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CMHS DEPARTMENT OF PHO
OBGYN SEMINAR: 3
prepared by
Outlines
Introduction
 Definitions
Classification of HDP
Clinical manfestation
Complications
Management and treatment
Introduction to
HYPERTNSIVE Disorders of Pregnancy.
• Hypertensive disorders of pregnancy remain among
the most fatal and unsolved problems in obstetrics.
• Along with hemorrhage and infection it contributes
greatly to maternal morbidity and mortality.
• Among the spectrum of HDP, PE either alone or
superimposed on chronic HPN, is the most
dangerous.
Definition
HDP are one of the most common obstetric
complications, affecting 5-10% of all pregnancy.
Along with hemorrhage and infection it forms the
deadly triad during pregnancy as a cause of maternal
mortality.
Triads of maternal mortality including.
√ Hemorrhage
√ Infection
√ Hypertensive disorders
Cont---
Hypertension (HTN) is diagnosed when
appropriately# taken blood pressure exceeds
140mmHg systolic or 90mmmHg of diastolic,
observed at least on two occasions 4hrs
apart but not more than 7days apart.
Appropriate BP measurement
include:
Avoiding smoking, caffeine and exercise for 30min
prior to measurement
Patient should sit quietly for 5min (10min, old JUSH
guideline) in a chair with feet on the floor.
Measurement is taken from right arm at the level
of the heart
Using appropriate BP cuff size Width of the
inflatable bladder of the cuff should be about 40%
of the upper arm circumference (about 12- 14cm in
the average adult)
• NB. We don’t necessarily need both the
systolic and diastolic BP to be elevated to
diagnose HTN; elevation of one of them is
enough for diagnosis.
• Severe HTN is when sustained elevation of
SBP of ≥160mmHg or DBP of ≥ 110mmHg is
• observed on two occasions for at least 4hrs
apart but not more than 7days
Classification
According to ACOG (2013) there are four types of
hypertensive disorders during pregnancy
1. Gestational HTN (GH)
2. Preeclampsia eclampsia syndrome (PE-E
syndrome)
3. Chronic essential HTN
4. Preeclampsia-superimposed on chronic HTN
Overviews Of HDP classification
GH is a new onset elevated BP without proteinuria
or signs/symptoms of preeclampsia
related end organ dysfunction that is diagnosed for
the first time after 20 weeks of
pregnancy and resolves by 12 weeks postpartum in
previously normotensive lady
Preeclampsia
Preeclampsia is a multi-system progressive disorder
characterized by new onset of
hypertension and proteinuria or hypertension
and significant end-organ dysfunction
with or without proteinuria after 20 weeks of
gestation in a previously normotensive
woman.
PE = GH + proteinuria or severe features
Even though HTN is considered to be the hallmark of
PE, some patient with PE may
present with signs of PE without HTN, - and it is
referred to as atypical PE.
Eclampsia
Eclampsia is defined as the development of
convulsions (generalized tonic-clonic) or unexplained
coma during pregnancy or postpartum in patients
with signs and symptoms
of PE.
ACOG defines eclampsia as a new onset tonic-clonic,
focal or multifocal seizure in the absence of other
causative conditions,
such as, Epilepsy, Cerebral arterial ischemia or
infarction, ICH and Drug use.
It is tonic clonic convulsions or coma occurring
during pregnancy, labour or within 7 days
postpartum unrelated to other cerebral conditions
like epilepsy in a woman with neglected or fulminant
preeclampsia.
√It occurs in 50 % antepartum, 25% intrapartum
and 25% postpartum.
√Atypical ecclampsia is ecclampsia occurring before
20 weeks of gestation and after 48 hours
postpartum.
Chronic HTN and Superimposed PE
✓Chronic HTN: Is defined as an elevated BP
that is present prior to conception (pregnancy) or is
diagnosed before 20th week of gestation, or HTN
that persist for more than 12wks postpartum.
✓The frequency of chronic hypertension in pregnancy
is estimated at 1% to 5%.
√Women with chronic hypertension are at increased
risk for superimposed PE.
Superimposed PE
Superimposed preeclampsia is worsening of
hypertension (rise in systolic blood pressure by 30
mmhg or/and rise in diastolic blood pressure by 15
mmhg from mid pregnancy levels)
and worsening or development of proteinuria with or
without pathologic edema in a woman with chronic
hypertension.
Gestational HTN (GH)
• GH is a new onset elevated BP without proteinuria
or signs/symptoms ofpreeclampsia related end
organ dysfunction.
• That is diagnosed for the first time after 20 weeks
of pregnancy and resolves by 12 weeks postpartum
in previously normotensive lady
Cont---
√Gestational or transient hypertension is
recurrent mild hypertension that develops between
20 weeks of gestation and 24 hours postpartum
without other signs of preeclampsia
or chronic hypertension and resolves within 10 days
postpartum.
It is the most frequent cause of HTN during
pregnancy.
√The incidence ranges from 6-29% in nulliparous
women and from 2-4% in multiparous, the incidence
increases in multiple gestation.
• Almost half of these women develop PE syndrome.
• The likelihood of progression to PE depends on
gestational age (GA) at the time of diagnosis, with
higher rates if the onset of HTN is before 35wks
(32wks, ACOG 2019) of gestation. Fortunately, most
cases of GH develop at or beyond 37wks of
gestation.
• GH is divided in to two: Mild GH and Severe GH
• Criteria for the diagnosis of mild GH
• Systolic blood pressure >140 mm Hg but <160 mm
Hg and diastolic blood pressure >90 mm Hg but
<110 mm Hg.
• Proteinuria of <300 mg per 24hr collection
• Platelet count of >100,000/mm3Normal liver
enzymes
• Absent maternal symptoms
• Absent intrauterine growth restriction and
oligohydramnios by ultrasound.
• Criteria for the diagnosis of severe GH there
is some confusion about whether sever GH is
separate thing or it is just PE with severity feature.
• Women with GH who present with severe range BP
should be managed in the same approach as for
women with severe PE.
• GH and PE may also be undistinguishable in long
term cardiovascular risks, like chronic HTN. (ACOG
2019)
• The overall pregnancy outcome of GH depends on
GA at time of diagnosis and the type of GH.
• Most cases of mild GH which develop after 37wks
of gestation usually have similar outcome as
normotensive pregnancy, other than higher rate of
induction of labor.
• Women with severe GH has increased risk of
maternal and perinatal morbidities,
• (greater than those with mild PE), including
placental abruption, preterm delivery, and
delivery of small for gestational age baby
• Some reclassify GH as transient hypertension, if
evidence of PE doesn’t develop and the BP returns
to normal by 12 weeks postpartum.
Risk factors GH
√First pregnancy
√ Age
√family history
√multipl pregnancy
√ obesity
√preexisting medical conditions
√ previous hx of preeclampsia
√ race and ethnicity
Complications of GH
Management of GH
√ Regular prenatal care Life style modification
√ Close monitoring. Hospitalization
√medication.
√Delivery. <37 wk and stable __Expectant Mgt.
(Steroids <32_34 wks).
