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Hypertensive Hypertensive Hypertensive Hypertensive Disorders Disorders Disorders Disorders
of of of of PregnancyPregnancyPregnancyPregnancy
Joshi Suyajna D.Professor of OBG,
VIMS- Bellary
HYPERTENSIVE DISORDERS OF PREGNANCYHYPERTENSIVE DISORDERS OF PREGNANCYHYPERTENSIVE DISORDERS OF PREGNANCYHYPERTENSIVE DISORDERS OF PREGNANCY
• PIH also known as preeclampsia
• Eclampsia present when seizures superimposed on preeclampsia
• HELLP syndrome:
(H) hemolysis, (EL) elevated liver enzymes, (LP) low platelet count
Definition of HYPERTENSION
a. One measurement of
DIASTOLIC BLOOD PRESSURE (DBP) more than 110 mm Hg
b.TWO consequestive measurement of DBP more than 90 mm Hg –
4 hours apart.
ISSHP 1986
HYPERTENSION IN PREGNANCY
Classification (ACOG):
• Pregnancy Induced Hypertension
Pre-eclampsia
Eclampsia
• Chronic Hypertension
• PIH superimposed on chronic hypertension
• Transient hypertension
• Unclassified hypertensive disorders
National Institute of Health (National High Blood Pressure Education Program Working
Group- NHBPEPNHBPEPNHBPEPNHBPEP 2000)
�1. Chronic Hypertension
�2. Preeclampsia
�3. Preeclampsia superimposed on chronic hypertension
�4. Gestational Hypertension. (Transient
hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy).
International Society for the Study of Hypertension in Pregnancy (ISSHP)
Classification (ISSHP)
Known hyper-tension prior topregnancy or at
booking (<20 weeks)
Chronichypertension,renal disease
Hypertension(without proteinuria)
arising inpregnancy
Gestationalhypertension
Gestationalhypertension
plus proteinuria
Pre-eclampsia
Compulsionsassociated with
pregnancy
Eclampsia
No information onpre-pregnancy
or pre-20weeks GP
Unclassifiablehypertension
HypertensiveDisorders ofPregnancy
Introduction
World wide each year
• 1,500,000 to 1,800,000 women develop Preeclampsia
• Upto 1,50,000 women have eclamptic convulsions
• 90% of these women are from developing countries
MATERNAL MORTALITYMATERNAL MORTALITYMATERNAL MORTALITYMATERNAL MORTALITY
• Hypertensive disorders particularly severe hypertension of preeclampsia is the leading cause of maternal and perinatal mortality and morbidity.
Lewis G et al RCOG Press –2001
Perinatal Outcome
UK India
Overall Perinatal Mortality
(per 1000 live births) 15 34%
Proportion due to
Hypertensive disease 18% 18%
Increased risk with
Hypertensive disease 2.3 4.76
Douglas KA et al, BMJ 1994Shah DS, FOGSI Perinatal Survey, 1994
Sardesai Jr Obstet Gynecol 2003
Zweifel …. 1916
Pre-eclampsia
Disease of many theories
Chesley Chesley Chesley Chesley …………. 1978. 1978. 1978. 1978
The most common definitions :The most common definitions :
• Hypertension that develops de novo as a consequence of pregnancy after 20th
week of gestation, returning to normal after 6 weeks of delivery.
• PE is present when diastolic BP> 90 mmHg or Systolic >140 or a systolic BP rises at least 30 mm Hg over base line values or diastolic BP rises at least 15 mm Hg over base line value at least at two different occasions and at least 6 hours apart (ACOG)
Acog bulletin 2002
INCIDENCE
• PRE-ECLAMPSIA 5 to 10%
• Eclampsia
• Developed countries 1 : 2000
• INDIA 1:30 TO 1: 500
• MATERNAL MORTALITYMATERNAL MORTALITYMATERNAL MORTALITYMATERNAL MORTALITY:
• U.S.A 17.6%
• INDIA 25.5%Walker JJ, Lancet:2000;356:1260Walker JJ, Lancet:2000;356:1260--6565
Sawhney H et al,
Some observations
�‘PRIMI’…Mac Gillivray..1958
�‘PRIMIPATERNITY’…Feeny & Scott…1980
�‘SINGLE GENE DISORDER’
Chesley and Cooper…1986
Pathogenesis
‘unknown’ (Barton& Sibai, 2008).
