HYPERTENSIVE

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HYPERTENSIVE DISORDERS IN PREGNANCY
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Hypertension in PregnancyClassification

• Chronic hypertension
• Gestational hypertension (only during pregnancy)
• Preeclampsia Superimposed upon chronic
  hypertension or Renal Disease
• Preeclampsia - eclampsia
• Transient hypertension (only after pregnancy)

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Chronic Hypertension

• Defined as hypertension diagnosed
• Before pregnancy
• Before the 20th week of gestation
• During pregnancy and not resolved postpartum

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Gestational Hypertension

• Gestational Hypertension
• Systolic gt140
• Diastolicgt90
• No Proteinurea
• 25 Develop Pre-eclampsia

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Gestational Hypertension

• Diagnosis of gestational hypertension
• Detected for first time after midpregnancy
• No proteinuria
• Only until a more specific diagnosis can be
  assigned postpartum
• If preeclampsia does not develop and
• BP returns to normal by 12 weeks postpartum,
  diagnosis is transient hypertension.
• BP remains high postpartum, diagnosis is chronic
  hypertension.
• Proteinurea develops Preeclampsia is diagnosed
  (25 incidence)

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Hypertension in Pregnancy

• Complicates 7-10 of pregnancies
• 70 Preeclampsia-eclampsia
• 30 Chronic hypertension
• Eclampsia 0.05 incidence
• 20 of Maternal Deaths
• Cause of 10 of Preterm birth
• Etiology unknown

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Hypertension in Pregnancy

• Young female 3 fold increased risk
• Africans 2 fold increased risk
• Multifetal pregnancies
• Twins
• Triplets
• Hypertension
• Renal Disease
• Collagen Vascular Disease

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• Blood pressure
• Measure blood pressure in the sitting position,
  with the cuff at the level of the heart. Inferior
  vena caval compression by the gravid uterus while
  the patient is supine can alter readings
  substantially, leading to an underestimation of
  the blood pressure. Blood pressures measured in
  the left lateral position similarly may yield
  falsely low values if the blood pressure is
  measured in the higher arm and the cuff is not
  maintained at heart level.
• Allow women to sit quietly for 5-10 minutes
  before measuring the blood pressure.

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• Record Korotkoff sounds I (the first sound) and
  IV (the muffling of sound) to denote the systolic
  blood pressure (SPB) and DPB, respectively. In
  about 5 of women, an exaggerated gap exists
  between the fourth (muffling) and fifth
  (disappearance) Korotkoff sounds, with the fifth
  sound approaching zero. In this setting, record
  both the fourth and fifth sounds (eg, 120/80/40
  with sound I 120, sound IV 80, sound V 40).
  

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Pre-eclampsia
Case Study
19 years old lady G1 P0 was seen at the antenatal
clinic at 32 weeks gestation for routine check
up. On examination she looked generally well,
blood pressure was 150/90 pulse 80/m with lower
limb oedema . Uterus was appropriate for date
with a viable fetus. Urine analysis showed
protein. Q- what is the diagnosis Q- what
investigations to perform Q- what treatment to
commence
19 years old lady G1 P0 was seen at the antenatal
clinic at 32 weeks gestation for routine check
up. On examination she looked generally well,
blood pressure was 150/95 pulse 80/m with lower
limb oedema . Uterus was appropriate for date
with a viable fetus. Urine analysis showed
protein. Q- what is the diagnosis Q- what
investigations to perform Q- what treatment to
commence
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Pre-eclampsia
Case Study
19 years old lady G1 P0 was admitted to the
labour word at 32 weeks gestation complaining of
headache. On examination she looked generally
unwell, irritable, epigastric pain, nausea
blood pressure was 160/110 pulse 90/m with lower
limb and abdominal wall oedema , reflexes
exaggerated. Uterus was small for date with a
viable fetus. Urine analysis showed
protein. Q- what is the diagnosis Q- what
investigations to perform Q- what treatment to
commence
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Pre-eclampsia
INCIDENCE 5-10 0f all pregnancies . 20
recurrence This is the third most important cause
of maternal mortality worldwide

• DEFINITION OF HYPEWRTENSION
• D.B.P. gt 90 mmHg or
• S.B.P. gt 140 mmHg or
• Rise in D.B.P. of at least 15 mmHg
  (physiological changes) or
• Rise in S.B.P. of at least 30 mmHg

abandoned
PROTIENUREA Proteinurea is defined as
urinary excretion 0.3 g protein or greater
in a 24-hour 30 mg/dl (1 or greater on
urine dip specimen)
/-
OEDEMA 90 pregnancy. progressive
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Pre-eclampsia
Risk Fac tors

• Enlarged placenta e.g.
• Pre-existing hypertension, renal
• Pre-existing vascular disease
• P0 gtgtgtgt multip
• Family history
• New husband

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Pre-eclampsia
Aetiology

• Abnormal trophoblast invasion
• first 12 weeks, the decidual segments of the
  spiral arteries are invaded increased flow to
  interrvellous space by 20 weeks trophoblast
  invades intramyometrial segment of spiral
  arteriesgtgtgt reduce resistance to blood flow to
  placenta.(high volume)
• In P-E trophoblast invasion is patchy spiral
  arteries retain their muscular walls. Reason
  ????

