Transcript Module 3 chapter 1c - The Association of Physicians of India

MODULE 3 CHAPTER 2 E
PLAN
• Diagnosis and classificaton of hypertension in
pregnancy
• Pathophysiology
• Evaluation of newly diagnosed Hypertension
Gestational Vs Preeclampsia
Mild or severe
Measure protein excretion
Look for high risk symptoms
Perform lab evaluation
Assess fetal wellbeing
• Management
• Conclusion
DIAGNOSIS AND CLASSIFICATION
Introduction
• Most common medical complication of pregnancy
• 5-10 % of gestations in India.
• In 2000, the National High Blood Pressure Education
Program Working Group on High Blood Pressure in
Pregnancy defined four categories of hypertension in
pregnancy:
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Chronic hypertension
Gestational hypertension
Preeclampsia
Preeclampsia superimposed on chronic hypertension
MEASUREMENT TECHNIQUE
• In seated position- Relaxed
• Use correct cuff size
• Avoid Vena-caval compression when supine –
left lateral decubitus
• Avoid terminal digit preference– Read off to
the nearest 2mm of Hg.
• Diastolic pressure is at K V
• If K sounds heard till zero both K 4 and 5 levels
to be mentioned eg 140/70/0
Chronic Hypertension Defined
1. BP measurement of 140/90 mm Hg or more
on two occasions six hours apart
2. Before 20 weeks of gestation OR
beyond 12 weeks postpartum
Persisting
Gestational Hypertension
• Formerly called PIH (Pregnancy Induced HTN)
• HTN without proteinuria occurring after 20
weeks gestation and returning to normal within
12 weeks after delivery.
• 50% of women diagnosed with gestational
hypertension between 24 and 35 weeks develop
preeclampsia.
Older Criteria for Gestational
HTN
• 30/15 increase in BP over baseline levels
• No longer appropriate
• 73% of patients will exceed 30 mm systolic
and 57% will exceed 20 mm diastolic
Preeclampsia
• New onset hypertension with proteinuria after 20
weeks gestation.
• Resolves by 6 weeks postpartum.
• Characterized as mild or severe based on the degree
of hypertension and proteinuria, and the presence of
symptoms resulting from involvement of the kidneys,
brain, liver, and cardiovascular system
PATHOPHYSIOLOGY
Risk Factors
FACTOR
Renal disease
RISK RATIO
20:1
Chronic hypertension
Antiphospholipid
syndrome
10:1
10:1
Family history of PIH
Twin gestation
5:1
4:1
Nulliparity
Age > 40
3:1
3:1
Diabetes mellitus
2:1
African American
1.5:1
EVALUATION
EVALUATION
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Chronic Vs pregnancy induced hypertension
Gestational Vs preeclampsia
Mild Vs severe gestational hypertension
Mild Vs severe preeclampsia
Preclampsia Vs eclampsia
GESTATIONAL VS PREECLAMPSIA
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GESTATIONAL
Primi not a strong RF
Recurrent risk 20-47%
Total blood and plasma
volume not low
• Proteinuria absent
• Odema absent
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PREECLAMPSIA
Primi
Recuurent risk 5%
Total blood and plasma
volume low
• Proteinuria present
• Odema present
GESATATIONAL HYPERTENSION
MILD VS SEVERE
• MILD
• SEVERE
• SBP 140- 160
• DBP 90- 110
• SBP >160
• DBP>110
THERE IS NO MODERATE HYPERTENSION IN PREGNANCY
PREECLAMPSIA - MILD VS SEVERE
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Multiorgan Effects of Preeclamsia
• Cardiovascular – HTN, increased cardiac
output, increased systemic vascular
resistance, hypovolemia
• Neurological – Seizures-eclampsia, headache,
cerebral edema, hyperreflexia
• Pulmonary – Capillary leak, reduced colloid
osmotic pressure, pulmonary edema
Multiorgan Effects cont….
