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HYPERTENSIVE DISORDERS
IN PREGNANCY
DR. SALWA NEYAZI
CONSULTANT OBSTETRICIAN GYNECOLOGIST
PEDIATRIC & ADOLESCENT GYNECOLOGIST
TYPES OF HYPERTENSIVE DISEASE IN
PREGNANCY
1-Gestational hypertension
2-PET
3-Eclampsia
4-Chronic hypertension
5-PET superimposed on chronic hypertension
1-Gestational hypertension
BP ≥ 140/90 mm Hg for the first time during pregnancy
No proteinuria
BP returns to N < 12 Wk postpartum
Final Dx made only postpartum
May have other signs of PET eg. Headache, epigastric
discomfort or thrombocytopenia
PET
Minimum criteria
BP ≥ 140/90 mm Hg after 20 Wk gestation
Proteinuria ≥ 300 mg/24 hrs or ≥ 1+ dipstick
Increased certainty of PET
BP ≥ 160/110 mm Hg
Proteinuria ≥ 2 gm/24 hrs or ≥ 2+ dipstick
Serum creatinine > 1.2 mg/dl unless known to be
previously elevated
Platelets < 100 000/mm³
Increased certainty of PET
Microangiopathic hemolysis (increased LDH)
Elevated ALT or AST
Persistant headache or other cerebral/ visual
disturbance
Persistant epigastric pain
ECLAMPSIA
Seizures that can not be attributed to other causes in
a woman with PET. 1% of Pt with PET develop EC
CHRONIC HYPERTENSION
BP ≥ 140/90 mm Hg before pregnancy or Dx before 20
Wk gestation
HPT first Dx after 20 Wk gestation & persistant after 12
Wk postpartum
PET SUPERIMPOSED ON CHRONIC HYPERTENSION
New onset proteinuria ≥ 300 mg/24 hrs in hypertensive
women but no proteinuria before 20 Wk gestation
A sudden increase in proteinuria or BP or
Plt count < 100 000/ mm³in women with HPT &
proteinuria before 20 Wk gestation
INCIDENCE & RISK FACTORS
PET occurs in 6-8% of all live birth
RISK FACTORS
Extremes of reproductive age
15 < & >35 Y
Nulliparity
Black race
Hx of PET in a 1st degree
female relative
Hx of PET in prior pregnancy
DM
Chronic renal disease
Ch HPT
Multiple pregnancy  twins 13
vs 6%
Hydatidiform mole
Nonimmune hydrops fetalis
Obesity  4.3%  BMI < 19.8
kg/m²
 13.3%  BMI ≥ 35
kg/m²
Smoking  ↓ risk of HPT
PATHOGENESIS
Endothelial cell injury ↓ ↓ prostacyclin & ↑ thromboxaneA2
Rejection phenomenon (inadequate matenal Ab response)
Compromised placental perfusion
Altered vascular reactivity  ↑sensitivity to vaspressin EPN,
NEPN & angiotensin
↓ GFR with retention of salt & water
↓ intravascular volume
↑ CNS irritability
DIC
Uterine muscle stretch & ischemia
Dietary factors
Genetic factors
PATHOGENESIS
Summary of current hypothesis:
Immunological disturbance  abnormal placental
implantation ↓ placental perfusion  production of
substances that activate or injure endothelial cells of the
blood vessels  multiple organ system involvement
PATHOPHYSIOLOGY
MULTIPLE ORGAN SYSTEM
INVOLVMENT
1- CNS
Similar to hypertensive encephalopathy
Petechial Hg
Gross hemorrhages due to ruptured arteries
Thrombosis of the arterioles
Microinfarcts
Fibrinoid necrosis in the walls of blood vessels
Cerebral edema  confusion, blurred vision / coma
Brain stem herniation is a serious complication of cerebral
edema  death