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Pre-eclampsia
Pathophysiology

• Normal pregnancy marked peripheral
  vasodilatation. 4 fold increase in prostacyclin
  (PGI2) normal thromboxane and increased nitric
  oxide by vascular endothelium
• Pre-eclampsia no change/reduction in
  prostacyclin and N.O. synthesis. Vasospasm and
  endothelial cell dysfunctiongtgtgt platelet
  activation and micro aggregate formation
• It is a multi organ affecting disease/ syndrome
• hemorrhage and necrosis in many organs,,
  arteriolar constriction
• kidneys glomerioloendotheliosis
• acute atherosis of spiral arteries, platelets
  micro-aggregatesthrombosis
• liver damagegtgtgtgt cerebral vasospasm

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Pathophysiology
Pathophysiologic Abnormalities in
Preeclampsia   Generalized vasospasm  Activation
of coagulation system  Abnormal
hemostasis  Altered thromboxane-prostacyclin
ratio  Endothelial cell injury  Abnormal
hemodynamics  Reduced uteroplacental blood flow
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Pathophysiology

• Heart Generally unaffected cardiac
  decompensation in the presence of preexisting
  heart disease.
• Kidney Renal lesions (glomerular
  endotheliosis) GFR and renal blood flow
  decrease hyperuricemia proteinuria may appear
  late in clinical course hypocalciuria
  alterations in calcium regulatory hormones
  impaired sodium excretion suppression of renin
  angiotensin system.

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Pathophysiology

• Coagulation System Thrombocytopenia low
  antithrombin III higher fibronectin.
• Liver HELLP syndrome (hemolysis, elevated ALT
  and AST, and low platelet count).
• CNS Eclampsia is the convulsive phase of
  preeclampsia. Symptoms may include headache and
  visual disturbances, including blurred vision,
  scotomata, and, rarely, cortical blindness.

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Symptoms of Preeclampsia

• Visual disturbances typical of preeclampsia are
  scintillations and scotomata. These disturbances
  are presumed to be due to cerebral vasospasm.
• Headache is of new onset and may be described as
  frontal, throbbing, or similar to a migraine
  headache. However, no classic headache of
  preeclampsia exists.
• Epigastric pain is due to hepatic swelling and
  inflammation, with stretch of the liver capsule.
  Pain may be of sudden onset, it may be constant,
  and it may be moderate-to-severe in intensity.

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Symptoms of preeclampsia

• While mild lower extremity edema is common in
  normal pregnancy, rapidly increasing or
  nondependent edema may be a signal of developing
  preeclampsia. However, this signal theory remains
  controversial and recently has been removed from
  most criteria for the diagnosis of preeclampsia.
• Rapid weight gain is a result of edema due to
  capillary leak as well as renal sodium and fluid
  retention.

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Physical Findings in Preeclampsia

• Blood Pressure
• Proteinurea
• Retinal vasospasm or Retinal edema
• Right upper quadrant (RUQ) abdominal tenderness
  stems from liver swelling and capsular stretch

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Physical findings in Preeclampsia

• Brisk, or hyperactive, reflexes are common during
  pregnancy, but clonus is a sign of neuromuscular
  irritability that raises concern.
• Among pregnant women, 30 have some lower
  extremity edema as part of their normal
  pregnancy. However, a sudden change in dependent
  edema, edema in nondependent areas such as the
  face and hands, or rapid weight gain suggests a
  pathologic process and warrants further evaluation

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Pre-eclampsia
Screening tests

• Why screening
• Accuracy. Uterine artery doppler at 24 weeks,
  notching on both uterine arteries identifies 80
  who will develop PET,,, 5 false positive