�Impaired trophoblast differentiation& invasion
�Placental & endothelial dysfunction
�Immune maladaptation to paternal Ags
�Exaggerated systemic inflam. response.
‘Hypertensive Disorders in Pregnancy’, published in 1978
Leon Chesley
“The Remote Prognosis of Eclamptic Women: Sixth Periodic Report,"
1908-2000
Leon Chesley's death on March 29, 2000,Leon Chesley's death on March 29, 2000,Leon Chesley's death on March 29, 2000,Leon Chesley's death on March 29, 2000,marked the end of an era in academic obstetrics and gynecology. It is doubtful that anyone in the second half of the 20th century equaled his depth and breadth of influence on the intellectual life of our discipline.
Leon Chesley
SIBAI BAHA MOHAMMED
Sibai B.M.
�Magnesium sulfate is
the ideal anticonvulsant in preeclampsia-eclampsia. Am J Obstet
Gynecol. 1990; 162: 1141–1145
� Sibai BM. Eclampsia VI. Maternal-perinatal
outcome in 254254254254 cases. Am J Obstet Gynecol.
1990; 163: 1049–1055JOSHI SUYAJNA D.
High Risk Factors
Primigravida : Extremes of reproductive age (young and elderly)
Socio economic (status) : DisadvantagedEthnicity : African AmericanFamily history : Hypertension, pre-eclampsia, (First degree relatives) eclampsia
Placental abnormalities : Molar pregnancyHyperplacentosis – multiple pregnancyPlacental ischaemia
Associated medical conditions : Obesity, Diabetes, Renal disease,Collagen vascular disease
Thrombophilias : Anti-phospholipid syndrome, Protein C, S deficiency, Factor V Leiden
Genetic : History of pre-eclampsia in sister, mother (Multi-factorial inheritance)
Immunological
Preconceptional Risk Factors
Rates of preeclampsia depend on: severity of underlying complications &combinations of risk factors.
Risk %Risk factors
15-40Chronic hypertension/renal disease
10-35Pre gestational DM
10-20Connective tissue disease (lupus, rheumatoid arthritis)
10-40Thrombophilia (acquired or congenital)
10-15Obesity/insulin resistance
10-20Age older than 40 y
10-35Limited sperm exposure
10-15Family history of preeclampsia/ cardiovascular disease
1.5 foldWoman born as SFGA
2-3 foldAdverse outcome in a previous pregnancy: IUGR, ab placentae, IUFD
DEGREE OF PE
• DEPENDS ON:
1. Degree of impairment of trophoblastic invasion
2. Time of detection of
continuous process
SYMPTOMS
�HEADACHE- vascular origin
�VISUAL DISTURBANCES-
retinal vascular spasm…..detachment
• Blurring
• Diplopia
• Scotoma
MacGillivary 1983
EPIGASTRIC PAIN
RUQ PAIN:
Stretching of the Liver capsule
Subcapsular haematoma
DISTENSION OF LIVER
Arias & Mancilla – Jimenez 1976
EDEMA
• Early but non specific sign
• Rapid weight gain
• Edema of PE is due to sodium retention and thus not limited to dependent edema
• Edema of hands and face more reliable than dependent edema
• Parasthesia due to medial or ulnar nerve compression
EDEMA
• 1. Persistent ankle edema
• 2. Rapidly progressing edema
• 3. Edema of the Upper part of body
EDEMA SUBSIDES ON RESTEDEMA SUBSIDES ON RESTEDEMA SUBSIDES ON RESTEDEMA SUBSIDES ON REST----
GOOD PROGNOSISGOOD PROGNOSISGOOD PROGNOSISGOOD PROGNOSIS
Occult edema