MECHANISM  cerebral hyperperfusion ,vasospasm
&forced dilation
1- CNS
CT Scan  ½ of the pt focal hypodensities in the white
matter / post half of the cerebral hemisphere &
occasionally in the grey matter may represent
petechial Hg
Severe cases IV Hg or subarachnoid Hg
MRI  Abnormalities in the cortical & subcortical white
matter of the occipital & parietal areas
EEG nonspecific changes
2-PULMONARY SYSTEM
Pulmonary edema
May occur with sever PET OR EC
Usually postpartum
May be due to excessive fluid administration with
crystalloids + ↓ plasma colloid pressure due to
proteinuria
↑ in Pt with ch HPT & hypertensive cardiac disease
Aspiration of gastric content with EC
3-CVS
Plasma volume is reduced, the cause is unknown
theories:
1-Generalized vasoconstriction with ↑ vascular
permeability  Advocate the use of vasodilators
2-1ry hypovolemia  hypoperfusion of the uterus
release of pressor substances  HPT
 Advocate the use of volume expanders & avoidance
of diuretics
3-CVS
High systemic vascular resistance & hyperdynamic
ventricular function avoid aggressive fluid
adminstration
Loss of the normal refractoriness to angiotensin II
4-BLOOD
Hemoconcentration
Thrombocytopenia < 150 000  15-20% of PT
Fibrinogen ↑
Thrombin time ↑ in 1/3 of the Ptwith EC
FDP ↑  20% of the Pt
DIC  5%
Microangiopathic hemolytic anemia 5%
HEELP hemolytic anemia, ↑↑ liver enzymes, low Plt
-LDH > 600 U/L
-T bilirubin >1.2 mg/dl
-AST > 70U/L
-Plt < 100 000/mm³
Found in 10% of the Pt with severe PET
5-KIDNEY
Characteristic lesion glomeruloendotheliosis  swelling
of the gromelular capillary endothelium  ↓↓GFR
↓↓ creatinine clearance/ ↑↑plasma creatinine
↑↑ uric acid
Proteinuria
Renal tubular necrosis &renal failure
6-Eyes
Visual disturbances  due to retinal artery vasospasm
Retinal detachment
Cortical blindness occipital lobe ischemia infarction or
edema lasting hrs –up to 8 days
7-Liver
Minimal involvement with fibrin deposition
Periportal hemorrhagic necrosis ↑↑ serum liver
enzymes
Bleeding from these lesions  Subcapsular hematoma
 hepatic rupture
Hepatic infarction
HEELP SYNDROME
8-Endocrine & metabolic changes
↓↓ plasma renin, angiotensin II & aldosterone to the
normal prepregnancy values
Vasopressin levels are N
Atrial natriuretic peptide ↑↑
Volume expansion in PET ↑ ANP  ↑ COP &↓
periephal vascular resistance
Expansion of the extracellular fluid volume (edema)
Proteinuria ↓↓ plasma oncotic pressure displacement
of intravascular fluid to interstitium
9-Uteroplacental perfusion
Vasospasm  compromised placental perfusion ↑↑
perinatal morbidity & mortality
Doppler velocimetry (systolic /diastolic velocity ratio of
umbilical& uterine arteries )20% N
15% N Umbilical / Abnormal uterine
40% Both Abnormal
Histological changes in placental bed
Defective trophoblastic invasion of spiral arteries /
decidual vessels but not myometrial vessels are invaded
by trophoblast
Charecteristic lipid rich lesions in the uteroplacental
arteries
PREVENTION
Calcium supplementation??
