Transcript โดย พญ. มนทินี ใช้ปัญญา PIH(Pregnancy-induced- hypertension)

PIH(Pregnancy-inducedhypertension)
โดย
พญ. มนทินี ใช้ ปัญญา
17 มิถุนายน 2546
ห้ องประชุมชัยพฤกษ์
โรงพยาบาลโพธาราม
ความสาคัญ
Common and form one of the deadly triad
(hemorrhage,infection)
 most common medical risk factor (Ventura
and colleagues,2000, National Center for
Health Statistics)
 18% of maternal deaths in USA(19871990) were from complication of PIH
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Terminology

Any new-onset pregnancy-related
hypertension
include hypertension without proteinuria
 potential precursor to preeclampsia or
eclampsia
 most hypertensive nulliparous women had
only transient uncomplicated hypertension
that subsided promptly after delivery
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Diagnosis
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Gestational hypertension
( PIH or transient hypertension )
Preeclampsia
Eclampsia
Preeclampsia superimposed on chronic
hypertension
Chronic hypertension
Gestational hypertension
(PIH or transient hypertension)
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BP >/= 140/90 mmHg for first time during
pregnancy
No proteinuria
BP return to normal < 12 weeks’ postpartum
Final diagnosis made only postpartum
May have other signs of preeclampsia, for
example, epigastric discomfort or
thrombocytopenia
Transient hypertension
:preeclampsia does not develop and BP has
turned to normal by 12 weeks’ postpartum
Preeclampsia

Minimal criteria :
1.BP >/= 140/90 mmHg after 20 weeks’
gestation
2.Proteinuria >/= 300 mg/24 hours or >/= 1+
dipstick
Increased certainty of preeclampsia :
BP >/= 160/110mmHg
 Proteinuria 2.0 g/24 hours or >/= 2+ dipstick
 Serum creatinine > 1.2 mg/dL unless known to be
previously elevated
 Platelets < 100,000/mm3
 Microangiopathic hemolysis (increased LDH)
 Elevated ALT or AST
 Persistent headache or other cerebral or visual
disturbance
 Persistent epigastric pain
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Severity of preeclampsia
Mild
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DBP : < 100 mmHg
proteinuria : trace to
1+
headache : absent
visual disturbance :
absent
upper abdominal pain :
absent
oliguria : absent
convulsion : absent
Severe
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>/= 110 mmHg
>/= 2+
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present
present
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present
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present
present(eclampsia)
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Severity of preeclampsia(2)
Mild
Severe
Serum creatinine :
normal
 thrombocytopenia :
absent
 liver enzyme elevation
:minimal
 fetal growth
restriction : absent
 pulmonary edema :
absent

elevated

present

marked

obvious

present
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Eclampsia
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Preeclampsia that is complicated by
generalized tonic-clonic convulsions
fatal coma without convulsions
All pregnant women with convulsions should
be considered to have eclampsia
Most common in the last trimester
increasingly more frequent as term
approaches
Eclampsia (2)
Seizures may appear before, during or
after labor
 Seizures that develop more than 48 hours
postpartum may be encountered up to 10
days postpartum
 the convulsive movements
---> facial twitchings

---> generalized muscular contraction
---> jaws open and close violently
---> all muscles alternately contract and relax
---> lies motionless
Complication of eclampsia
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respiratory arrest, coma, hypoxemia --> lactic acidosis
fever : from CNS hemorrhage
fetal bradycardia (usually recovers 3
- 5 min, if > 10 min --->placental
abruption must be considered
Complication (2)
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pulmonary edema : aspiration
pneumonitis, cardiac failure
blindness : retinal detachment,
occipital lobe ischemia, infarction,
edema (prognosis is good and usually
complete return to normal < 1 wk)
psychosis : usually lasts for < 2 wk
Superimposed Preeclampsia
( on chronic hypertension )
New-onset proteinuria >/= 300 mg/24
hours in hypertensive women but no
proteinuria before 20 weeks’ gestation
 A sudden increase in proteinuria or blood
pressure or platelet count < 100,000/mm3
in women with hypertension and
proteinuria before 20 weeks’ gestation
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Chronic hypertension
BP >/= 140/90 mmHg before pregnancy or
diagnosed before 20 weeks’ gestation or
 Hypertension first diagnosed after 20
weeks’ gestation and persistent after 12
weeks’ postpartum
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Underlying chronic hypertension
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Essential familial hypertension
arterial abnormalities
renovascular hypertension
coarctation of aorta
endocrine disorders
diabetes
cushing syndrome
primary aldosteronism
pheochromocytoma
thyrotoxicosis
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Glomerulonephritis (acute and chronic)
renoprival hypertension
chronic glomerulonephritis
chronic renal insufficiency
diabetic nephropathy
polycystic kidney disease
acute renal failure
obesity
connective-tissue diseases
lupus erythematosus
scleroderma
periarteritis nodosa
Risk factor
Multiple pregnancy
 Familial history of PIH
 DM
 Antiphospholipid syndrome
 History of chronic hypertension
 Maternal age > 35 year
 Obesity
 African-American ethnicity(Conde - Agudelao and
Beligan,2000;Sibai and
colleagues,1997;Walker,2000)