ABNORMAL WEIGHT GAINABNORMAL WEIGHT GAINABNORMAL WEIGHT GAINABNORMAL WEIGHT GAIN
Mudaliar & Krishna Menon
SIGNSSIGNSSIGNSSIGNS
HYPERTENSION
�MILD:
140/90 mm Hg – 150/100 mm Hg
�MODERATE: 150/100 to 160/110
�SEVERE:
160-180/110 and more
Drugs and Therapeutics Bulletin 1993
FUNDOSCOPY
• ARTERIOLAR CONSTRICTION
• RETINAL EDEMA
• HAEMORRHAGES & EXUDATES –
NOT COMMON
MacGillivary 1983
INVESTIGATIONS
• PROTEINURIA:
300mg. Or more in 24 hours
300 mg/dl – 2 random samples
6 hours apart
PERINATAL MORTALITY DOUBLED
Cowles et al 1994
PLATELET COUNT
• Thrombocytopenia- ≤ 150000/ml
20% of PE
Mild PE:Mild PE:Mild PE:Mild PE: 7%7%7%7%
Severe PE: 50%Severe PE: 50%Severe PE: 50%Severe PE: 50%
Giles and Inglis 1981
SERUM URIC ACID
• MORE THAN – 330 mmol/l:
• 1. Foetal Distress-
• 2. Low Birthweight Foetus
• 3. PNM-
Varma 1982
LIVER FUNCTION TESTSLIVER FUNCTION TESTSLIVER FUNCTION TESTSLIVER FUNCTION TESTS
• SERUM GLUTAMIC OXALOACETIC TRANSAMINASE
• ASPARATE TRANSAMINASE
• LDH
Magann and Martin 1995
STEROID PROPHYLAXISSTEROID PROPHYLAXISSTEROID PROPHYLAXISSTEROID PROPHYLAXIS
• ACCELERATED LUNG MATURITY X
SAME PROBABILITY
HMDGluk and Kulovich 1973
Carvalho 1997
Out Patient Management
Gestational Hypertension less than
160/100 mm Hg
• Bed rest at home (controversial)
• Home BP monitoring, weight and urine protein.
• Referred for Day Assessment Unit (DAU) for evaluation like NST and USG
DAU managementDAU management
• 4 to 6 hourly BP recording.
• Mid stream urine analysis.
• Proteinuria, protein creatinine ratio.
• CTG
• Hb, platelets, creatinine, liver function tests (enzymes, AST/ALT), uric acid.
• Review.
Indications for Hospitalization from Day Care Unit
• BP equal to or more than 160/100 mm Hg
• Uric acid equal to or more than 450 mmol/L
• Platelets less than 1,50,000
• Proteinuria equal to or more than 5 gm in 24 hrs
• Oliguria
• S creatinine more than 1 mg%
• Cerebral or visual disturbances
• Impaired liver function
• Non reactive CTG
• IUGR/Oligohydramnios
Maternal SURVEILLANCE
Bed restVital parametersBP measurement 6 hourly Daily weightInput /output chartingUrine protein estimation dailyPremonitory symptomsDeep tendon reflexesFundoscopy
BIOCHEMICAL MONITORING
CBCUrine routine and microscopy24 hour urineRFT, BUN, Creatinine, uric acid, creatinine cleareanceLFT: enzymes, bilirubin, proteinsPlatelet countCoagulation profile
Fetal Well-being
•Delay the delivery if mother is safe•Prematurity is the most important determinant of perinatal outcome•Antenatal Corticosteroids
Fetal Surveillance
- Daily Fetal Movement Count- Fetal growth clinically and by USG- Amount of liquor- Cardiotocogram- Doppler velocimetry of the
umbilical artery
Control of Hypertension
• Aims of antihypertensive therapy
- To increase renal perfusion
- To increase uteroplacental perfusion
- To prevent intracranial bleeding
- To prevent Left ventricular failure
- To prevent the selective cerebral
arterial vasospasm that causes
eclamptic seizures
Indications for Antihypertensive Therapy
Role of antihypertensive therapy in Mild to Moderate Hypertension is
unclear.
