病 例
张平, 女,36岁，以“停经九个月，胎动五个
月，双下肢浮肿两周，头晕眼花一小时。”为主诉
入院。早孕反应及胎动如期出现，两周前无明显诱
因双下肢浮肿，休息后无好转。一小时前出现头晕
眼花。既往无高血压，慢性肾炎病史。
查体,T36.7℃, P78次 /分,BP175/110mmHg,
心肺听诊无异常，腹膨隆，足月腹型,LOA,浮肿
+++。
实验室检查：血常规示 PL258G/L,HGB108g /
L,HCT0.45。 尿常规示蛋白 +++。
辅助检查,B超示 BPD9.0cm,FL7.2cm,胎盘
钙化 Ⅱ 级。 NST有反应型。
Hypertensive disorder
complicating pregnancy
妊娠期高血压疾病
H y pe rt e n s i v e d i s e a s e i n pre g na n c y
1, g e s t a t i o n a l h y p e r t e n s i o n ( t r a n s i e n t h y p e r t e n s i o n )
( a B P g r e a t e r t h a n 140 m m H g / 90 m m H g wit h o u t pr ot e i nu r i a or
e n d - or g a n da m a ge )
2,p r e e c l a m p s i a
( n or m ot e ns i v e,pr e gn a n t pa t i e n t s w h o h a v e s us t a i n e d hy p e r t e ns i o n,
pr ot e i nu r i a,a n d e de m a a f t e r t h e 20t h we e k of g e s t a t i o n ) 50- 70%
3, E c l a m p s i a
Oc c u r r e n c e of s e i z u r e s i n a wo m e n wit h pr e e c l a m p s i a t ha t c a n n ot
be a t t r i bu t e d t o ot h e r c a us e s,I t m a y a ppe a r be f or,d u r i ng a n d a f t e r
l a bor,
4, c h r o n i c h y p e r t e n s i o n w i t h s u p e r i m p o s e d p r e e c l a m p s i a ;
15- 30%
5,c h r o n i c h y p e r t e n s i o n b e g i n s p r i o r t o p r e g n a n c y,
( A B P g r e a t e r t h a n 140 m m H g / 90 m m H g oc c u r s pr i or t o t he 20t h
we e k of g e s t a t i o n,i s n ot a s s oc i a t e d wit h s i gn i f i c a n t pr ot e i nu r i a or
e n d - or g a n da m a ge,a n d c o n t i nu e s we l l a f t e r de l i v e r y )
Preeclampsia
Preeclampsia is defined as the combination of
high blood pressure (hypertension),swelling
(edema),and protein in the urine (albuminuria,
proteinuria) developing after the 20th week of
pregnancy.
? Mild preeclampsia is characterized by a systolic BP
greater than 140 mm Hg or a diastolic BP greater than 90
mm Hg in a pregnant patient with minimal
proteinuria((>300mg/d )and pathologic edema.
? Severe preeclampsia A systolic BP greater than 160 mm
Hg or a diastolic BP greater than 110 mm Hg with
significant proteinuria (>5.0 g/d) and evidence of end-
organ damage,Serum creatinine>106μmol/L,
Platelet:<100x109/L elevated LDH,ALT or AST
Risk factors
extremes of maternal age,primigravida,
multiple gestations,molar pregnancy,
diabetes mellitus (DM),renal disease,
connective tissue disease,vascular
disease,prior history of preeclampsia or
eclampsia,and family history of
preeclampsia or eclampsia.
? The fetus is a semi-allograft to the mother,Immune
interaction between decidual leukocytes and invading
cytotrophoblast cells is essential for normal trophoblast
invasion and development,Immune maladaptation may
cause shallow invasion of spiral arteries by endovascular
cytotrophoblast cells and endothelial cell dysfunction
mediated by an increased decidual release of cytokines,
proteolytic enzymes,and free radical species.
? Genetic gactor
? Development of preeclampsia-eclampsia may be based on
a single recessive gene or a dominant gene with incomplete
penetrance,Penetrance may be dependent on fetal
genotype,The possibility of genetic imprinting should be
considered in future genetic investigations of preeclampsia.