Fish oil ineffective
Low dose aspirin selective supression of throboxane
synthesis by the plt & sparing endothelial prostacyclin
production Not effective in preventing PET
Antioxidants Vit C & E supplementation  significant
reduction in PET
SYMPTOMS & SIGNS
↑ BP
Proteinuria
Edema of the face & hands ( but it has been dropped of
the definition due to poor predictive value)
Headache
Visual disturbance
Epigastric pain
Exaggerated reflexes
Fetal & maternal risks
Fetal
IUGR
Oligohydramnios
Placental infarcts
Placental abruption
Prematurity
Uteroplacental
insufficiency
Perinatal death
Maternal
CNS seizures & stroke
DIC
↑↑ CS
Renal failure
Hepatic failure or rupture
Death
CLASSIFICATION OF PET
SEVERE PET
Systolic BP >160 mmHg or diastolic >110 mmHg on two
occasions at least 6 hrs apart
Proteinuria ≥ 5 g/24 hrs
Oliguria < 500 cc /24 hrs
Cerebral or visual symptoms
Epigastric or Rt upper quadrant pain
Pulmonary edema or cyanosis
Low PLt
↑↑ liver enzymes
IUGR
MILD PET  any PET that is not considered severe
MANEGEMENT OF PET &
EC
Manegement
OBJECTIVES
Terminaton of pregnancy with the least possible trauma
to the mother & fetus
Birth of an infant who subsequently thrives
Complete restoration of health to the mother
1- Hospitalization
Women with new onset BP ≥ 140/90
Worsening BP
Development of proteinuria in addition to existing BP
INITIAL HOSPITAL MANAGEMENT
Observe for headache , visual disturbance, epigastric
pain & rapid wt gain
Wt daily
Analysis for proteinuria every 2 days / daily
BP in sitting position every 4 hrs except during sleep
Blood investigations  Hct, Plt, S creatinine, liver
enzymes
Frequent evaluation of fetal size & AF
Reduced physical activity but not absolute bed rest
N diet & fluid intake
FURTHER MANAGEMENT
Depends on:
Severity of PET
Duration of gestation
Condition of the Cx
Complete resolution of the signs & symptoms does not
occur till after delivery
Lines of management
Termination of pregnancy
Antihypertensive therapy
Anticonvulsant therapy
Home health care if BP improved within few days Pt
can be managed as outpatient Home BP & urine
protein monitoring . Instruction to come to hospital if she
has waning symptoms . Rest at home
Termination of pregnancy
Indications
Term pregnancy with mild or severe PET
Severe PET regardless of the gestational age
Warning signs  headache , visual disturbance, epigastric
pain, oliguria
Eclampsia Pt must be stabilized & delivered immediately
Preterm with mild PET  Assess fetal wellbeing by NST,
BPP, Doppler
Methods of termination
IOL with prostaglandines to ripen the Cx followed by IV
oxytocin
Elective CS  Severe PET with unfavorable Cx
Antihypertensive therapy
Mild PET
There is no benefit of antihypertensive therapy
Reduction in the maternal BP with labetalol or nifedipine
IUGR
ACI contraindicated  IUGR, boney malformations,
limb contracture, PDA, pulmonary hypoplasia, RDS,
hypotension &death
Severe PET
Antihypertensive therapy is used to control BP untill the Pt
delivers or in preterm for 48 hrs to allow time for
glucocorticoid administration for fetal lung maturity then
delivery
Antihypertensive therapy for severe PET & EC
Hydralazine
 IV infusion or IV 5-10 mg bolus at 15-20 min interval
 when diastolic BP ≥100-110 mm Hg or systolic BP ≥
160 mmHg
Nifedipine 10 mg po repeated in 30 min
Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after
10min/80 mg (not to exceed 220 mg)
Nitroprusside used only in PT not responding to other
drugs
Diuretics not recommended because intravascular
volume depletion already exists in PET
Fluid therapy
Hyperosmotic agents not recommended because
intravascular influx of fluid subsequent escape of
fluid to vital organs pulmonary edema & cerebral
edema
LR 60-120 ml/hr Excessive fluid administration