Drugs and therapy Perceptive 2001,17(18),11-15
INDICATIONS FOR ANTI-HYPERTENSIVES IN
PEPEPEPEGROUP ‘A’
1.Persistent rise of BP in mild to moderate PE
2.Severe preeclampsia-EXPECTANT
GROUP ‘B’
Hypertensive crisis
Antihypertensive for mild PE
• Methyldopa : A drug of First Choice
• Labetalol : A reasonable Alternative
• Atenolol : To be avoided
• Nifedipine : Calcium channel blocker in late
pregnancy
• Propranolol : can be used in late pregnancy
• Hydralazine : add on therapy to Methyldopa
• ACE inhibitors : To be avoided
• Diuretics : not to be used as
antihypertensive
Following are the criteria for delivery in mild preeclampsia
1) Gestational age >/ = 40 weeks
2) Gestational age >/ = 37 weeksa) Fetal weight < 10th percentile b) Bishop score >/= 6 c) Non reactive NST pattern
3) Gestational age >/ = 34 weeks witha) Laborb) Rupture of membranesc) Vaginal bleedingd) Imminent symptoms
4) Abnormal biophysical profile.5) Criteria for severe preeclampsia met
DIURETICS IN PE:NO
1. GROSS ANASARCA
2. 2. PULMONARY EDEMA
• No reduction in the incidence of PE or perinatal mortality
• May have deleterious effects: • reduced renal & placental perfusion. • (Cochrane Library 2007 Issue 1:CD004451
Diagnostic criteria for
severe preeclampsia –ACOG PRACTICE BULLETIN
• Blood pressure >160-180 mm Hg systolic or >110 mm Hg diastolic
• Proteinuria >5g per 24 hr
• Oliguria defined as <500 mL per 24 hr
• Cerebral or visual disturbances• Pulmonary edema • Epigastric or right upper quadrant pain
• Impaired liver function of unclear etiology• Thrombocytopenia• Fetal intrauterine growth retardation or oligohydramnios• Elevated serum creatinine
• Grand mal seizures (eclampsia)
SEVERESEVERESEVERESEVERE----PEPEPEPEHYPERTENSION
� MILD:
140/90 mm Hg – 150/100 mm Hg
� MODERATE: 150/100 to 160/110
�SEVERE:
160-180/110 and moreDrugs and Therapeutics Bulletin 1993
Antihypertensive for Control of Acute or Severe
Hypertension in Pregnancy
Labetalol : 20 mg IV, repeated every 30 min & can be doubled maximum
upto 80 mg
Nifedipine : 5 to 10 mg every
15 min to maximum upto 30 mg
Antihypertensive for Control of Acute or Severe Hypertension in Pregnancy
Short Acting Antihypertensive agents :
• Hydralazine : 5 mg IV repeated after 20 min
Other Antihypertensive agents :
Diazoxide : 30 to 50 mg IV, repeated every 10
to 15 min or by continuous infusion.