Smoking during pregnancy has been
associated with a reduced risk of
hypertension during pregnancy( Zhang and
colleagues, 1999)
 Placenta previa has also been claimed to
reduce risk of hypertensive disorders due
to pregnancy(Ananth and colleagues, 1997 )
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Pathogenesis
Risk factors
Vasospasm
platelet aggregation
PGI2
TXA2,
vasoconstrictor
microangiopathy
regional bl. flow
Pathology
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Cardiovascular changes :
Hypovolemia :
- from vasospasm and
increased vascular permeability
---> hemoconcentration
---> edema
Coagulation :
- thrombocytopenia
- microthrombi ---> DIC
- decreased antithrombin III ---> prolong PT
-microangiopathy ---> fragmentation hemolysis
Pathology (2)
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Fluid and electrolyte changes :
HCO3 is lowered following an eclamptic convulsion
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Kidney :
Decreased GFR
---> oliguria
---> renal failure
---> uric acid, creatinine is elevated
Glomerulopathy
---> proteinuria
Increased tubular reabsorption
---> increased serum calcium
Pathology(3)
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Liver : elevated liver enzyme in severe case
subcapsular hematoma
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Brain : infarction, hemorrhage, cerebral edema --
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Placenta : decreased blood flow
-> headache, visual disturbance, convulsion
EEG --->nonspecific change
---> IUGR, fetal distress
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Lung : pulmonary edema
HELLP Syndrome
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Hemolysis
Elevated liver enzymes
Low Platelet
Prediction
Angiotensin sensitivity test : angiotensin II
infusion
 roll over test
 uric acid
 Ca metabolism
 fibronectin
 urinary kallikrein excretion
 coagulation activator
 marker of oxidative stress
 immunological factors
 placental peptides
 doppler velocimetry of the uterine arteries
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Prevention
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Early prenatal detection :
1 -28 wk., ANC every 4 wk.
28 - 36 wk., ANC every 2 wk.
> 36 wk., ANC every 1 wk.
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Dietary manipulation :
salt restriction, high calcium, fish oil
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Low dose aspirin :
suppression of thromboxane synthesis
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Antioxidant : control lipid peroxidation --/-->
endothelial cell dysfunction
Management
Objective
 termination of pregnancy with the least
possible trauma to mother and fetus
 birth of an infant who subsequently thrives
 complete restoration of health to the
mother
Hospital management
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Detailed examination
BW. OD
Urine protein on admittance
and at least every 2 days thereafter
BP every 4 hours, except between midnight and
morning
Plasma creatinine, Hct., platelet count, liver
enzymes
Frequent evaluation of fetal size and amniotic
fluid volume either clinlcally or with sonography
Hospital management(2)
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Reduce physical activity is beneficial (absolute bed
rest is not necessary, sedatives and transquilizers
are not prescribed)
protein and calories should be included in the diet
sodium and fluid intake should not be limited or
forced
further management depends upon
1. Severity of preeclampsia
2. Duration of gestation
3. Condition of the cervix
Specific treatment
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Prevent convulsion
control BP
termination of
pregnancy
Prevent convulsion
MgSO4 therapy is superior to phenytoin in
preventing eclamptic seizures
 Hallak and associates (1999) ---> maternal
seizures were associated with fetal brain
injury due to maternal hypoxia during the
convulsion
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MgSO4 dosage schedule
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Continuous intravenous infusion
1. MgSO4 4 - 6 g. + 100 mL of IV fluid IV
drip in 15 - 20 min.
2. Begin 2 g/h in 100 mL of IV maintenance
infusion
3. Serum Mg level at 4 - 6 h, keep levels
between 4 -7 mEq/L
4. MgSO4 is discontinued 24 h after delivery
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Intermittent intramuscular injections
1. 20%MgSO4 4 g IV push (rate < 1 g/min)
2. 50% MgSO4 10 g IM at buttock
(ข้างละ5 g+1.0 mL of 2%lidocaine )
If convulsions persist after 15 min,
--- 20% MgSO4 2-4 g IV push (rate < 1 g/min)
3. 50% MgSO4 5 g IM alternate buttock q 4 hr.
but only after assuring that :
a. the patellar reflex is present
b. respirations are not depressed
c. urine output >/= 100 ml /4 hr.
4. MgSO4 is discontinued 24 h after delivery
Antihypertensive drug therapy
Sibai and associates (1987) --->growthrestricted infants were twice as frequent
in patient given labetalol compared with
those treated by hospitalization alone
 Von Dadelszen and associates (2000) -->treatment - induced decreases in maternal
BP may adversely affect fetal growth
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Antihypertensive drug therapy (2)
Easterling and colleagues (1999) ---> women
at risk for preeclampsia ( high cardiac
output measured by doppler technique at
24 wk) were randomized to prophylactic
atenolol or placebo, the incidence of
preeclampsia in control group : atenolol
group = 18 : 4
 the use of ACEI during second and third
trimesters should be avoided
 diuretics should not be used
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Hydralazine
SBP >/= 160 mmHg and/or DBP > 105 mmHg
(National High Blood Pressure Education
Program, 2000 )
 5 mg IV as the initial dose
 5 - 10 mg IV q 15 - 20 min. until a
satisfactory response is achieved
 Satisfactory response = DBP 90 - 100
mmHg
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Labetalol
Lower BP more rapidly, and associates
tachycardia was minimal, but hydralazine
lowered MAP to save levels more
effectively
 The Working Group(2000) recommends 20
mg IV bolus.
 If not effective within 10 min, this is
followed by 40 mg, then 80 mg every 10 min
but not to exceed a 220 mg total dose
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Termination of pregnancy
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Severe preeclampsia
Near term
Post-partum
Physiologic diuresis : 12 -72 h postpartum
 proteinuria and edema disappear < 1 wk
 BP returns to normal within a few days to 2
weeks
 Gestational hypertension must resolve
within 12 weeks
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Counseling for future pregnancies
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Women who had preeclampsia are
more prone to hypertensive
complications in future pregnancies
The earlier diagnosis, the greater
recurrence
Multiparous are at increased risk
compared with nulliparas
Counseling (2)
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Women with early-onset severe PIH
may be at risk for underlying
thrombophilias (factor V Leiden,
protein S and C deficiency,
antiphospholipid antibodies)
Preeclampsia does not cause chronic
hypertension