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Pre-eclampsia
Investigations
Maternal
Fetal
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Pre-eclampsia
Prevention
Methods Used to Prevent Hypertensive Disorders of
Pregnancy  Proper prenatal care  Low-salt
diet  Diuretics  Antihypertensive
drugs  Nutritional supplementation   Magnesium
(365 mg/d)  Zinc (20 mg/d)  Calcium (1500200
mg/d)  Fish oil  Antithrombotic agents
  Low-dose aspirin (50150 mg/d)  Dipyridamole
(225300 mg/d)  Subcutaneous heparin (15,000
IU/d)
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Prevention
Low doses of aspirin do help prevent
pre-eclampsia, but there is little information
about whether they are of benefit for treatment
of established pre-eclampsia cochrane 22
April 2003
Pre-eclampsia is a condition in pregnancy
involving high blood pressure and protein in the
urine. It can lead to serious complications and
death. As pre-eclampsia affects blood clotting,
antiplatelets (drugs like aspirin which can
prevent blood clots) are used for pre-eclampsia.
The review of trials found that low doses of
aspirin lowered the risk of pre-eclampsia a
little (15 lowering in the risk), with a similar
lowering in the risk of the baby dying (14) and
a very small lowering in the risk of the baby
being born too early (8). Doses less than 75mg
appear to be safe. Higher doses may be better,
but as the risks of adverse effects may also
increase, more research is needed.
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Prevention
Calcium supplements may prevent high blood
pressure and help prevent preterm labour
cochrane 22 April 2003
Main results Eleven studies were included, all
of good quality. There was a modest reduction in
high blood pressure with calcium supplementation
. The effect was greatest for women at high risk
of hypertension (relative risk 0.45, 95
confidence interval 0.31 to 0.66) and those with
low baseline dietary calcium (relative risk 0.49,
95 confidence interval 0.38 to 0.62).
Reviewers' conclusions Calcium supplementation
appears to be beneficial for women at high risk
of gestational hypertension and in communities
with low dietary calcium intake. Optimum dosage
requires further investigation.
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• SERIOUS COMPLICATIONS -

• HELLP SYNDROME
• ABRUPTIO PLACENTAE
• PULMONARY OEDEMA
• ACUTE RENAL FAILURE
• CEREBRAL HAEMORRHAGE
• VISUAL DISTURBANCES BLINDNESS
• HEPATIC RUPTURE
• ELECTROLYTIC IMBALANCE
• POSTPARTUM COLLAPSE

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HYPERTENSION DURING PREGNANCY
OBJECTIVES OF MANAGEMENT

• CURE / PREVENT PROGRESSION -
• CLOSE MONITORING
• REDUCE BLOOD PRESSURE -TATRGET- 140/90
• PROMOTE FOETAL MATURITY
• PROLONG PREGNANCY (34 - 36 WEEKS)
• TO ACHIEVE FOETAL MATURITY ? TERMINATION
• DELIVERY- BEST DAY, BEST WAY BEST PLACE
• PREVENT / MANAGE COMPLICATIONS

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HYPERTENSION DURING PREGNANCY
MONITORING
MATERNAL

• LOOK FOR APPEARANCE OF OMINOUS FEATURES
• DAILY- RECORD B.P 4 TIMES, MONITOR URINE OUTPUT
  TEST FOR PROTEINURIA QUALI. / QUANT
• ALT.DAY- BODY WEIGHT
• EVERY 4TH DAY- URIC ACID, PLATELET COUNT, L.F.T.
  (LDH)
• WEEKLY- CREATININE

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HYPERTENSION DURING PREGNANCY
MONITORING
FOETAL

• DAILY - CLINICAL FOETAL MONITORING - FHS, FUNDAL
  Ht. ABDOMINAL GIRTH, LIQUOR, FOETAL MOVEMENT
  COUNT, C.T.G
• USG - ON ADMISSION THEN 3 WEEKLY FOR FOETAL
  BIOPHYSICAL PARAMETERS, PLACENTA AND LIQUOR
  VOLUME
• DOPLLER USG FOR PLACENTAL BLOOD FLOW VELOCITY
  EVERY 4TH DAY
• L/S RATIO FOR MATURITY