pulmonary edema & cerebral edema
PREVENTION /CONTROL OF CONVULSIONS
Magnesium sulfate IV infusion  4 gm loading dose in 100
ml of IV fluid over 20 min  2 gm /hr maintenance
Measure serum MG level at 4-6hrs maintain at 4-7 mEq /L
D/C 24 hrs after delivery25% of seiz occur post partum
Avoid toxicity by :
-monitoring patellar reflexes
-respiratory rate
-urine output
Antidote calcium gluconate 1gm IV
MgS ↓ myometrial contractility
Compared to phenytoin or diazepam 50% ↓ in maternal
mortality ,67% ↓ in convulsions
Infants were less likely to be admitted to NICU/ intubation
Prognosis
Maternal death rare due to cerebral Hg, aspiration
pneumonia, hypoxic encephalopathy, thromboembolism,
hepatic rupture, renal failure, ansthesia
Recurrence  25-33% primipara
 70% multipara
PG, PET before 30 wk 40%
HEELP 5%
CHRONIC HYPERTENSION
in pregnancy
CHRONIC HYPERTENSION
Incidence of ch HPT 0.5-4%
80% essential HPT
20% due to renal disease
Symptoms & signs
↑risk in  Age > 30, obese, multipara, DM, renal
disease, black race, family Hx
Difficult to deffirentiate HPT with superimposed PET from
HPT with renal disease both have proteinuria
INVESTIGATIONS
Chest x ray  cardiomegaly
ECG  Lt vent hypertrophy
↑ serum creatinine, ↓ creatinine clearance & proteinuria
5-10%
MATERNAL COMPLICATIONS
Superimposed PET in 1/3 of Pt
↑ risk of abruptio placentae 0.4-10% DIC, acute tubular
& cortical necrosis
If renal function is well creatinine < 1.5 mg/dl
pregnancy does not change the coarse of renal
disease
If renal function is affected prior to pregnancy
deterioration of renal function occur more rapid in
pregnancy
FETAL COMPLICATIONS
Prematurity 25-30%
IUGR 10-15%
Stillbirth & fetal distress due to abruptio placentae or ch
intrauterine asphyxia
TREATMENT
No benefit of treating mild CH HPT ( 140-179/90-109)
in pregnancy  should be monitered for worsening HPT or
superimposed PET
Pt with severe CH HPT should have their BP controlled
before pregnancy & continue Rx in pregnancy
α Methyle Dopa
Calcium channel blockers
B blockers can be used but  IUGR
Labetalol
Obstetric management
Serial U/S for fetal growth. BPP, NST34wk
Follow up every 2 wks till 30 then weekly
Warn the mother about symptoms of superimposed PET
Investigations Renal function test,uric a , calcium ,LFT,
24hrs urine for creatinine clearance & protein, CBC,
Urinalysis, ECG.GTT
Early U/S for dating of preg
Not allowed to continue past 40wks
IOL at40 wks
Regular diet no salt restriction
IOL for superimposed PET,IUGR, fetal distress,
worsening renal function

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07. HYPERTENSIVE DISORDERS IN PREGNANCY.ppt

  • 1. HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI CONSULTANT OBSTETRICIAN GYNECOLOGIST PEDIATRIC & ADOLESCENT GYNECOLOGIST
  • 2. TYPES OF HYPERTENSIVE DISEASE IN PREGNANCY 1-Gestational hypertension 2-PET 3-Eclampsia 4-Chronic hypertension 5-PET superimposed on chronic hypertension
  • 3. 1-Gestational hypertension BP ≥ 140/90 mm Hg for the first time during pregnancy No proteinuria BP returns to N < 12 Wk postpartum Final Dx made only postpartum May have other signs of PET eg. Headache, epigastric discomfort or thrombocytopenia
  • 4. PET Minimum criteria BP ≥ 140/90 mm Hg after 20 Wk gestation Proteinuria ≥ 300 mg/24 hrs or ≥ 1+ dipstick Increased certainty of PET BP ≥ 160/110 mm Hg Proteinuria ≥ 2 gm/24 hrs or ≥ 2+ dipstick Serum creatinine > 1.2 mg/dl unless known to be previously elevated Platelets < 100 000/mm³
  • 5. Increased certainty of PET Microangiopathic hemolysis (increased LDH) Elevated ALT or AST Persistant headache or other cerebral/ visual disturbance Persistant epigastric pain ECLAMPSIA Seizures that can not be attributed to other causes in a woman with PET. 1% of Pt with PET develop EC