<37 wk and indications* for delivery consider
inducing delivery (steroids<32_34wks)
≥37wks considers inducing delivery
Antihypertensive drugs
• Labetalol ____10_20mg Iv then 20_ 80mg every
10_30 minutes to maximum cumulative dosage of
300mg; constant infusion 1_2mg/min I
• Hydralazine ___5mg Iv or Im,then 5_10mg Iv every
20_40 minutes to maximum cumulative dosage of
20mg;or constant infusion of 0.5_10mg/hr
• Nifedipine____10_20mg orally, repeated in
20minutes if needed,then 10_20mg every 2_6hrs.
Maximum daily dose is 80 mg .
• Methyldopa ___4gm/day in divided doses depend
on the response
Preeclampsia And
Elampsia
PREECLAMPSIA (PE)
• PE is a part of PIH which define as
BP>140/90 in the presence of significant
proteinuria of 300gm/24hr urine specimen
or less acurate more than 1+
protein(100mg/dl) on dipstick in at least two
randomly collected urine at least 6hrs apart
after 20th wks of gestation /up to 6wks post
partum.
• PE = GH + proteinuria or severe feature
Classification PE
PE is categorized as,
1. PE with severity features (PE -SF)and
2. PE without- severity features(PE w/o SF)
Criteria to diagnosed Preeclampsia with Severity
Features
Preeclampsia, with severe features, is defined when
the disorder is present in association with any one of
the following abnormalities.
SBP ≥160 mm Hg or DBP ≥110 mmHg on two
occasions at least 4 hours apart while the patient
is on bed rest or once if the patient has received
prior antihypertensive therapy.
New-onset persistent cerebral symptoms:
headaches or visual disturbances
Impaired liver function as indicated by
abnormally elevated liver enzymes (at least twice
the upper limit of normal [ULN]); severe,
persistent right upper quadrant or epigastric pain
that is unresponsive to medications .
Pulmonary edema (often develop in postpartum)
Thrombocytopenia (platelet count<100,000/μl)
Progressive renal insufficiency (serum creatinine
>1.1 mg/dl);
•NB, the amount of proteinuria (≥500gm
in a 24hr urine specimen or ≥3+ on
dipstick), oliguria, and presence of
intrauterine growth restriction (IUGR) or
fetal growth restriction (FGR) by
ultrasound have been removed as
criteria for the diagnosis of severe
disease.
• Even though HTN is considered to be the hallmark
of PE, some patient with PE may present with signs
of PE without HTN, - and it is referred to as
atypical PE.
The criteria for atypical preeclampsia include
gestational proteinuria or FGR plus one or more of
the following. Severity features preeclampsia without
hypertension:
hemolysis, thrombocytopenia, elevated liver
enzymes
 Early signs and symptoms of PE-E syndrome
earlier than 20 weeks.
Late postpartum PE-E syndrome (>48 hours
postpartum but less than six weeks after delivery).
Risk factors PE
Nulliparity, (limited sperm exposure)
Age <20yrs or >40yrs (35yrs ACOG)
Race, (higher in the Black population because of
genetic predisposition)
Multifetal gestation (increase risk to 13%)
Obesity/gestational diabetes mellitus (BMI
≥35kg/m2 increase risk to 13.3%)
PE in previous pregnancy
Preexisting medical-genetic conditions
Chronic hypertension
 Renal disease
 Type 1 DM
 Antiphospholipid antibody syndrome
Thrombophilia, Factor V Leiden mutation
Pregnancy with the aid of artificial reproductive
technology(ART)
Family history of preeclampsia
Woman born small for gestational age
Poor outcome in previous pregnancy like
Fetal growth restriction (FGR), placental
abruption (PA), fetal death.
Factors that reduce risk of PE
Smoking, unlike its effect in many obstetric
and gynecologic abnormalities, it carries a
reduced risk for hypertension during
pregnancy, because it up-regulates placental
adrenomedullin expression which regulates
volume homeostasis
Long term sperm exposure with the same
partner
Pathophysiologic changes in PE
Hematological changes
• Thrombocytopenia
NB, once it developed thrombocytopenia usually
continues to worsen, so delivery is recommended
• Hemolysis, (Microangiopathic Hemolysis
Renal changes
• Reduced renal perfusion and GFR (up to 25%
below normal pregnancy)
• Oliguria, NB, Intensive IV fluid therapy is not
indicated as a treatment for preeclamptic women
with oliguria, unless urine output is diminished
• Proteinuria, may develop late, for example,
approximately 10- 15% of HEELP syndrome and
17% of patient with eclampsia don’t have
proteinuria at the time of presentation.
• Increased urine sodium level
• Increased serum creatinine and uric acid level
• AKI in patients with comorbid hemorrhage with
hypovolemia and hypotension (for example, in
patient with severe placenta abruption)
NB, PE is the most common cause of AKI
in pregnancy
Hepatic changes
Hepatic function may be significantly altered in
women with PE with SF (indicated by elevated
AST and ALP)
AST is the dominant transaminase released in
liver dysfunction due to PE, and is related to
periportal necrosis. (AST>ALT)
Evaluation of these coagulation parameters is
useful when there is:
Thrombocytopenia
Significant liver dysfunction
Suspected placental abruption
RUQ or epigastric pain is thought to be from
HELLP syndrome
 Is one of the more severe forms of PE,
because it is associated with increased rates
of maternal morbidity and mortality
Is mostly a 3rd TM condition, but in 30% of
cases it is 1st expressed or progress
postpartum (i.e., 70% antepartum)
RUQ pain and generalized malaise are the
main presenting symptoms in 90% of cases.
Nausea and vomiting in 50% of cases
Criteria to establish diagnosis of
HELLP syndrome
Hemolysis (at least two of the following signs of hemolysis)
Peripheral blood smear showing schistocytes, or burr cells
Serum Bilirubin ≥1.2mg/dl
Late manifestation
Low serum haptoglobin
Severe anemia (Microangiopathic Hemolytic Anemia) unrelated to
blood loss
 LDH >600U/L (>2x the ULN)
Elevated liver enzymes
ALT/AST at least twice the ULN (upper limits of the normal)
AST level >2000IU/L
Low platelets (≤100,000/µl)
Classification of HELLP syndrome
.Based on the level of Plt count, LDH and AST/ALT
Neurologic changes
• Both sudden elevation in BP (hyperperfusion=>
disruption of end capillaries, and vasogenic edema)
and hypoperfusion (=> Ischemia, cytotoxic edema
and tissue
Headache, (in 75% of severe PE)
• HA usually start from occipital area, because of the
cerebrovascular hyperperfusion that has a
predilection for the occipital lobes
• Frequently improve after MgSO4
Visual changes and & temporary blindness (lasting
a few hours to a week)
Generalized cerebral edema
Cognitive decline
Clinical manifestations of PE
The clinical findings of PE can manifest as either a
maternal syndrome or a fetal syndrome.