• Hematologic – Volume contraction, elevated
hematocrit, low platelets, anemia due to
hemolysis
• Renal – Decreased GFR, increased
BUN/creatinine, proteinuria, oliguria, ATN
• Fetal – Increased perinatal morbidity,
placental abruption, fetal growth restriction,
oligohydramnios, fetal distress
Eclampsia
• New onset of seizures in a woman with preeclampsia.
• Preceded by increasingly severe preeclampsia, or
it may appear unexpectedly in a patient with
minimally elevated blood pressure and no
proteinuria.
• Blood pressure is only mildly elevated in 30-60%
of women who develop eclampsia.
• Occurs: Antepartum - 53%, intrapartum - 19%, or
postpartum - 28%
Diagnostic Criteria for
Preeclampsia
1.
SBP of 140 mm Hg or more or a DBP of 90 mm Hg or more on two
occasions at least six hours apart after 20 weeks of gestation AND
2.
Proteinuria –> 300 mg in a 24-hour urine specimen or 1+ or greater on
urine dipstick testing of two random urine samples collected at least
four hours apart.
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A random urine protein/creatinine ratio < 0.21 indicates that significant
proteinuria is unlikely with a NPV of 83%;,values >0.7 indicates definite
proteinuria.
Generalized edema (affecting the face and hands) is often present in
patients with preeclampsia but is not a diagnostic criterion.
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Headache
Visual disturbance
Dyspnoea
Right upper
quadrant
pain
Low urine
output
Chest pain
Pregant woman with these
Symptoms should be
Suspected to have preeclampsia
Even when there is no
proteinuria
Severe odema
MATERNAL INVESTIGATION
• Full blood count:- Haemoglobin,
hematocrit, platelet count and blood film if
there is any evidence of hemolysis
• Biochemistry:Urea, Creatinine, electrolytes,
and uric acid, LFT
• 24 hr. urine save: total protein assessment
+- catecholamines
• Others:ANA, anti-cardiolipin, lupus
anticoagulant, for early onset PET ( ie <32
weeks)
HELLP Syndrome
• Is a variant of severe preeclampsia
• Occurs in up to 20% of pregnancies
complicated by severe preeclampsia.
• Variable clinical presentation; 12 to 18% are
normotensive and 13% do not have
proteinuria.
• At diagnosis, 30% of women are postpartum,
18% are term, and 52% are preterm.
HELLP Syndrome
• Common presenting complaints are RUQ or
epigastric pain, N/V, malaise or nonspecific
symptoms suggesting an acute viral syndrome.
• Any patient with these symptoms or signs of
preeclampsia should be evaluated with CBC, platelet
count, and liver enzymes.
• When platelet count < 50,000/mm3 or active
bleeding occurs, coagulation studies needed to R/O
DIC.
FETAL ASSESSMENT
• Ultrasound estimation of fetal size:head and
abdominal circumferences and the ratio
between the two
• Biophysical profile: fetal movement, tone,
breathing movements & liquor volume + fetal
heart rate assessment
• Cardiotocography:Standard or computerised
• Doppler ultrasound: uterine arteries, umblical
arteries, +- fetal regional studies
• Others: amniocentesis, fetal blood sample
UMBILICAL ARTERY DOPPLER
NORMAL
HIGH RISK
MANAGEMENT
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WHEN TO START
WHAT LEVEL TO START
WHAT LEVEL TO BE ACHIEVED
WHAT IS FETAL OUTCOME
WHICH IS IDEAL DRUG
WHAT SPEED
WHEN TO START SECOND DRUG
Blood pressure goal
• A reasonable goal of therapy in women
without end-organ damage is systolic pressure
between 140 and 150 mmHg and diastolic
pressure between 90 and 100 mmHg . Overly
aggressive blood pressure reduction could be
harmful.
• One analysis reported that a 10 mmHg fall in
mean arterial pressure was associated with a
176 g decrease in birth weight . This effect was
unrelated to the type of hypertension or
choice of medication.