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MANAGEMENT OF PRE-ECLAMPSIA
the principles are early recognition of
the symptomless syndrome awareness of serious
nature of the condition in its severe form
without over-reacting to mild disease agreed
guidelines for admission to hospital,
investigation, and use of anti hypertensive and
anticonvulsant therapy well-timed delivery to
pre-empt serious maternal or fetal complications
postnatal follow-up and counselling for future
pregnancies.
Clinical observation and investigation
Examination (over and above routine) palpation
of the femoral pulses (to exclude coarctation of
aorta) look for hyperreflexia and ankle
clonus check optic fundi for silver wiring,
arterio-venous nipping, exudates and haemorrhage.
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Laboratory investigation Proteinuria-. If
present also check urine microscopy and culture
to exclude urinary infection. Serum urate levels
increase early in pre-eclampsia. Levels gt350
pmol/L are abnormal in pregnancy but gradually
increasing levels are more significant. Serum
urea and creatinine. Rising levels are
significant but not such sensitive indicators of
pre-eclampsia as uric acid. The upper limits of
normal in pregnancy are 5 mmol/L for serum urea
and 100 pmol/L for creatinine, but trends are
even more important than specific levels.
Platelet count gradually falls if disseminated
Intravascular coagulation is occurring.
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Laboratory investigation
Liver function-this should be checked once
persistent proteinuria is present, or if platelet
count is significantly reduced. It can be
detected by elevation of liver enzymes (not
alkaline phosphatase, which is normally raised
because it is produced by the placenta).
Coagulation studies should be carried out if
platelet count is reduced, and in severe
disease. Tests of fetal growth and well-being
Each of these tests should be repeated as often
as is clinically necessary.
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Pre-eclampsia
Treatment
definite treatment is delivery (ending the
pregnancy). But, Mother vs. Fetus
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Pre-eclampsia
Treatment
Mild pre-eclampsia
diastolic /90-95 proteinurea trace-1
Moderate pre-eclampsia Severe pre-eclampsia
Does the treatment improve the condition? Then
why. Adv/disadv
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Management of mild (non-proteinuric)
pre-eclampsia The principles are uncomplicated
hypertension is suitable for careful supervision
at home by the primary health care team anti
hypertensive therapy is not indicated admission
to hospital is indicated when -SBP is 160
and/or DBP 100 mmHg or greater -proteinuria is
detected in a clean (i.e. mid-stream) urine
sample in the absence of a urinary
infection -the patient is symptomatic with e.g.
visual disturbances, unusual headache, epigastric
pain, or vomiting (URGENT!) there is clinical
evidence of intrauterine growth retardation
tests of fetal welfare have deteriorated -4-a
previous bad obstetric history suggests that
closer surveillance would be worthwhile.
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MANAGEMENT OF SEVERE HYPERTENSION
The maternal risks of cerebrovascular accident
and of left ventricular or renal failure begin to
increase significantly when hypertension is
severe. The choice has then to be made between
delivery and antihypertensive therapy. Among
the factors to be considered are gestational
age-it is seldom justified to commence long-term
oral therapy from 34 weeks the severity of other
signs and symptoms availability of intensive
neonatal care facilities. gtK Treatment neither
influences the progression of underlying
preeclampsia nor significantly improves fetal
outcome. It helps to protect the mother and
enables many pregnancies to continue that
otherwise would be ended because of maternal
risk.
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CONTROL OF ACUTE SEVERE HYPERTENSION
There is no consensus on the optimum acute
treatment. The important objective is to reduce
the blood pressure to safe levels (but not too
low!). Parenteral hydralazine is used most
commonly but oral nifedipine should be considered
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LONGER-TERM CONTROL OF SEVERE HYPERTENSION
The combined a- and (B- blocking agent labetalol
is commonly used. The potent vasodilator and
calcium channel blocker nifedipine is a useful
second-line treatment. Its major drawback is
severe headache. Angiotensin-converting enzyme
(ACE) inhibitors have deleterious fetal effects
and their use is not recommended. If a woman with
chronic hypertension becomes pregnant on an ACE
inhibitor, change to another anti-hypertensioe
agent is advised.
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LONGER-TERM CONTROL OF SEVERE HYPERTENSION
There is still insufficient trial evidence to
determine whether the benefits outweigh any
disadvantages. If it is to be used, the
suggested indications are ,-DBP gt_100
mmHg -pregnancy lt_34 weeks fetal and maternal
state otherwise good. Methyldopa remains the
drug of first choice. The combined a- and (B-
blocking agent labetalol is commonly used. The
potent vasodilator and calcium channel blocker
nifedipine is a useful second-line treatment. Its
major drawback is severe headache. Angiotensin-con
verting enzyme (ACE) inhibitors have deleterious
fetal effects and their use is not recommended.
If a woman with chronic hypertension becomes
pregnant on an ACE inhibitor, change to another
anti-hypertensioe agent is advised.
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TTiming of delivery The most common grounds for
delivery are progressive fetal compromise (i.e.
when the baby is safer delivered) uunacceptable
risk to maternal health, e.g. uncontrollable BP,
impending renal failure or heart failure, HELLP
syndrome, DIC, eclampsia (see below). .
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The mode of delivery (caesarean section versus
vaginal) depends on -the seriousness of the
situation -the gestational age -the degree of
fetal/maternal compromise. Epidural analgesia
is the method of choice for labour (as long as a
coagulation defect has been excluded).
Appropriate facilities for the care of the
newborn available