Maternal syndrome
Symptoms
Headache (severe, global type, which is
unresponsive to NSAIDs)
Blurring of vision, or less commonly double
vision and blindness (from retinal detachment)
 Right upper quadrant or Epigastric pain
Swelling of the face or vulva
Vaginal bleeding
Nausea/vomiting
Difficulty of breathing
Signs
Elevated BP, (NB, BP could be normal and patient still
can have PE)
Facial/generalized edema
Signs of pleural effusion and ascites
RUQ tenderness
Mental status change (confusion to coma, result of
cerebral edema)
Hyperreflexia
Laboratory findings
• Proteinuria(U/A)
• Thrombocytopenia(CBC)
• Elevated serum AST/ALT (2x ULN), LDH, creatinine
and bilirubin level(LFT andRFT) and Findings of DIC
Fetal manifestations include: -
 Oligohydramnios
FGR
 Abruption
Vascular stillbirth
 Preterm delivery
ECLAMPSIA
• Eclampsia is defined as the development of
convulsions (generalized tonic-clonic) or
unexplained coma during pregnancy or
postpartum in patients with signs and
symptoms of PE.
Eclampsia=PE+convulsion(unexplained coma)
Diagnosis
• The diagnosis of eclampsia is secure in the
presence of
generalized edema
hypertension
proteinuria, and
 convulsions.
Eclampsia often (in 78-83%, ACOG 2019) is preceded by
premonitory signs of cerebral irritation, (signs of
impending eclampsia) such as:
Persistent occipital or frontal headache
Blurring of vision (blindness is seen in up to 10-15%
of eclamptic patients, and it is mainly due to occipital
lobe edema)
Photophobia
 Altered mental status
Seizure may lead to severe maternal hypoxia, trauma
and aspiration pneumonia
Severity of Eclampsia
Eclampsia is considered severe if one or more of the
following are present (Eden’s criteria)
Coma of 6 or more hours
Temp >39oc
PR > 120bpm
SBP >200mmHg
 RR >40
>10 convulsions
Maternal and fetal outcomes of eclampsia
Maternal (with incidence): - PA (7-10%), DIC (7-10%),
Pulmonary edema (3-5%), AKI (5-9%) Aspiration
pneumonia (2-3%) and Cardiopulmonary arrest (2 5%)
Fetal or perinatal: - Prematurity, PA, Severe FGR,
Preterm delivery, is about 50% and about 25% occur
before 32wks of gestation
Prevention of eclampsia Can be: -
I. Primary: by preventing the development and /or
progression of PE,
II. Secondary: by using pharmacologic agents that
prevent convulsions in women with established PE.
III. Tertiary: by preventing subsequent convulsions in
women with established eclampsia
Management of PE-Esyndrome
• Management of PE depends on the severity of PE
and the GA.
It can be an expectant and
definitive management.
•NB, termination of pregnancy is the
only definitive management for PE
Antepartum management
Mild PE (PE w/o severity feature) and GH
Can be managed as outpatient, but if follow up is difficult, admit.
Expectant management Follow up
• Twice weekly ANC
• Daily fetal kick count
• Serial ultrasonography
• Weekly antepartum testing
• Closely monitoring BP, twice weekly
• Steroids, if <37wks
• twice weekly testing for PE (in those with GH)
U/A, CBC, RFT. liver enzymes
Following initial documentation of proteinuria, and dx of PE,
• The patient should be reminded to report any sign of
severity if developed during the expectant
management period.
• NB. In women with GH w/o SF, progression to PE with
SF can occur within 1-3wks,
• and in those with PE w/o SF, progression to PE with
SF can occur within days
indication for delivery (definitive mgt)
• GA ≥37+0/7 wks. (ACOG 2019) or ≤ 28wks
• If cervical status is favorable, induction is initiated. If
the cervical status is unfavorable, pre- induction
cervical ripening agents are used as needed
• Abnormal antepartum testing
• Fetal death
• Fetal condition incompatible with life
• If evidence of worsening preeclampsia is seen
(development of any SF)
• Eclampsia
• Prophylactic intrapartum magnesium sulfate is
indicated to prevent convulsions
Severe preeclampsia (PE with SF)
• Severe preeclampsia mandates hospitalization.
Expectant management
Is given until development of maternal or fetal
indications for delivery or until achievement of fetal
lung maturity or 34 weeks' gestation.
IV MgSO4 is begun to prevent convulsions for the first
24-48 hours, anticonvulsant
should be discontinued if no indications for delivery
develop
 Corticosteroids to accelerate fetal lung maturity
(Dexamethasone 6mg IM BID four doses) and delivery
after 48 hours
• Fetal kick chart daily
• Laboratory evaluation includes
 CBC every other day
 liver enzymes, and serum creatinine twice a
weekly
• Fetal evaluation includes fetal heart
monitoring,and fetal growth assessment twice
weekly
Antihypertensive therapy
The aim of this therapy is to: -
keep the SBP between 140 & 160mand DBP
between 90 & 110mmHg, and prevent CHF,
AKI, and Stroke
Acute blood pressure control
Hydralazine (peripheral vasodilator) 5–10 mg IV. The
onset of action is 10–20 minutes, and the dose can be
repeated in 20–30 minutes if necessary (maximum of
60 mg IV or 300 mg PO in 24 hours)
 Labetalol (Beta blocker) 5–20 mg by slow IV push.
The dose can be repeated in 10–20 minutes
Nifedipine (calcium channel blocker) 5–10 mg orally.
The dose can be repeated in 20–30 minutes, as
needed
Maintenance antihypertensive therapy
• Methyldopa up to 4gm/day PO in divided doses
depending on the response
• Nifedipine 10-20mg PO every 6hrs
Neuroprophylaxis—Prevention of Seizures
• Magnesium sulfate (MgSO4) Is the most preferred and
effective anticonvulsant prophylaxis
Mechanism of action
• reduced presynaptic release of the neurotransmitter
glutamate
• blockade of glutamatergic N-methyl D-aspartate (NMDA)
receptors
• potentiation of adenosine action
• improved calcium buffering by mitochondria, and
• blockage of calcium entry via voltage-gated channels
Dosage
• IV loading dose of 4gm over 20–60 minutes and 10gm
IM half on each buttock, followed by a maintenance
dose of 3gm/hour IV or 5gm IM in alternate buttocks
every 4 hours. If convulsion occurs after MgSO4 is
started, give 2gm MgSO4 IV.
Toxicity
i. Loss of deep tendon reflexes (patella)occurs at 8 to 10
mEq/L
ii. Respiratory paralysis at 10 to 15 mEq/L
iii. Cardiac arrest at 20 to 25 mEq/L
In the event of these adverse effects MgSO4 should
be discontinued and Calcium gluconate (10 mL of
10% solution over 3min) given
contraindication
Severe renal impairment
 Hypermagnesemia
Hypocalcemia
Skeletal muscle disorders, progressive muscle
weakness with carcinoma
Myasthenia gravis and Allergies
Absence of magnesium sulfate, one may use
diazepam 30mg/1000ml D5W 30 drops per minute
and 10mg IV bolus if convulsion occurs.
Indications for definitive management (delivery) in
Severe PE
The gestational age is ≥34wks.