  • 6. CHRONIC HYPERTENSION BP ≥ 140/90 mm Hg before pregnancy or Dx before 20 Wk gestation HPT first Dx after 20 Wk gestation & persistant after 12 Wk postpartum PET SUPERIMPOSED ON CHRONIC HYPERTENSION New onset proteinuria ≥ 300 mg/24 hrs in hypertensive women but no proteinuria before 20 Wk gestation A sudden increase in proteinuria or BP or Plt count < 100 000/ mm³in women with HPT & proteinuria before 20 Wk gestation
  • 7. INCIDENCE & RISK FACTORS PET occurs in 6-8% of all live birth RISK FACTORS Extremes of reproductive age 15 < & >35 Y Nulliparity Black race Hx of PET in a 1st degree female relative Hx of PET in prior pregnancy DM Chronic renal disease Ch HPT Multiple pregnancy  twins 13 vs 6% Hydatidiform mole Nonimmune hydrops fetalis Obesity  4.3%  BMI < 19.8 kg/m²  13.3%  BMI ≥ 35 kg/m² Smoking  ↓ risk of HPT
  • 8. PATHOGENESIS Endothelial cell injury ↓ ↓ prostacyclin & ↑ thromboxaneA2 Rejection phenomenon (inadequate matenal Ab response) Compromised placental perfusion Altered vascular reactivity  ↑sensitivity to vaspressin EPN, NEPN & angiotensin ↓ GFR with retention of salt & water ↓ intravascular volume ↑ CNS irritability DIC Uterine muscle stretch & ischemia Dietary factors Genetic factors
  • 9. PATHOGENESIS Summary of current hypothesis: Immunological disturbance  abnormal placental implantation ↓ placental perfusion  production of substances that activate or injure endothelial cells of the blood vessels  multiple organ system involvement
  • 11. 1- CNS Similar to hypertensive encephalopathy Petechial Hg Gross hemorrhages due to ruptured arteries Thrombosis of the arterioles Microinfarcts Fibrinoid necrosis in the walls of blood vessels Cerebral edema  confusion, blurred vision / coma Brain stem herniation is a serious complication of cerebral edema  death MECHANISM  cerebral hyperperfusion ,vasospasm &forced dilation
  • 12. 1- CNS CT Scan  ½ of the pt focal hypodensities in the white matter / post half of the cerebral hemisphere & occasionally in the grey matter may represent petechial Hg Severe cases IV Hg or subarachnoid Hg MRI  Abnormalities in the cortical & subcortical white matter of the occipital & parietal areas EEG nonspecific changes
  • 13. 2-PULMONARY SYSTEM Pulmonary edema May occur with sever PET OR EC Usually postpartum May be due to excessive fluid administration with crystalloids + ↓ plasma colloid pressure due to proteinuria ↑ in Pt with ch HPT & hypertensive cardiac disease Aspiration of gastric content with EC
  • 14. 3-CVS Plasma volume is reduced, the cause is unknown theories: 1-Generalized vasoconstriction with ↑ vascular permeability  Advocate the use of vasodilators 2-1ry hypovolemia  hypoperfusion of the uterus release of pressor substances  HPT  Advocate the use of volume expanders & avoidance of diuretics
  • 15. 3-CVS High systemic vascular resistance & hyperdynamic ventricular function avoid aggressive fluid adminstration Loss of the normal refractoriness to angiotensin II
  • 16. 4-BLOOD Hemoconcentration Thrombocytopenia < 150 000  15-20% of PT Fibrinogen ↑ Thrombin time ↑ in 1/3 of the Ptwith EC FDP ↑  20% of the Pt DIC  5% Microangiopathic hemolytic anemia 5% HEELP hemolytic anemia, ↑↑ liver enzymes, low Plt -LDH > 600 U/L -T bilirubin >1.2 mg/dl -AST > 70U/L -Plt < 100 000/mm³ Found in 10% of the Pt with severe PET
  • 17. 5-KIDNEY Characteristic lesion glomeruloendotheliosis  swelling of the gromelular capillary endothelium  ↓↓GFR ↓↓ creatinine clearance/ ↑↑plasma creatinine ↑↑ uric acid Proteinuria Renal tubular necrosis &renal failure 6-Eyes Visual disturbances  due to retinal artery vasospasm Retinal detachment Cortical blindness occipital lobe ischemia infarction or edema lasting hrs –up to 8 days