Criteria for Treatment
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Diastolic BP > 105-110
Systolic BP > 160
Avoid rapid reduction in BP
Do not attempt to normalize BP
Goal is DBP < 105 not < 90
May precipitate fetal distress
Gestational HTN at Term
• Delivery is always a reasonable option if term
• If cervix is unfavorable and maternal disease is
mild, expectant management with close
observation is possible
Mild Gestational HTN Not at Term
140-150/90-100
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Rule out severe disease
Conservative management
Serial labs
Twice weekly visits
Antenatal fetal surveillance
Outpatient versus inpatient
Ideal time of delivery is 40 weeks
Anti hypertensive therapy in young patients
with low pre pregancy BP with high risk
symptoms
Management of Preeclampsia
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The ultimate cure is DELIVERY.
Assess gestational age
Assess cervix
Fetal well-being
Laboratory assessment
Rule out severe disease
Indications for Delivery in Preeclampsia
• Maternal indications
– Gestational age of 38 weeks or greater
– Platelet count below 100,000
– Progressive deterioration of hepatic or renal
function
– Suspected placental abruption
– Persistent severe headache or visual changes
– Persistent severe epigastric pain, nausea, or
vomiting
– Eclampsia
Indications for Delivery in Preeclampsia
• Fetal indications
– Severe intrauterine growth restriction
– Nonreassuring fetal surveillance
– Oligohydramnios
ANTI HYPERTENSIVE DRUGS
Hypertensive Emergencies
• Fetal monitoring
• IV access
• IV hydration to maintain urine output > 30 mL
per hour, limit to 100 mL per hour.
• The reason to treat is maternal, not fetal
• May require ICU
Characteristics of Severe HTN
• Crises are associated with hypovolemia
• Clinical assessment of hydration is inaccurate
• Unprotected vascular beds are at risk, ie.,
uterine
Key Steps Using Vasodilators
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250-500 cc of fluid, IV
Avoid multiple doses in rapid succession
Allow time for drug to work
Maintain LLD position
Avoid over treatment
Acute Medical Therapy
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Hydralazine
Labetalol
Nifedipine
Nitroprusside
Clonidine
Hydralazine
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Dose: 5-10 mg every 20 minutes
Onset: 10-20 minutes
Duration: 3-8 hours
Side effects: headache, flushing, tachycardia,
lupus like symptoms
• Mechanism: peripheral vasodilator
Labetalol
• Dose: 20 mg, then 40, then 80 every 20
minutes, for a total of 220mg
• Onset: 1-2 minutes
• Duration: 6-16 hours
• Side effects: hypotension
• Mechanism: Alpha and Beta blockade
Nifedipine
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Dose: 10 mg po, not sublingual
Onset: 5-10 minutes
Duration: 4-8 hours
Side effects: chest pain, headache, tachycardia
Mechanism: CA channel blockade
Clonidine
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Dose: 1 mg po
Onset: 10-20 minutes
Duration: 4-6 hours
Side effects: unpredictable, avoid rapid
withdrawal
• Mechanism: Alpha agonist, works centrally
Nitroprusside
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Dose: 0.2 – 0.8 mg/min IV
Onset: 1-2 minutes
Duration: 3-5 minutes
Side effects: cyanide accumulation,
hypotension
• Mechanism: direct vasodilator
Seizure Prophylaxis
• Magnesium sulfate
• Loading dose of 4 to 6 g diluted in 100 mL of
normal saline, given IV over 15 to 20 minutes,
followed by a continuous infusion of 1-2 g per
hour
• Monitor urine output, RR and DTR’s
• With renal dysfunction, may require a lower
dose
Treatment of Eclampsia
• Protecting the patient and her airway
• Place patient on left side and suction to
minimize the risk of aspiration
• Give oxygen
• Avoid insertion of airways and padded tongue
blades
• IV access
• Mag Sulfate 4-6 g IV bolus, if not effective,
give another 2 g
Magnesium Sulfate
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Is NOT a hypotensive agent
Works as a centrally acting anticonvulsant
Also blocks neuromuscular conduction
Serum levels: 4-7 mg/dL
Additional benefit of reducing the incidence of
placental abruption
Toxicity
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Respiratory rate < 12
DTR’s not detectable
Altered sensorium
Urine output < 25-30 cc/hour
Antidote: 10 ml of 10% solution of calcium
gluconate 1 g IV over 2 minutes.