 Failure to control hypertension with two antihypertensive
drugs with a maximum dose in 48 hours. Resistant HTN
 Persistent maternal severity symptoms (severe headache,
visual changes and abdominal and/or epigastric pain with
elevated liver enzymes).
HEELP Syndrome
Eclampsia
 Pulmonary edema or left ventricular failure
IUFD
 DIC
Severe renal dysfunction
Management of eclampsia
ABCD of life, and basic supportive care
 Prevent aspiration
Positioning in lateral decubitus position
 Give oxygen and monitor saturation
Control convulsion
Anticonvulsants –
MgSO4 (same dosage as in severe PE)
NB. MgSo4 isn’t necessary to arrest the current
seizure, rather to prevent recurrence
 If refractory to MgSO4, (still seizing after 20min or
>2 recurrence) Use sodium amobarbital (250mg IV in
3min), thiopental or phenytoin (1250mg IV at a rate
of 50mg/min)
Alternative supplementary anticonvulsant medication
include: -
Intravenous barbiturate (given slowly).
Midazolam or lorazepam may also be given in a
small single dose, but prolonged use is avoided
because it is associated with a higher mortality rate
from aspiration pneumonia Sedation and ICU may
be necessary, if all medical interventions fail
Women who developed PE have an increased risk
cardiovascular disease (HTN, MI, and CHF)
cerebrovascular disease (stroke)
peripheral arterial disease
cardiovascular mortality later in life
CHRONIC HYPERTENSION
& SIPE
Introduction
1/27/2024 68
• Hypertensive disorders represent the most
common medical complications of pregnancy
• Chronic hypertension in pregnancy is defined
by ACOG as blood pressure > or = 140mmHg
systolic and /or 90 mmHg dystolic before
pregnancy or before 20 weeks of gestation .
Defnition
1/27/2024 69
• Chronic HTN is defined as hypertension
present before the pregnancy or that is
Dxed before the 20th week of gestation or
HTN that persists for more than 12 weeks
postpartum
• Chronic hypertension is primary disorder in
90-95% of cases, which is essential or
secondary to some identifiable risk factors
such as, renal parenchymal disease, renal
vascular disease & endocrine disorders,
Cont...
1/27/2024 70
• Women with low rsk CH have satisfactory maternal
and fetal outcome without any hypertensive
therapy by life style modification.
• Those are - weight loss,
- consuming fruits and vegetables more, -
- limiting salt intake.
- stopping smoking and alcohol.
Epidemology
1/27/2024 71
• Incidence of chronic hypertension in pregnancy is
estimated to be 1-5%.
• It is more common in older , obese and Dm
women.
Classification of chronic
hypertension
1/27/2024 72
• Based on rise in BP,
- Mild CH.
- Severe CH
• Based on its cause,
- - primary CH.
- Secondary CH
• Based on severity.
- Low Risk CH.
- High risk CH
Mild CH
1/27/2024 73
• Mild CH is blood pressure of 140-159mmHg systolic
and/or 90-109mmHg dystolic.
• It may proceed to severe in third trimester.
• 14-28% develop SIPE
Severe CH
1/27/2024 74
• It is blood pressure of >160mmHg systolic and /or
>110 mmHg dystolic.
• It has high chance of progressing to superimposed
preeclampsia.
• In addition to life style modification
antihypertensive therapy is important to control BP
• 50-79% develop SIPE
Primary CH
1/27/2024 75
• Abnormal high BP that is not due to medical
disorders
• Condition is reversible with life style modification
and medication.
• This factors are obesity, family History of
hypertension , unhealthy diet,age, alcohol and etc
• In early stage it is asymptomatic.
• 90% of cases are primary hypertension .
Secondary CH
1/27/2024 76
• Abnormal high BP due to medical disorders.
• Those medical disorders are
- kidney disease.
- pheochromocytoma.
- Thyroid disorders.
- medications
• 10% of cases are due to other medical disorders
Low risk hypertension
1/27/2024 77
• Is controlled BP to <160mmHg systolic and
<110mmHg dystolic without organ damage
• It is also primary hypertension which is not result of
other medical disorders.
• Life style modification is an advised measure.
• The use of anti hypertensive therapy is not
identified.
High risk chronic hypertension
1/27/2024 78
It is high risk if one or more of the following present
- severe chronic hypertension
- secondary hypertension
- any organ damage
Management
1/27/2024 79
Management depend on the ethiology & severity of
hypertension.
* Low Risk - has to be followed for it's progression
to severe hypertension which easily proceed to
SIPE.
-Frequent ANC follow
-Termination if associated with SIPE
* High risk- anti hypertensive therapy to control BP
and improve fetal outcome and maternal wellbeing.
Acute SH - hydralazine 10-20mg iv
- labetalol 20- 40mg iv
Postpartum management
1/27/2024 80
• In those with high risk chronic hypertension BP
must be controlled for at least 24hr after delivery.
• Methyldopa and labetalol are recommended while
diuretics and other beta blockers not.
• MgSo4 as anticonvulsant if SIPE developed to avoid
seizure
Complication
1/27/2024 81
• Maternal
- SIPE.
- placental abruption
- hypertensive encephalopathy.
- poluminary edema.
- Cerebral hemorhage
• Fetal
- premature delivery
-perinatal mortalityg
Superimposed preeclampsia
1/27/2024 82
Refers to chronic hypertension that develop to
preeclampsia.
Womens with high risk Chronic hypertension are
more at risk for SIPE.
Womens with SIPE are delivered earlier in
pregnancy.
Cont....
1/27/2024 83
• Complicates about 20% of pregnancy in women
with chronic hypertension and is associated with
increased maternal and perinatal morbidity
• The overall rate of superimposed PE is 25% (14% to
28% in mild HTN and 50% to 79% in severe HTN),
the rate is not affected by maternal age, race, or
presence of proteinuria early in pregnancy._x0000_
Cont....
1/27/2024 84
• The diagnosis of superimposed preeclampsia is based
on one or more of the following findings:
development of new-onset proteinuria is defined as the
urinary excretion of 0.3g/24-hour specimen in women
with hypertension and no proteinuria before 20 weeks'
gestation or in women with hypertension and
proteinuria before 20 weeks
severe exacerbation in hypertension plus development
of Symptoms or thrombocytopenia & abnormal liver
enzymes in women with HTN & proteinuria before 20
weeks
1/27/2024 85
A diagnosis of SUPERIMPOSED PREECLAMPSIA with
severe feature is made in the presence of any of the
following
1)BP of >or=160mmHg systolic and >or=110mmHg
dystolic despite any hypertensive drug
2) Persistent cerebral symptoms
3) Increase in liver enzymes
4) Decrease in platlet
5)New onset or worsening of renal insufficiency
Prevention
1/27/2024 86
* To prevent SIPE;
Low dose aspirin 81 mg is recommended until
delivery for women with chronic hypertension.
Management
1/27/2024 87
If there is evidence of SIPE
1) Antihypertensive drug recommended in
pregnancy and frequent follow up.
2) corticosteroid at 31 week
3) If it is without severity features
Induce labor at 37 week
4) If with severity features
-increase antihypertensive dosage
-MgSo4 for seizure prophylaxis
- Induce labor at 34 week
References
Medstar OBGYN 2nd edition.