  • 18. 7-Liver Minimal involvement with fibrin deposition Periportal hemorrhagic necrosis ↑↑ serum liver enzymes Bleeding from these lesions  Subcapsular hematoma  hepatic rupture Hepatic infarction HEELP SYNDROME
  • 19. 8-Endocrine & metabolic changes ↓↓ plasma renin, angiotensin II & aldosterone to the normal prepregnancy values Vasopressin levels are N Atrial natriuretic peptide ↑↑ Volume expansion in PET ↑ ANP  ↑ COP &↓ periephal vascular resistance Expansion of the extracellular fluid volume (edema) Proteinuria ↓↓ plasma oncotic pressure displacement of intravascular fluid to interstitium
  • 20. 9-Uteroplacental perfusion Vasospasm  compromised placental perfusion ↑↑ perinatal morbidity & mortality Doppler velocimetry (systolic /diastolic velocity ratio of umbilical& uterine arteries )20% N 15% N Umbilical / Abnormal uterine 40% Both Abnormal Histological changes in placental bed Defective trophoblastic invasion of spiral arteries / decidual vessels but not myometrial vessels are invaded by trophoblast Charecteristic lipid rich lesions in the uteroplacental arteries
  • 21. PREVENTION Calcium supplementation?? Fish oil ineffective Low dose aspirin selective supression of throboxane synthesis by the plt & sparing endothelial prostacyclin production Not effective in preventing PET Antioxidants Vit C & E supplementation  significant reduction in PET
  • 22. SYMPTOMS & SIGNS ↑ BP Proteinuria Edema of the face & hands ( but it has been dropped of the definition due to poor predictive value) Headache Visual disturbance Epigastric pain Exaggerated reflexes
  • 23. Fetal & maternal risks Fetal IUGR Oligohydramnios Placental infarcts Placental abruption Prematurity Uteroplacental insufficiency Perinatal death Maternal CNS seizures & stroke DIC ↑↑ CS Renal failure Hepatic failure or rupture Death
  • 24. CLASSIFICATION OF PET SEVERE PET Systolic BP >160 mmHg or diastolic >110 mmHg on two occasions at least 6 hrs apart Proteinuria ≥ 5 g/24 hrs Oliguria < 500 cc /24 hrs Cerebral or visual symptoms Epigastric or Rt upper quadrant pain Pulmonary edema or cyanosis Low PLt ↑↑ liver enzymes IUGR MILD PET  any PET that is not considered severe
  • 26. Manegement OBJECTIVES Terminaton of pregnancy with the least possible trauma to the mother & fetus Birth of an infant who subsequently thrives Complete restoration of health to the mother 1- Hospitalization Women with new onset BP ≥ 140/90 Worsening BP Development of proteinuria in addition to existing BP
  • 27. INITIAL HOSPITAL MANAGEMENT Observe for headache , visual disturbance, epigastric pain & rapid wt gain Wt daily Analysis for proteinuria every 2 days / daily BP in sitting position every 4 hrs except during sleep Blood investigations  Hct, Plt, S creatinine, liver enzymes Frequent evaluation of fetal size & AF Reduced physical activity but not absolute bed rest N diet & fluid intake
  • 28. FURTHER MANAGEMENT Depends on: Severity of PET Duration of gestation Condition of the Cx Complete resolution of the signs & symptoms does not occur till after delivery Lines of management Termination of pregnancy Antihypertensive therapy Anticonvulsant therapy Home health care if BP improved within few days Pt can be managed as outpatient Home BP & urine protein monitoring . Instruction to come to hospital if she has waning symptoms . Rest at home
  • 29. Termination of pregnancy Indications Term pregnancy with mild or severe PET Severe PET regardless of the gestational age Warning signs  headache , visual disturbance, epigastric pain, oliguria Eclampsia Pt must be stabilized & delivered immediately Preterm with mild PET  Assess fetal wellbeing by NST, BPP, Doppler Methods of termination IOL with prostaglandines to ripen the Cx followed by IV oxytocin Elective CS  Severe PET with unfavorable Cx