? preeclampsia is a disease of first pregnancies,The
protective effect of multiparity,however,is lost
with change of partner,Also,exposure to semen
provides protection against developing
preeclampsia,Analogous to altered paternity,
artificial donor insemination and oocyte donation
are reported to result in a substantial increase of
preeclampsia,Thus,epidemiologic studies
strongly suggest that immune maladaptation is
involved in the etiology of preeclampsia.
? Normal placental development involves progressive loss of the musculoelastic tissue in
the spiral arteries that feed the vessels of the intervillous spaces,which results in uterine
blood flow increases of nearly 25% during the first trimester,In women destined to
develop preeclampsia,this physiologic dilatation of the spiral arteries does not occur
because the placental trophoblast cells do not invade the spiral arteries,In severe cases,
other pathologic changes also occur,Accumulation of fat-laden macrophages with
fibrinoid necrosis (ie,acute atherosis),disruption of the basement membranes,platelet
deposition,mural thrombi,and proliferation of intimal and smooth muscle cells all
decrease the luminal diameter,
? The narrowed and damaged spiral arteries become thrombosed,resulting in placental
infarction and necrosis,Uteroplacental blood flow then is reduced by 50-75%,The
anatomical reduction in blood flow may be complicated by vasospasm of the
uteroplacental bed,
? Decreased placental perfusion is thought to lead to fetoplacental ischemia,The ischemic
placenta may produce a circulating agent,which is currently unidentified but causes the
widespread dysfunction of the maternal vascular endothelium that leads to the systemic
manifestations of preeclampsia
Pathophysiologic changes
Pathological deterioration of function I a
numner of organs and systems has
been identified as a consequence of
Generalized vasospasm
Pathologic changes in
main organs ①
?Brain, blindness
? cerebral edema
? cerebral hemmorage
?cardiovascular change
? increased cardiac after load
? myocardial ischemia,edema
? pulmonary edema
Pathologic changes in
main organs ②
?Liver, periportal hemorrhagic necrosis
（ 门 脉周围出血坏死）
?kidneys,endothelial edema of glomerulus
?placenta, atherosclerosis
low placental perfusion
?Blood volume,hemoconcentration
?Hematological changes
? thrombocytopenia
?endocrine and metabolic changes
diagnosis
?History hypertension
proteinuria
?sign edema
symptom
convulsion,coma
blood examination
? axillary liver and renal functions
examination funduscopy of eyes
others
Differential diagnosis
?Essential hypertension and chronic
nephritis
?convulsive disorders
?the screening test,
mean arterial blood pressure
roll over test
blood variation
calcium amount in urine
Management
?Gestional hypertension
A rest
B diet
C medication,
phnobarbital （ 苯巴比妥）
diazepam（ 安定）
preeclampsia
?A,Hospitalization
?B,antispasm medication
magnesium sulfate（ 硫酸镁）
?B sedative drugs
diazepam
?C antihypertensive drugs
?D expansive volume treatment
albumin （ 白蛋白）
plasma （ 血浆）
whole blood（ 全血）
?E Diuretics,furosemide （ 速尿）
20% mannitol （ 甘露醇）
?F Termination of pregnancy
a indications,
b methods, induction of labor （ 引产）
cesarean section（剖宫产）
?G The management of eclampsia
a controlling convulsion
b nursing
c closely monitoring
Classification of PIH syndrome
classif
ication
-catiou
criteria
BP edema p r o t e i n u r i a
Mild
Moderate
present
>18.7/12KPa(140/
9 0 m m H g ￡| o r > 4 / 2 K P a
(30/15mmHg) than
basic BP
<21.3/14.6KPa
160/110mmHg
?ù 21.3/14.6KPa persrent
with symptoms
sever
+
+ ++ +++
mild
c o n v u l s i o n
preeclamp s i a
eclampsia sion
vul
sia
á? ?¤ìμ °? èe ?è
D°ì ì ó￠ 32°? ?í 2￥ ?íó? ?? óμ òe
IUGR
é¤ ′? ?o ??