Gabbes obstetrics Normal and problem pregnancy
7th. edition.
Obs protocol MoH edited 2020.
William obstetrics 2016 edition
Pocket obstetrics and gynecology
1/27/2024 89
THANK YOU!!!

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Seminar 3 Hhypertensive Disorder in Pregnancy .pptx

  • 1. CMHS DEPARTMENT OF PHO OBGYN SEMINAR: 3 prepared by
  • 2. Outlines Introduction  Definitions Classification of HDP Clinical manfestation Complications Management and treatment
  • 3. Introduction to HYPERTNSIVE Disorders of Pregnancy. • Hypertensive disorders of pregnancy remain among the most fatal and unsolved problems in obstetrics. • Along with hemorrhage and infection it contributes greatly to maternal morbidity and mortality. • Among the spectrum of HDP, PE either alone or superimposed on chronic HPN, is the most dangerous.
  • 4. Definition HDP are one of the most common obstetric complications, affecting 5-10% of all pregnancy. Along with hemorrhage and infection it forms the deadly triad during pregnancy as a cause of maternal mortality. Triads of maternal mortality including. √ Hemorrhage √ Infection √ Hypertensive disorders
  • 5. Cont--- Hypertension (HTN) is diagnosed when appropriately# taken blood pressure exceeds 140mmHg systolic or 90mmmHg of diastolic, observed at least on two occasions 4hrs apart but not more than 7days apart.
  • 6. Appropriate BP measurement include: Avoiding smoking, caffeine and exercise for 30min prior to measurement Patient should sit quietly for 5min (10min, old JUSH guideline) in a chair with feet on the floor. Measurement is taken from right arm at the level of the heart Using appropriate BP cuff size Width of the inflatable bladder of the cuff should be about 40% of the upper arm circumference (about 12- 14cm in the average adult)
  • 7. • NB. We don’t necessarily need both the systolic and diastolic BP to be elevated to diagnose HTN; elevation of one of them is enough for diagnosis. • Severe HTN is when sustained elevation of SBP of ≥160mmHg or DBP of ≥ 110mmHg is • observed on two occasions for at least 4hrs apart but not more than 7days
  • 8. Classification According to ACOG (2013) there are four types of hypertensive disorders during pregnancy 1. Gestational HTN (GH) 2. Preeclampsia eclampsia syndrome (PE-E syndrome) 3. Chronic essential HTN 4. Preeclampsia-superimposed on chronic HTN
  • 9. Overviews Of HDP classification GH is a new onset elevated BP without proteinuria or signs/symptoms of preeclampsia related end organ dysfunction that is diagnosed for the first time after 20 weeks of pregnancy and resolves by 12 weeks postpartum in previously normotensive lady
  • 10. Preeclampsia Preeclampsia is a multi-system progressive disorder characterized by new onset of hypertension and proteinuria or hypertension and significant end-organ dysfunction with or without proteinuria after 20 weeks of gestation in a previously normotensive woman. PE = GH + proteinuria or severe features
  • 11. Even though HTN is considered to be the hallmark of PE, some patient with PE may present with signs of PE without HTN, - and it is referred to as atypical PE.
  • 12. Eclampsia Eclampsia is defined as the development of convulsions (generalized tonic-clonic) or unexplained coma during pregnancy or postpartum in patients with signs and symptoms of PE. ACOG defines eclampsia as a new onset tonic-clonic, focal or multifocal seizure in the absence of other causative conditions, such as, Epilepsy, Cerebral arterial ischemia or infarction, ICH and Drug use.
  • 13. It is tonic clonic convulsions or coma occurring during pregnancy, labour or within 7 days postpartum unrelated to other cerebral conditions like epilepsy in a woman with neglected or fulminant preeclampsia. √It occurs in 50 % antepartum, 25% intrapartum and 25% postpartum. √Atypical ecclampsia is ecclampsia occurring before 20 weeks of gestation and after 48 hours postpartum.
  • 14. Chronic HTN and Superimposed PE ✓Chronic HTN: Is defined as an elevated BP that is present prior to conception (pregnancy) or is diagnosed before 20th week of gestation, or HTN that persist for more than 12wks postpartum. ✓The frequency of chronic hypertension in pregnancy is estimated at 1% to 5%. √Women with chronic hypertension are at increased risk for superimposed PE.
  • 15. Superimposed PE Superimposed preeclampsia is worsening of hypertension (rise in systolic blood pressure by 30 mmhg or/and rise in diastolic blood pressure by 15 mmhg from mid pregnancy levels) and worsening or development of proteinuria with or without pathologic edema in a woman with chronic hypertension.
  • 16.
  • 17. Gestational HTN (GH) • GH is a new onset elevated BP without proteinuria or signs/symptoms ofpreeclampsia related end organ dysfunction. • That is diagnosed for the first time after 20 weeks of pregnancy and resolves by 12 weeks postpartum in previously normotensive lady
  • 18. Cont--- √Gestational or transient hypertension is recurrent mild hypertension that develops between 20 weeks of gestation and 24 hours postpartum without other signs of preeclampsia or chronic hypertension and resolves within 10 days postpartum. It is the most frequent cause of HTN during pregnancy. √The incidence ranges from 6-29% in nulliparous women and from 2-4% in multiparous, the incidence increases in multiple gestation.
  • 19. • Almost half of these women develop PE syndrome. • The likelihood of progression to PE depends on gestational age (GA) at the time of diagnosis, with higher rates if the onset of HTN is before 35wks (32wks, ACOG 2019) of gestation. Fortunately, most cases of GH develop at or beyond 37wks of gestation.
  • 20. • GH is divided in to two: Mild GH and Severe GH • Criteria for the diagnosis of mild GH • Systolic blood pressure >140 mm Hg but <160 mm Hg and diastolic blood pressure >90 mm Hg but <110 mm Hg. • Proteinuria of <300 mg per 24hr collection • Platelet count of >100,000/mm3Normal liver enzymes • Absent maternal symptoms • Absent intrauterine growth restriction and oligohydramnios by ultrasound.
  • 21. • Criteria for the diagnosis of severe GH there is some confusion about whether sever GH is separate thing or it is just PE with severity feature. • Women with GH who present with severe range BP should be managed in the same approach as for women with severe PE. • GH and PE may also be undistinguishable in long term cardiovascular risks, like chronic HTN. (ACOG 2019)
  • 22. • The overall pregnancy outcome of GH depends on GA at time of diagnosis and the type of GH. • Most cases of mild GH which develop after 37wks of gestation usually have similar outcome as normotensive pregnancy, other than higher rate of induction of labor.
  • 23. • Women with severe GH has increased risk of maternal and perinatal morbidities, • (greater than those with mild PE), including placental abruption, preterm delivery, and delivery of small for gestational age baby • Some reclassify GH as transient hypertension, if evidence of PE doesn’t develop and the BP returns to normal by 12 weeks postpartum.