  • 30. Antihypertensive therapy Mild PET There is no benefit of antihypertensive therapy Reduction in the maternal BP with labetalol or nifedipine IUGR ACI contraindicated  IUGR, boney malformations, limb contracture, PDA, pulmonary hypoplasia, RDS, hypotension &death Severe PET Antihypertensive therapy is used to control BP untill the Pt delivers or in preterm for 48 hrs to allow time for glucocorticoid administration for fetal lung maturity then delivery
  • 31. Antihypertensive therapy for severe PET & EC Hydralazine  IV infusion or IV 5-10 mg bolus at 15-20 min interval  when diastolic BP ≥100-110 mm Hg or systolic BP ≥ 160 mmHg Nifedipine 10 mg po repeated in 30 min Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after 10min/80 mg (not to exceed 220 mg) Nitroprusside used only in PT not responding to other drugs Diuretics not recommended because intravascular volume depletion already exists in PET
  • 32. Fluid therapy Hyperosmotic agents not recommended because intravascular influx of fluid subsequent escape of fluid to vital organs pulmonary edema & cerebral edema LR 60-120 ml/hr Excessive fluid administration pulmonary edema & cerebral edema
  • 33. PREVENTION /CONTROL OF CONVULSIONS Magnesium sulfate IV infusion  4 gm loading dose in 100 ml of IV fluid over 20 min  2 gm /hr maintenance Measure serum MG level at 4-6hrs maintain at 4-7 mEq /L D/C 24 hrs after delivery25% of seiz occur post partum Avoid toxicity by : -monitoring patellar reflexes -respiratory rate -urine output Antidote calcium gluconate 1gm IV MgS ↓ myometrial contractility Compared to phenytoin or diazepam 50% ↓ in maternal mortality ,67% ↓ in convulsions Infants were less likely to be admitted to NICU/ intubation
  • 34. Prognosis Maternal death rare due to cerebral Hg, aspiration pneumonia, hypoxic encephalopathy, thromboembolism, hepatic rupture, renal failure, ansthesia Recurrence  25-33% primipara  70% multipara PG, PET before 30 wk 40% HEELP 5%
  • 36. CHRONIC HYPERTENSION Incidence of ch HPT 0.5-4% 80% essential HPT 20% due to renal disease Symptoms & signs ↑risk in  Age > 30, obese, multipara, DM, renal disease, black race, family Hx Difficult to deffirentiate HPT with superimposed PET from HPT with renal disease both have proteinuria
  • 37. INVESTIGATIONS Chest x ray  cardiomegaly ECG  Lt vent hypertrophy ↑ serum creatinine, ↓ creatinine clearance & proteinuria 5-10% MATERNAL COMPLICATIONS Superimposed PET in 1/3 of Pt ↑ risk of abruptio placentae 0.4-10% DIC, acute tubular & cortical necrosis If renal function is well creatinine < 1.5 mg/dl pregnancy does not change the coarse of renal disease If renal function is affected prior to pregnancy deterioration of renal function occur more rapid in pregnancy
  • 38. FETAL COMPLICATIONS Prematurity 25-30% IUGR 10-15% Stillbirth & fetal distress due to abruptio placentae or ch intrauterine asphyxia
  • 39. TREATMENT No benefit of treating mild CH HPT ( 140-179/90-109) in pregnancy  should be monitered for worsening HPT or superimposed PET Pt with severe CH HPT should have their BP controlled before pregnancy & continue Rx in pregnancy α Methyle Dopa Calcium channel blockers B blockers can be used but  IUGR Labetalol
  • 40. Obstetric management Serial U/S for fetal growth. BPP, NST34wk Follow up every 2 wks till 30 then weekly Warn the mother about symptoms of superimposed PET Investigations Renal function test,uric a , calcium ,LFT, 24hrs urine for creatinine clearance & protein, CBC, Urinalysis, ECG.GTT Early U/S for dating of preg Not allowed to continue past 40wks IOL at40 wks Regular diet no salt restriction IOL for superimposed PET,IUGR, fetal distress, worsening renal function