è? é¤
è? °ò
íá 1? ?±? §
á? ±? ?§
á? ?§ è¨
?? è¤ ( 1±í ? ￡|
2? è? ó3
?¨ ?í í? ′ˉ ??
?2 ??
?? ?? ì? í?
3? ?￥ ?? 2?
ê¨ê μ í? ?? 1D
μ? ?§ ??
3°° 3? ÷ ?|
é? ?· ?÷ ?|
?§ ?· ?¨è ?
è? ó3
3°° 3á ?
140/9 0? ?
BP<160/110mm
Hg? ú ê2é ×
?¨ ?í í? è? ó3
±· 2¤?? à?
á? è? ó3￡ ? μ? è?
H C T ?ù 0, 3 5
?§ o? e¤′? ?ù 1,6
?¨ ?§ e¤′? ?ù 3.6
á? ±? ó? ￡? 1.020
?? °Y ó? ??
o3 ??
oü ?2
ò? ?°
o3 á? ??
?? á?
íù ì￠,3 ? °′ ??
?? ￡? ?? ?±
ACE-￠ ? ?′
μ? ê¨3 ? ú3? ? 1?
a-? ? é? ?ó ó? 1?
?? èμ à?
￡ ¨3 ￠ ?ü ′? í? 2 D￥ ￡|
° ′¨￡ ? ′? à?
?′ ?| ??
±? àü 2é 1¤￡? ?¤
?μ ￡? ?? ?′ °?
μ? ?′ 21
è? á? ￡? μ? ?′ 21
°33 °° 3￡ ? ?§ o?
D? íù é? ?ò ￡? ?¨ ?§
?| ?ù
3D e? ?¤?í
ê2? ? ê2ê 2
DP? ù 110 o r
mABP? ù >120
é¤ ?é
é¤ ?é ?? °ú
′?
áμ
?§ ?? ?| ò? 1?
张平, 女,36岁，以“停经九个月，胎动五个
月，双下肢浮肿两周，头晕眼花一小时。”为主诉
入院。早孕反应及胎动如期出现，两周前无明显诱
因双下肢浮肿，休息后无好转。一小时前出现头晕
眼花。既往无高血压，慢性肾炎病史。
查体,T36.7℃, P78次 /分,BP175/110mmHg,
心肺听诊无异常，腹膨隆，足月腹型,LOA,浮肿
+++。
实验室检查：血常规示 PL258G/L,HGB108g /
L,HCT0.45。 尿常规示蛋白 +++。
辅助检查,B超示 BPD9.0cm,FL7.2cm,胎盘
钙化 Ⅱ 级。 NST有反应型。
Hypertensive disorder
complicating pregnancy
妊娠期高血压疾病
H y pe rt e n s i v e d i s e a s e i n pre g na n c y
1, g e s t a t i o n a l h y p e r t e n s i o n ( t r a n s i e n t h y p e r t e n s i o n )
( a B P g r e a t e r t h a n 140 m m H g / 90 m m H g wit h o u t pr ot e i nu r i a or
e n d - or g a n da m a ge )
2,p r e e c l a m p s i a
( n or m ot e ns i v e,pr e gn a n t pa t i e n t s w h o h a v e s us t a i n e d hy p e r t e ns i o n,
pr ot e i nu r i a,a n d e de m a a f t e r t h e 20t h we e k of g e s t a t i o n ) 50- 70%
3, E c l a m p s i a
Oc c u r r e n c e of s e i z u r e s i n a wo m e n wit h pr e e c l a m p s i a t ha t c a n n ot
be a t t r i bu t e d t o ot h e r c a us e s,I t m a y a ppe a r be f or,d u r i ng a n d a f t e r
l a bor,
4, c h r o n i c h y p e r t e n s i o n w i t h s u p e r i m p o s e d p r e e c l a m p s i a ;
15- 30%
5,c h r o n i c h y p e r t e n s i o n b e g i n s p r i o r t o p r e g n a n c y,
( A B P g r e a t e r t h a n 140 m m H g / 90 m m H g oc c u r s pr i or t o t he 20t h
we e k of g e s t a t i o n,i s n ot a s s oc i a t e d wit h s i gn i f i c a n t pr ot e i nu r i a or
e n d - or g a n da m a ge,a n d c o n t i nu e s we l l a f t e r de l i v e r y )
Preeclampsia
Preeclampsia is defined as the combination of
high blood pressure (hypertension),swelling
(edema),and protein in the urine (albuminuria,
proteinuria) developing after the 20th week of
pregnancy.