  • 24. Risk factors GH √First pregnancy √ Age √family history √multipl pregnancy √ obesity √preexisting medical conditions √ previous hx of preeclampsia √ race and ethnicity
  • 26. Management of GH √ Regular prenatal care Life style modification √ Close monitoring. Hospitalization √medication. √Delivery. <37 wk and stable __Expectant Mgt. (Steroids <32_34 wks). <37 wk and indications* for delivery consider inducing delivery (steroids<32_34wks) ≥37wks considers inducing delivery
  • 27. Antihypertensive drugs • Labetalol ____10_20mg Iv then 20_ 80mg every 10_30 minutes to maximum cumulative dosage of 300mg; constant infusion 1_2mg/min I • Hydralazine ___5mg Iv or Im,then 5_10mg Iv every 20_40 minutes to maximum cumulative dosage of 20mg;or constant infusion of 0.5_10mg/hr • Nifedipine____10_20mg orally, repeated in 20minutes if needed,then 10_20mg every 2_6hrs. Maximum daily dose is 80 mg . • Methyldopa ___4gm/day in divided doses depend on the response
  • 29. PREECLAMPSIA (PE) • PE is a part of PIH which define as BP>140/90 in the presence of significant proteinuria of 300gm/24hr urine specimen or less acurate more than 1+ protein(100mg/dl) on dipstick in at least two randomly collected urine at least 6hrs apart after 20th wks of gestation /up to 6wks post partum. • PE = GH + proteinuria or severe feature
  • 30. Classification PE PE is categorized as, 1. PE with severity features (PE -SF)and 2. PE without- severity features(PE w/o SF) Criteria to diagnosed Preeclampsia with Severity Features Preeclampsia, with severe features, is defined when the disorder is present in association with any one of the following abnormalities.
  • 31. SBP ≥160 mm Hg or DBP ≥110 mmHg on two occasions at least 4 hours apart while the patient is on bed rest or once if the patient has received prior antihypertensive therapy. New-onset persistent cerebral symptoms: headaches or visual disturbances Impaired liver function as indicated by abnormally elevated liver enzymes (at least twice the upper limit of normal [ULN]); severe, persistent right upper quadrant or epigastric pain that is unresponsive to medications .
  • 32. Pulmonary edema (often develop in postpartum) Thrombocytopenia (platelet count<100,000/μl) Progressive renal insufficiency (serum creatinine >1.1 mg/dl); •NB, the amount of proteinuria (≥500gm in a 24hr urine specimen or ≥3+ on dipstick), oliguria, and presence of intrauterine growth restriction (IUGR) or fetal growth restriction (FGR) by ultrasound have been removed as criteria for the diagnosis of severe disease.
  • 33. • Even though HTN is considered to be the hallmark of PE, some patient with PE may present with signs of PE without HTN, - and it is referred to as atypical PE. The criteria for atypical preeclampsia include gestational proteinuria or FGR plus one or more of the following. Severity features preeclampsia without hypertension: hemolysis, thrombocytopenia, elevated liver enzymes  Early signs and symptoms of PE-E syndrome earlier than 20 weeks. Late postpartum PE-E syndrome (>48 hours postpartum but less than six weeks after delivery).
  • 34. Risk factors PE Nulliparity, (limited sperm exposure) Age <20yrs or >40yrs (35yrs ACOG) Race, (higher in the Black population because of genetic predisposition) Multifetal gestation (increase risk to 13%) Obesity/gestational diabetes mellitus (BMI ≥35kg/m2 increase risk to 13.3%) PE in previous pregnancy
  • 35. Preexisting medical-genetic conditions Chronic hypertension  Renal disease  Type 1 DM  Antiphospholipid antibody syndrome Thrombophilia, Factor V Leiden mutation Pregnancy with the aid of artificial reproductive technology(ART) Family history of preeclampsia Woman born small for gestational age Poor outcome in previous pregnancy like Fetal growth restriction (FGR), placental abruption (PA), fetal death.
  • 36. Factors that reduce risk of PE Smoking, unlike its effect in many obstetric and gynecologic abnormalities, it carries a reduced risk for hypertension during pregnancy, because it up-regulates placental adrenomedullin expression which regulates volume homeostasis Long term sperm exposure with the same partner
  • 37. Pathophysiologic changes in PE Hematological changes • Thrombocytopenia NB, once it developed thrombocytopenia usually continues to worsen, so delivery is recommended • Hemolysis, (Microangiopathic Hemolysis Renal changes • Reduced renal perfusion and GFR (up to 25% below normal pregnancy) • Oliguria, NB, Intensive IV fluid therapy is not indicated as a treatment for preeclamptic women with oliguria, unless urine output is diminished
  • 38. • Proteinuria, may develop late, for example, approximately 10- 15% of HEELP syndrome and 17% of patient with eclampsia don’t have proteinuria at the time of presentation. • Increased urine sodium level • Increased serum creatinine and uric acid level • AKI in patients with comorbid hemorrhage with hypovolemia and hypotension (for example, in patient with severe placenta abruption) NB, PE is the most common cause of AKI in pregnancy
  • 39. Hepatic changes Hepatic function may be significantly altered in women with PE with SF (indicated by elevated AST and ALP) AST is the dominant transaminase released in liver dysfunction due to PE, and is related to periportal necrosis. (AST>ALT) Evaluation of these coagulation parameters is useful when there is: Thrombocytopenia Significant liver dysfunction Suspected placental abruption RUQ or epigastric pain is thought to be from
  • 40. HELLP syndrome  Is one of the more severe forms of PE, because it is associated with increased rates of maternal morbidity and mortality Is mostly a 3rd TM condition, but in 30% of cases it is 1st expressed or progress postpartum (i.e., 70% antepartum) RUQ pain and generalized malaise are the main presenting symptoms in 90% of cases. Nausea and vomiting in 50% of cases
  • 41. Criteria to establish diagnosis of HELLP syndrome Hemolysis (at least two of the following signs of hemolysis) Peripheral blood smear showing schistocytes, or burr cells Serum Bilirubin ≥1.2mg/dl Late manifestation Low serum haptoglobin Severe anemia (Microangiopathic Hemolytic Anemia) unrelated to blood loss  LDH >600U/L (>2x the ULN) Elevated liver enzymes ALT/AST at least twice the ULN (upper limits of the normal) AST level >2000IU/L Low platelets (≤100,000/µl)
  • 42. Classification of HELLP syndrome .Based on the level of Plt count, LDH and AST/ALT
  • 43. Neurologic changes • Both sudden elevation in BP (hyperperfusion=> disruption of end capillaries, and vasogenic edema) and hypoperfusion (=> Ischemia, cytotoxic edema and tissue Headache, (in 75% of severe PE) • HA usually start from occipital area, because of the cerebrovascular hyperperfusion that has a predilection for the occipital lobes • Frequently improve after MgSO4
  • 44. Visual changes and & temporary blindness (lasting a few hours to a week) Generalized cerebral edema Cognitive decline Clinical manifestations of PE The clinical findings of PE can manifest as either a maternal syndrome or a fetal syndrome.