Sodium Nitroprusside : IV infusion 0.5 to 10
mg/kg/min
‘EXPECTANTEXPECTANTEXPECTANTEXPECTANT’ MANAGEMENTFETAL WELLBEING
�CTG: DAILY
�USGUSGUSGUSG---- FETAL WEIGHTFETAL WEIGHTFETAL WEIGHTFETAL WEIGHT
– GROWTH PROFILEGROWTH PROFILEGROWTH PROFILEGROWTH PROFILE---- ONCE IN 2 WksONCE IN 2 WksONCE IN 2 WksONCE IN 2 Wks
�AFI: TWICE WEEKLY
�UMBILICAL ARTERY DOPPLER –
TWICE WEEKLY
DAVID CHURCHILL 2000
DAVID CHURCHILL 2000
‘EXPECTANTEXPECTANTEXPECTANTEXPECTANT’ MANAGEMENTMATERNAL WELLBEING
�BLOOD PRESSURE: 4 HOURLY
�URINE FOR PROTEIN LOSS: DAILY
�PLATELET COUNT,
SERUM URIC ACID:TWICE WEEKLY
�LFT: WEEKLY
Criteria for delivering patient withEXPECTANT MANAGEMENT-PE
• BP persistently 160/110 or more inspite of treatment
• Urine output < 400 ml in 24 hrs
• Platelet count < 50,000/mm3
• Progressive increase in S. Creatinine
• LDH > 1000 IU/L
• Repetitive late decelaration with poor variability
• Severe IUGR with Oligohydramnios
• Reversed umbilical diastolic blood flow
Decision making in severe preeclampsia
Gestational Age Course
More than 34 weeks Delivery
Less than 26 weeks Delivery
26 to 34 weeks Expectant management v/s
Delivery
Planning Delivery
PlaceMultidisciplinary team and high dependency care availableNeonatal care facilities
Route
�Aim for vaginal deliveryLSCS required for obstetric indication or
maternal or fetal compromise�AVOID GENERAL ANAESTHESIA
TimeConservative v/s Early intervention
Labour Management• IV access
• Repeat haematological investigations
• Fluid management
• Seizure prophylaxis and anti hypertensives
• Electronic fetal monitoring
• Analgesia and Anaesthesia
• No ergometrine
•““““Like A Flash Of LighteningLike A Flash Of LighteningLike A Flash Of LighteningLike A Flash Of Lightening””””
• Acute Convulsive Disorder Acute Convulsive Disorder Acute Convulsive Disorder Acute Convulsive Disorder ––––
• Cause Cause Cause Cause –––– Hypertension Induced Or Induced Or Induced Or Induced Or Aggravated By PregnancyAggravated By PregnancyAggravated By PregnancyAggravated By Pregnancy.
BP may be normal !BP may be normal !BP may be normal !BP may be normal !
Treat all women with convulsions in pregnancy as
eclampsia until proven otherwise.
ECLAMPSIA
According to ACOG eclampsia is defined as convulsions occurring in a
patient with preeclampsia.
OR
Preeclampsia complicated with convulsion and /
or coma is called eclampsia. It can also occur in patients who have preeclampsia superimposed on essential hypertension or chronic nephritis
ECLAMPSIAECLAMPSIAECLAMPSIAECLAMPSIA
Pathogenesis of eclampsia - Unknown
- Severe arterial vasospasm
Rupture of the vascular endothelium
Pericapillary hemorrhage
Development foci of abnormal electrical discharge that may generalized
Convulsions
Period of gestation – convulsions
In 50% of cases >36 wks of gestation
Antepartum - 46.3%
Intrapartum - 16.4%
Postparum - 37.3%
usually within 48 hrs of delivery
Sibai BM et al Obstet Gynaecol 1981, 58 : 609.
HYPERTENSION IN ECLAMPSIAHYPERTENSION IN ECLAMPSIAHYPERTENSION IN ECLAMPSIAHYPERTENSION IN ECLAMPSIA
�Severe htn………..54%
�Mild htn…………..30%
�NORMAL BP…….16%
Temporary Blindness Temporary Blindness Temporary Blindness Temporary Blindness (amaurosis)(amaurosis)(amaurosis)(amaurosis)
Petechial hemorrhage
Focal vasogenic edema in the occipital cortex
cortical blindness …. 1 to 3%Cunningham, 1995
PERMANENT BLINDNESS
� cerebral infarction cerebral infarction cerebral infarction cerebral infarction
� retinal artery ischemia and retinal artery ischemia and retinal artery ischemia and retinal artery ischemia and infarction infarction infarction infarction
Lara-Torre and associates, 2002;
Moseman and Shelton, 2002.
