immune system
by the early conceptus is essential for
production of the blocking factors that
prevent rejection of the foetus and
placenta. Hypoimmune response results in
damage of the placenta and subsequent
pre-eclampsia.
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• It was found that the vascular sensitivity to
angiotensin II is reduced due to presence of
angiotesinase enzyme in normal pregnancy
while it increases in PIH.
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• Prostacyclin is a vasodilator and an inhibitor
for platelets aggregation while thromboxane
is a vasoconstrictor and platelets aggregator.
In PIH, there is imbalance towards an
increase in thromboxane production.
38. Pathological Changes>Sodium and water
retention
•There is haemoconcentration with fluid shift
from the intravascular to the extravascular
compartment.
•N.B. HELLP syndrome is described in PIH which
consists of: H = Haemolysis, EL= Elevated Liver
enzymes, LP= Low Platelet count.
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40. 2. Proteinuria (albuminuria):
It is urinary protein greater than 0.3gm/L in
24 hours collection or greater than 1gm/L
in two random samples obtained at least 6
hours apart.
Proteinuria is usually in the range of 1-3 gm
daily, of which 50-60% is albumin but in
severe cases it may exceed 15gm.
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3. Oedema:
a.It is weight gain of more than 1 kg in any
one week or 2.25 kg in any one month.
b.Clinical oedema is present in about two-
thirds(2/3) of patients with PIH.
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• Symptoms:These are usually manifestations
of severe pre-eclampsia.
• Headache: usually frontal but may be
occipital. It is due to cerebral oedema and
hypertension.
• Visual disturbances: blurring of vision, flashes
of light or blindness.
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3.Epigastric or right upper quadrant pain: due
to enlargement of the liver .
4.Nausea and vomiting: due to congestion of
gastric mucosa and/ or cerebral oedema.
3.Oliguria or anuria: due to kidney pathology.
44. Tests depend on blood
pressure
measurement
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• 1.Roll-over test:
After resting in the left lateral position turning
to a supine position induces a rise in diastolic
pressure of 20 mmHg or more is indicative of
tendency to develop pre-eclampsia.
Subsequent reports have indicated that the test
is less satisfactory.
45. Tests depend on blood
pressure
measurement
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• 2.Mid-trimester mean blood pressure:
If the mean arterial blood pressure (MAP)
(the diastolic pressure +1/3 the pulse pressure) is
more than 95 mmHg, the risk of developing
PIH increases by over four folds.
= 140/90 = 90+1/3*50 = 107mm of hg
Normally it is 90-93 mm of hg
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Pre-eclampsia Pre-existing (chronic)
Hypertension
Parity usually primigravida. usually multigravida.
Past History of pre-eclampsia may be present. of hypertension in between
pregnancies.
Hypertension after the 20th week of pregnancy
(except in vesicular mole) and
disappears within 6 weeks postpartum.
before pregnancy, during the
first 20 weeks and persists
after 6 weeks postpartum.
Proteinuria if present, it develops after
hypertension.
If present, it develops before
hypertension due to
underlying renal disease.
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1. Proper antenatal care:
1.To detect the high risk patients who
may
develop PIH through the screening tests.
a.Early detection of cases who are already
developed PIH and examine them more
frequently.
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2.Low dose aspirin:
a.It inhibits thromboxane production from the
platelets and the AII binding sites on platelets.
a.A low dose (60 mg daily) selectively inhibits
thromboxane due to higher concentration of
such a low dose in the portal circulation than
systemic affecting the platelets when pass
through the portal circulation. The prostacyclin
production form the systemic vessels will not be
affected.
53. www.freelivedoctor.com
Delivery of the foetus and placenta is the
only real treatment of pre-eclampsia. As the
conditions are not always suitable for this,
the treatment aims to prevent or minimise
the maternal and foetal complications till
reasonable maturation of the foetus.
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1.Hospitalisation: with complete bed rest more
in left lateral position to prevent
compression of the inferior vena cava. This
lowers the blood pressure, induces diuresis,
reduces oedema and increases renal and
placental blood flow.
2.High protein, low sodium diet.
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3. Observation:
A. Maternal:
> blood pressure twice daily.
> urine volume and proteinuria daily,
> oedema daily,
> body weight twice weekly,
> fundus oculi once weekly,
> blood picture including platelet count, liver and
renal functions particularly serum uric acid on
admission.
56. B. Foetal:
> daily foetal movement count,
> serial sonography,
> non-stress and stress test if needed.