  • 45. Maternal syndrome Symptoms Headache (severe, global type, which is unresponsive to NSAIDs) Blurring of vision, or less commonly double vision and blindness (from retinal detachment)  Right upper quadrant or Epigastric pain Swelling of the face or vulva Vaginal bleeding Nausea/vomiting Difficulty of breathing
  • 46. Signs Elevated BP, (NB, BP could be normal and patient still can have PE) Facial/generalized edema Signs of pleural effusion and ascites RUQ tenderness Mental status change (confusion to coma, result of cerebral edema) Hyperreflexia
  • 47. Laboratory findings • Proteinuria(U/A) • Thrombocytopenia(CBC) • Elevated serum AST/ALT (2x ULN), LDH, creatinine and bilirubin level(LFT andRFT) and Findings of DIC Fetal manifestations include: -  Oligohydramnios FGR  Abruption Vascular stillbirth  Preterm delivery
  • 48.
  • 49. ECLAMPSIA • Eclampsia is defined as the development of convulsions (generalized tonic-clonic) or unexplained coma during pregnancy or postpartum in patients with signs and symptoms of PE. Eclampsia=PE+convulsion(unexplained coma)
  • 50. Diagnosis • The diagnosis of eclampsia is secure in the presence of generalized edema hypertension proteinuria, and  convulsions.
  • 51. Eclampsia often (in 78-83%, ACOG 2019) is preceded by premonitory signs of cerebral irritation, (signs of impending eclampsia) such as: Persistent occipital or frontal headache Blurring of vision (blindness is seen in up to 10-15% of eclamptic patients, and it is mainly due to occipital lobe edema) Photophobia  Altered mental status Seizure may lead to severe maternal hypoxia, trauma and aspiration pneumonia
  • 52. Severity of Eclampsia Eclampsia is considered severe if one or more of the following are present (Eden’s criteria) Coma of 6 or more hours Temp >39oc PR > 120bpm SBP >200mmHg  RR >40 >10 convulsions
  • 53. Maternal and fetal outcomes of eclampsia Maternal (with incidence): - PA (7-10%), DIC (7-10%), Pulmonary edema (3-5%), AKI (5-9%) Aspiration pneumonia (2-3%) and Cardiopulmonary arrest (2 5%) Fetal or perinatal: - Prematurity, PA, Severe FGR, Preterm delivery, is about 50% and about 25% occur before 32wks of gestation Prevention of eclampsia Can be: - I. Primary: by preventing the development and /or progression of PE, II. Secondary: by using pharmacologic agents that prevent convulsions in women with established PE. III. Tertiary: by preventing subsequent convulsions in women with established eclampsia
  • 54. Management of PE-Esyndrome • Management of PE depends on the severity of PE and the GA. It can be an expectant and definitive management. •NB, termination of pregnancy is the only definitive management for PE
  • 55. Antepartum management Mild PE (PE w/o severity feature) and GH Can be managed as outpatient, but if follow up is difficult, admit. Expectant management Follow up • Twice weekly ANC • Daily fetal kick count • Serial ultrasonography • Weekly antepartum testing • Closely monitoring BP, twice weekly • Steroids, if <37wks • twice weekly testing for PE (in those with GH) U/A, CBC, RFT. liver enzymes Following initial documentation of proteinuria, and dx of PE,
  • 56. • The patient should be reminded to report any sign of severity if developed during the expectant management period. • NB. In women with GH w/o SF, progression to PE with SF can occur within 1-3wks, • and in those with PE w/o SF, progression to PE with SF can occur within days indication for delivery (definitive mgt) • GA ≥37+0/7 wks. (ACOG 2019) or ≤ 28wks • If cervical status is favorable, induction is initiated. If the cervical status is unfavorable, pre- induction cervical ripening agents are used as needed
  • 57. • Abnormal antepartum testing • Fetal death • Fetal condition incompatible with life • If evidence of worsening preeclampsia is seen (development of any SF) • Eclampsia • Prophylactic intrapartum magnesium sulfate is indicated to prevent convulsions
  • 58. Severe preeclampsia (PE with SF) • Severe preeclampsia mandates hospitalization. Expectant management Is given until development of maternal or fetal indications for delivery or until achievement of fetal lung maturity or 34 weeks' gestation. IV MgSO4 is begun to prevent convulsions for the first 24-48 hours, anticonvulsant should be discontinued if no indications for delivery develop  Corticosteroids to accelerate fetal lung maturity (Dexamethasone 6mg IM BID four doses) and delivery after 48 hours
  • 59. • Fetal kick chart daily • Laboratory evaluation includes  CBC every other day  liver enzymes, and serum creatinine twice a weekly • Fetal evaluation includes fetal heart monitoring,and fetal growth assessment twice weekly Antihypertensive therapy The aim of this therapy is to: - keep the SBP between 140 & 160mand DBP between 90 & 110mmHg, and prevent CHF, AKI, and Stroke
  • 60. Acute blood pressure control Hydralazine (peripheral vasodilator) 5–10 mg IV. The onset of action is 10–20 minutes, and the dose can be repeated in 20–30 minutes if necessary (maximum of 60 mg IV or 300 mg PO in 24 hours)  Labetalol (Beta blocker) 5–20 mg by slow IV push. The dose can be repeated in 10–20 minutes Nifedipine (calcium channel blocker) 5–10 mg orally. The dose can be repeated in 20–30 minutes, as needed
  • 61. Maintenance antihypertensive therapy • Methyldopa up to 4gm/day PO in divided doses depending on the response • Nifedipine 10-20mg PO every 6hrs Neuroprophylaxis—Prevention of Seizures • Magnesium sulfate (MgSO4) Is the most preferred and effective anticonvulsant prophylaxis Mechanism of action • reduced presynaptic release of the neurotransmitter glutamate • blockade of glutamatergic N-methyl D-aspartate (NMDA) receptors • potentiation of adenosine action • improved calcium buffering by mitochondria, and • blockage of calcium entry via voltage-gated channels
  • 62. Dosage • IV loading dose of 4gm over 20–60 minutes and 10gm IM half on each buttock, followed by a maintenance dose of 3gm/hour IV or 5gm IM in alternate buttocks every 4 hours. If convulsion occurs after MgSO4 is started, give 2gm MgSO4 IV. Toxicity i. Loss of deep tendon reflexes (patella)occurs at 8 to 10 mEq/L ii. Respiratory paralysis at 10 to 15 mEq/L iii. Cardiac arrest at 20 to 25 mEq/L
  • 63. In the event of these adverse effects MgSO4 should be discontinued and Calcium gluconate (10 mL of 10% solution over 3min) given contraindication Severe renal impairment  Hypermagnesemia Hypocalcemia Skeletal muscle disorders, progressive muscle weakness with carcinoma Myasthenia gravis and Allergies Absence of magnesium sulfate, one may use diazepam 30mg/1000ml D5W 30 drops per minute and 10mg IV bolus if convulsion occurs.