Alternate Anticonvulsants
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Diazepam 5-10 mg IV
Sodium Amytal 100 mg IV
Pentobarbital 125 mg IV
Dilantin 500-1000 mg IV infusion
After the Seizure
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Assess maternal labs
Fetal well-being
Effect delivery
Transport when indicated
No need for immediate cesarean delivery
Other Complications
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Pulmonary edema
Oliguria
Persistent hypertension
DIC
Pulmonary Edema
• Fluid overload
• Reduced colloid osmotic pressure
• Occurs more commonly following delivery as
colloid oncotic pressure drops further and
fluid is mobilized
Treatment of Pulmonary Edema
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Avoid over-hydration
Restrict fluids
Lasix 10-20 mg IV
Usually no need for albumin or Hetastarch
(Hespan)
Oliguria
• 25-30 cc per hour is acceptable
• If less, small fluid boluses of 250-500 cc as
needed
• Lasix is not necessary
• Postpartum diuresis is common
• Persistent oliguria almost never requires a PA
cath
Persistent Hypertension
• BP may remain elevated for several days
• Diastolic BP less than 100 do not require
treatment
• By definition, preeclampsia resolves by 6
weeks
Disseminated Intravascular
Coagulopathy
• Rarely occurs without abruption
• Low platelets is not DIC
• Requires replacement blood products and
delivery
Prevention of Preeclampsia
• Routine supplementation with calcium, magnesium, omega-3
fatty acids, or antioxidant vitamins is ineffective.
• Calcium reduces the risk of developing preeclampsia in high-risk
women and those with low dietary calcium intake.
• Low-dose aspirin (75 to 81 mg per day) is effective for women at
increased risk of preeclampsia, NNT = 69 ; NNT = 227 to
prevent one fetal death.
• Low-dose aspirin is effective for women at highest risk from
previous severe preeclampsia, diabetes, chronic hypertension,
or renal or autoimmune disease, NNT = 18.
LONG TERM MATERNAL RISKS
• The absolute risk that a woman with or without a
history of preeclampsia would develop one of these
cardiovascular events (hypertension, CAD,stroke,
venous thrombo embolism) at age 50 to 59 years
was estimated to be 17.8 and 8.3 percent,
respectively.
• Further review of these data show that women with
early onset/severe preeclampsia, recurrent
preeclampsia, gestational hypertension, or
preeclampsia with onset as a multipara appear to be
at highest risk of cardiovascular disease later in life,
including during the premenopausal period
Chronic Hypertension
• Treatment of mild to moderate chronic
hypertension neither benefits the fetus nor
prevents preeclampsia.
• Excessively lowering blood pressure may result in
decreased placental perfusion and adverse
perinatal outcomes.
• When BP is 150 to 180/100 to 110 mm Hg,
pharmacologic treatment is needed to prevent
maternal end-organ damage.
Treatment of Chronic Hypertension
• Methyldopa , labetalol, and nifedipine most common
oral agents.
• AVOID: ACEI and ARBs, atenolol, thiazide diuretics
• Women in active labor with uncontrolled severe
chronic hypertension require treatment with
intravenous labetalol or hydralazine.
CONCLUSION
The cure is achieved by delivery, which
removes the diseased tissue—the placenta.
In short, the need is to deliver before it is
too late. To achieve this apparently simple
end, the clinician must detect the
symptomless prodromal condition by
screening all pregnant women, admit to
hospital those with advanced preeclampsia
so as to keep track of an unpredictable
situation, and time preemptive delivery to
maximize the safety of mother and baby.
--REDMAN AND ROBERTS
END OF MODULE 3 CHAPTER 2 E