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a."Loop" diuretics: > Furosemide (Lasix): 20-40
mg IV repeated at intervals of 2-4 hours
>Thiazides: better to be avoided in pregnancy.
b.Osmotic diuretics: as mannitol or glucose
25%
62. Timing of delivery:
Severe pre-eclampsia is usually treated
conservatively till the end of the 36th week to
ensure reasonable maturation of the foetus.
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• Foetal: deteriorating placental function
as
judged by
a.intrauterine growth retardation,
b.oligohydramnios,
• reduced foetal movements,
a.abnormal foetal heart patterns, or
b.failing biochemical results.
65. • Maternal: deteriorating maternal condition as
judged by
blood pressure is sustained or
exceeds 180/110 mmHg,
urine proteinuria > 5 gm/24 hours,
oliguria,
evidence of DIC, or
imminent or already developed
eclampsia.
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a.Close monitoring of the foetus is indicated.
b.Proper sedation and analgesia to the
mother. Hypotensives may be given if
needed.
c.2nd stage of labour may be shortened by
forceps.
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a.Methergin is better avoided as it may
increase the blood pressure
a.Continue observation of the mother for 48
hours.
b.Sedatives and hypotensive drugs are
continued in a decreasing dose for 48 hours.
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can be treated as an outpatient with
sedatives
± hypotensive drugs with frequent follow up.
Pregnancy can be allowed . Delivery is usually
vaginal unless there is other indication for
caesarean section.
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• a. Premonitory stage/ stage of aura :olfactory hallucination
, false perceptin of smell, the eyes balls turns one side and
fix. It lasts for about ½ min.
• b. Tonic stage:involuntary contractin of vountary muscles ,
generalised tonic contraction of the whole body muscles
with opisthotonus and cyanosis. It lasts for about ½ min.
• c. Clonic stage: convulsions occur where there is
alternative contraction and relaxation of the body
muscles. The face is congested, tongue may be bitten,
blood-stained frothy saliva appears on the mouth,
temperature rises due to increased muscular activity
patient is unconscious. This lasts for about 1 min.
• d. Coma: it may last for few hours , unaware of previos
stages.
77. Severity of
Eclampsia
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• Eclampsia is considered severe if one or more
of
the follo iŶg is preseŶt ;EdeŶ’s ĐriteriaͿ:ǁ
• Coma of 6 or more hours.
• Temperature 390C or more.
• Pulse over 120/min.
• Systolic blood pressure over 200 mmHg.
• Respiratory rate over 40/min.
• More than 10 convulsions.
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> Morphine 10-20 mg IM or,
> Diazepam one ampule (10mg) IV over 4
min. then maintain by IV infusion 40 mg in
500 ml glucose 5% over 12-24 hours.
Diazepam is used as an anticonvulsant as
well.
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a."Loop" diuretics: > Furosemide (Lasix): 20-40
mg IV repeated at intervals of 2-4 hours
>Thiazides: better to be avoided in pregnancy.
b.Osmotic diuretics: as mannitol or glucose
25%
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• Obstetric measures
The policy is that there is no conservative treatment
in eclampsia and the patient should be delivered but
convulsions should be controlled first.
Spontaneous labour usually commences within 6
hours. If not induce labour by oxytocin as long as
there is no other indication for caesarean section and
vaginal delivery is anticipated within 8-12 hours.
Otherwise, caesarean section is indicated but never
give general anaesthesia before control of convulsions
or if the patient is in coma.
92. Effect of Pregnancy on
Chronic
Hypertension >Blood pressure falls by the second trimester in
most of cases, but rises during the third
trimester to a level some what above that in
early pregnancy.
>Deterioration of the underlying disease.
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93. Effect of Chronic Hypertension
on
Pregnancy Maternal:
> superimposed pre-eclampsia/ eclampsia in
15-
20% of cases.
Foetal:
>Intrauterine growth retardation.
>Intrauterine foetal death.
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94. General and medical treatment
> Rest,
> Sedatives,
> Antihypertensives,
> Diuretics,
> Observation.
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Obstetric measures
>Therapeutic abortion:
to treatment.
in severe cases not
responding
> Preterm delivery if there is
•marked deterioration of the underlying disease.
•indication for termination as in pre-eclampsia if it is
superimposed.
a.intrauterine growth retardation.
>Delivery at 37 completed weeks as intrauterine
foetal death may result from deteriorating placental
functions.