? Mild preeclampsia is characterized by a systolic BP
greater than 140 mm Hg or a diastolic BP greater than 90
mm Hg in a pregnant patient with minimal
proteinuria((>300mg/d )and pathologic edema.
? Severe preeclampsia A systolic BP greater than 160 mm
Hg or a diastolic BP greater than 110 mm Hg with
significant proteinuria (>5.0 g/d) and evidence of end-
organ damage,Serum creatinine>106μmol/L,
Platelet:<100x109/L elevated LDH,ALT or AST
Risk factors
extremes of maternal age,primigravida,
multiple gestations,molar pregnancy,
diabetes mellitus (DM),renal disease,
connective tissue disease,vascular
disease,prior history of preeclampsia or
eclampsia,and family history of
preeclampsia or eclampsia.
? The fetus is a semi-allograft to the mother,Immune
interaction between decidual leukocytes and invading
cytotrophoblast cells is essential for normal trophoblast
invasion and development,Immune maladaptation may
cause shallow invasion of spiral arteries by endovascular
cytotrophoblast cells and endothelial cell dysfunction
mediated by an increased decidual release of cytokines,
proteolytic enzymes,and free radical species.
? Genetic gactor
? Development of preeclampsia-eclampsia may be based on
a single recessive gene or a dominant gene with incomplete
penetrance,Penetrance may be dependent on fetal
genotype,The possibility of genetic imprinting should be
considered in future genetic investigations of preeclampsia.
? preeclampsia is a disease of first pregnancies,The
protective effect of multiparity,however,is lost
with change of partner,Also,exposure to semen
provides protection against developing
preeclampsia,Analogous to altered paternity,
artificial donor insemination and oocyte donation
are reported to result in a substantial increase of
preeclampsia,Thus,epidemiologic studies
strongly suggest that immune maladaptation is
involved in the etiology of preeclampsia.
? Normal placental development involves progressive loss of the musculoelastic tissue in
the spiral arteries that feed the vessels of the intervillous spaces,which results in uterine
blood flow increases of nearly 25% during the first trimester,In women destined to
develop preeclampsia,this physiologic dilatation of the spiral arteries does not occur
because the placental trophoblast cells do not invade the spiral arteries,In severe cases,
other pathologic changes also occur,Accumulation of fat-laden macrophages with
fibrinoid necrosis (ie,acute atherosis),disruption of the basement membranes,platelet
deposition,mural thrombi,and proliferation of intimal and smooth muscle cells all
decrease the luminal diameter,
? The narrowed and damaged spiral arteries become thrombosed,resulting in placental
infarction and necrosis,Uteroplacental blood flow then is reduced by 50-75%,The
anatomical reduction in blood flow may be complicated by vasospasm of the
uteroplacental bed,