  • 64. Indications for definitive management (delivery) in Severe PE The gestational age is ≥34wks.  Failure to control hypertension with two antihypertensive drugs with a maximum dose in 48 hours. Resistant HTN  Persistent maternal severity symptoms (severe headache, visual changes and abdominal and/or epigastric pain with elevated liver enzymes). HEELP Syndrome Eclampsia  Pulmonary edema or left ventricular failure IUFD  DIC Severe renal dysfunction
  • 65. Management of eclampsia ABCD of life, and basic supportive care  Prevent aspiration Positioning in lateral decubitus position  Give oxygen and monitor saturation Control convulsion Anticonvulsants – MgSO4 (same dosage as in severe PE) NB. MgSo4 isn’t necessary to arrest the current seizure, rather to prevent recurrence  If refractory to MgSO4, (still seizing after 20min or >2 recurrence) Use sodium amobarbital (250mg IV in 3min), thiopental or phenytoin (1250mg IV at a rate of 50mg/min)
  • 66. Alternative supplementary anticonvulsant medication include: - Intravenous barbiturate (given slowly). Midazolam or lorazepam may also be given in a small single dose, but prolonged use is avoided because it is associated with a higher mortality rate from aspiration pneumonia Sedation and ICU may be necessary, if all medical interventions fail Women who developed PE have an increased risk cardiovascular disease (HTN, MI, and CHF) cerebrovascular disease (stroke) peripheral arterial disease cardiovascular mortality later in life
  • 68. Introduction 1/27/2024 68 • Hypertensive disorders represent the most common medical complications of pregnancy • Chronic hypertension in pregnancy is defined by ACOG as blood pressure > or = 140mmHg systolic and /or 90 mmHg dystolic before pregnancy or before 20 weeks of gestation .
  • 69. Defnition 1/27/2024 69 • Chronic HTN is defined as hypertension present before the pregnancy or that is Dxed before the 20th week of gestation or HTN that persists for more than 12 weeks postpartum • Chronic hypertension is primary disorder in 90-95% of cases, which is essential or secondary to some identifiable risk factors such as, renal parenchymal disease, renal vascular disease & endocrine disorders,
  • 70. Cont... 1/27/2024 70 • Women with low rsk CH have satisfactory maternal and fetal outcome without any hypertensive therapy by life style modification. • Those are - weight loss, - consuming fruits and vegetables more, - - limiting salt intake. - stopping smoking and alcohol.
  • 71. Epidemology 1/27/2024 71 • Incidence of chronic hypertension in pregnancy is estimated to be 1-5%. • It is more common in older , obese and Dm women.
  • 72. Classification of chronic hypertension 1/27/2024 72 • Based on rise in BP, - Mild CH. - Severe CH • Based on its cause, - - primary CH. - Secondary CH • Based on severity. - Low Risk CH. - High risk CH
  • 73. Mild CH 1/27/2024 73 • Mild CH is blood pressure of 140-159mmHg systolic and/or 90-109mmHg dystolic. • It may proceed to severe in third trimester. • 14-28% develop SIPE
  • 74. Severe CH 1/27/2024 74 • It is blood pressure of >160mmHg systolic and /or >110 mmHg dystolic. • It has high chance of progressing to superimposed preeclampsia. • In addition to life style modification antihypertensive therapy is important to control BP • 50-79% develop SIPE
  • 75. Primary CH 1/27/2024 75 • Abnormal high BP that is not due to medical disorders • Condition is reversible with life style modification and medication. • This factors are obesity, family History of hypertension , unhealthy diet,age, alcohol and etc • In early stage it is asymptomatic. • 90% of cases are primary hypertension .
  • 76. Secondary CH 1/27/2024 76 • Abnormal high BP due to medical disorders. • Those medical disorders are - kidney disease. - pheochromocytoma. - Thyroid disorders. - medications • 10% of cases are due to other medical disorders
  • 77. Low risk hypertension 1/27/2024 77 • Is controlled BP to <160mmHg systolic and <110mmHg dystolic without organ damage • It is also primary hypertension which is not result of other medical disorders. • Life style modification is an advised measure. • The use of anti hypertensive therapy is not identified.
  • 78. High risk chronic hypertension 1/27/2024 78 It is high risk if one or more of the following present - severe chronic hypertension - secondary hypertension - any organ damage
  • 79. Management 1/27/2024 79 Management depend on the ethiology & severity of hypertension. * Low Risk - has to be followed for it's progression to severe hypertension which easily proceed to SIPE. -Frequent ANC follow -Termination if associated with SIPE * High risk- anti hypertensive therapy to control BP and improve fetal outcome and maternal wellbeing. Acute SH - hydralazine 10-20mg iv - labetalol 20- 40mg iv
  • 80. Postpartum management 1/27/2024 80 • In those with high risk chronic hypertension BP must be controlled for at least 24hr after delivery. • Methyldopa and labetalol are recommended while diuretics and other beta blockers not. • MgSo4 as anticonvulsant if SIPE developed to avoid seizure
  • 81. Complication 1/27/2024 81 • Maternal - SIPE. - placental abruption - hypertensive encephalopathy. - poluminary edema. - Cerebral hemorhage • Fetal - premature delivery -perinatal mortalityg
  • 82. Superimposed preeclampsia 1/27/2024 82 Refers to chronic hypertension that develop to preeclampsia. Womens with high risk Chronic hypertension are more at risk for SIPE. Womens with SIPE are delivered earlier in pregnancy.
  • 83. Cont.... 1/27/2024 83 • Complicates about 20% of pregnancy in women with chronic hypertension and is associated with increased maternal and perinatal morbidity • The overall rate of superimposed PE is 25% (14% to 28% in mild HTN and 50% to 79% in severe HTN), the rate is not affected by maternal age, race, or presence of proteinuria early in pregnancy._x0000_
  • 84. Cont.... 1/27/2024 84 • The diagnosis of superimposed preeclampsia is based on one or more of the following findings: development of new-onset proteinuria is defined as the urinary excretion of 0.3g/24-hour specimen in women with hypertension and no proteinuria before 20 weeks' gestation or in women with hypertension and proteinuria before 20 weeks severe exacerbation in hypertension plus development of Symptoms or thrombocytopenia & abnormal liver enzymes in women with HTN & proteinuria before 20 weeks
  • 85. 1/27/2024 85 A diagnosis of SUPERIMPOSED PREECLAMPSIA with severe feature is made in the presence of any of the following 1)BP of >or=160mmHg systolic and >or=110mmHg dystolic despite any hypertensive drug 2) Persistent cerebral symptoms 3) Increase in liver enzymes 4) Decrease in platlet 5)New onset or worsening of renal insufficiency
  • 86. Prevention 1/27/2024 86 * To prevent SIPE; Low dose aspirin 81 mg is recommended until delivery for women with chronic hypertension.
  • 87. Management 1/27/2024 87 If there is evidence of SIPE 1) Antihypertensive drug recommended in pregnancy and frequent follow up. 2) corticosteroid at 31 week 3) If it is without severity features Induce labor at 37 week 4) If with severity features -increase antihypertensive dosage -MgSo4 for seizure prophylaxis - Induce labor at 34 week
  • 88. References Medstar OBGYN 2nd edition. Gabbes obstetrics Normal and problem pregnancy 7th. edition. Obs protocol MoH edited 2020. William obstetrics 2016 edition Pocket obstetrics and gynecology