? Decreased placental perfusion is thought to lead to fetoplacental ischemia,The ischemic
placenta may produce a circulating agent,which is currently unidentified but causes the
widespread dysfunction of the maternal vascular endothelium that leads to the systemic
manifestations of preeclampsia
Pathophysiologic changes
Pathological deterioration of function I a
numner of organs and systems has
been identified as a consequence of
Generalized vasospasm
Pathologic changes in
main organs ①
?Brain, blindness
? cerebral edema
? cerebral hemmorage
?cardiovascular change
? increased cardiac after load
? myocardial ischemia,edema
? pulmonary edema
Pathologic changes in
main organs ②
?Liver, periportal hemorrhagic necrosis
（ 门 脉周围出血坏死）
?kidneys,endothelial edema of glomerulus
?placenta, atherosclerosis
low placental perfusion
?Blood volume,hemoconcentration
?Hematological changes
? thrombocytopenia
?endocrine and metabolic changes
diagnosis
?History hypertension
proteinuria
?sign edema
symptom
convulsion,coma
blood examination
? axillary liver and renal functions
examination funduscopy of eyes
others
Differential diagnosis
?Essential hypertension and chronic
nephritis
?convulsive disorders
?the screening test,
mean arterial blood pressure
roll over test
blood variation
calcium amount in urine
Management
?Gestional hypertension
A rest
B diet
C medication,
phnobarbital （ 苯巴比妥）
diazepam（ 安定）
preeclampsia
?A,Hospitalization
?B,antispasm medication
magnesium sulfate（ 硫酸镁）
?B sedative drugs
diazepam
?C antihypertensive drugs
?D expansive volume treatment
albumin （ 白蛋白）
plasma （ 血浆）
whole blood（ 全血）
?E Diuretics,furosemide （ 速尿）
20% mannitol （ 甘露醇）
?F Termination of pregnancy
a indications,
b methods, induction of labor （ 引产）
cesarean section（剖宫产）
?G The management of eclampsia
a controlling convulsion
b nursing
c closely monitoring
Classification of PIH syndrome
classif
ication
-catiou
criteria
BP edema p r o t e i n u r i a
Mild
Moderate
present
>18.7/12KPa(140/
9 0 m m H g ￡| o r > 4 / 2 K P a
(30/15mmHg) than
basic BP
<21.3/14.6KPa
160/110mmHg
?ù 21.3/14.6KPa persrent
with symptoms
sever
+
+ ++ +++
mild
c o n v u l s i o n
preeclamp s i a
eclampsia sion
vul
sia
á? ?¤ìμ °? èe ?è
D°ì ì ó￠ 32°? ?í 2￥ ?íó? ?? óμ òe
IUGR
é¤ ′? ?o ??
è? é¤
è? °ò
íá 1? ?±? §
á? ±? ?§
á? ?§ è¨
?? è¤ ( 1±í ? ￡|
2? è? ó3
?¨ ?í í? ′ˉ ??
?2 ??
?? ?? ì? í?
3? ?￥ ?? 2?
ê¨ê μ í? ?? 1D
μ? ?§ ??
3°° 3? ÷ ?|
é? ?· ?÷ ?|
?§ ?· ?¨è ?
è? ó3
3°° 3á ?
140/9 0? ?
BP<160/110mm
Hg? ú ê2é ×
?¨ ?í í? è? ó3
±· 2¤?? à?
á? è? ó3￡ ? μ? è?
H C T ?ù 0, 3 5
?§ o? e¤′? ?ù 1,6
?¨ ?§ e¤′? ?ù 3.6
á? ±? ó? ￡? 1.020
?? °Y ó? ??
o3 ??
oü ?2
ò? ?°
o3 á? ??
?? á?
íù ì￠,3 ? °′ ??
?? ￡? ?? ?±
ACE-￠ ? ?′
μ? ê¨3 ? ú3? ? 1?
a-? ? é? ?ó ó? 1?
?? èμ à?
￡ ¨3 ￠ ?ü ′? í? 2 D￥ ￡|
° ′¨￡ ? ′? à?
?′ ?| ??
±? àü 2é 1¤￡? ?¤
?μ ￡? ?? ?′ °?
μ? ?′ 21
è? á? ￡? μ? ?′ 21
°33 °° 3￡ ? ?§ o?
D? íù é? ?ò ￡? ?¨ ?§
?| ?ù
3D e? ?¤?í
ê2? ? ê2ê 2
DP? ù 110 o r
mABP? ù >120
é¤ ?é
é¤ ?é ?? °ú
′?
áμ
?§ ?? ?| ò? 1?