• Eclampsia
• Epilepsy
• Cerebral malaria in tropics
• Encephalitis
• Meningitis
• Intracranial tumors
• Peripheral cerebral thrombosis
• Poisoning
• Hysteria
Differential Diagnosis
• General management
• To control convulsions using MgSO4
• To control Hypertension
• To avoid Diuretics
• To limit IV fluids unless excessive fluid loss
• To investigate
�TERMINATION OF PREGNANCY
• Care in puerperium
• Follow up.
Principles of Management of Eclampsia
General management
• To place in a railed cot in an isolated place
• To maintain airway
– To administer oxygen
– To take detail history from relatives
– After proper sedation quick examination
– Catheterization and check for proteinuria
– ½ an hourly Pulse, Temp, RR, BP, uterine contraction, FHS.
– 1 hrly urine output
– Maintain fluid balance with CVP monitoring
– To administer antibiotics
Management of Eclampsia
Cure for severe PreCure for severe PreCure for severe PreCure for severe Pre----eclampsia/ eclampsia/ eclampsia/ eclampsia/ Eclampsia is delivery of fetus & placenta Eclampsia is delivery of fetus & placenta Eclampsia is delivery of fetus & placenta Eclampsia is delivery of fetus & placenta
Treat with
anticonvulsants &
antihypertensives
Stabilize
Deliver
Rushed delivery in an unstable patient is dangerous
Transfer if necessary
Lytic cocktail regimen
On admission
25mg chlorpromazine +100mg pethidine in 20ml of
5% solution iv followed by 50mg chlorpromazine +
25 mg promethazine im.
Later on
Promethazine 25mg and chlorpromazine 50mg given alternately lM till
24 hr of last fit or
IV 500ml containing 100mg pethidine drip rate adjusted to 20-30
drops/min till 24 hrs of last fit and not to exceed 300 mg /day.
Maternal Mortality (MM): 2.2%
Diazepam regimen:
Initial drug of 100mg iv further 40mg in
500ml of Ringer lactate i. v. at 30 drops/min
M.M. 5%
LEAN’S regimen
Lean T.H. Et al 1968
RYAN’ REGIMEN
• Phenytoin therapy :
• 10mg/kg IV followed by 5mg/kg 2
hrs later
• Sedatives can be used with above
regimen
Ryan G. et al 1989
Best Anticonvulsive
is the drug of choice for routine anti- convulsant management of women with eclampsia, when compared to Diazepam & Phenytoin.
Evidence from the Collaborative Eclampsia Trial.Evidence from the Collaborative Eclampsia Trial.Evidence from the Collaborative Eclampsia Trial.Evidence from the Collaborative Eclampsia Trial.
• Lancet. 1995 Jun 10. 345(8963). pp 1455Lancet. 1995 Jun 10. 345(8963). pp 1455Lancet. 1995 Jun 10. 345(8963). pp 1455Lancet. 1995 Jun 10. 345(8963). pp 1455----1463.1463.1463.1463.
Specific management
control seizures and to prevent its recurrence
Regimens Loading dose Maintenance dose
Pritchard 4gm IV over 3 to 4 min 5gm buttock 4 hrly10gm deep IM
Zuspan 4gm IV over 5 to 10 min 1-2gm hrly IV infu
Sibai 6gm IV over 20 min 2gm hrly IV infusion
Sardesai 4 gm IV or IM 2 gm 3 hrly IV or IM
Therapeutic level of MgSO4 – 4 to 7mRQ/litre
Monitor
Presence of patellar reflex (8 to 10mEQ/litre ���� diagnose)
Respiratory rate >16 (>12mEQ /litre ���� depression)
Urinary output 30ml/hr
Continuation for 24 hrs after the last seizure
M.M. 0.4%
Serum levels of Magnesium Serum levels of Magnesium Serum levels of Magnesium Serum levels of Magnesium toxicity toxicity toxicity toxicity
Normal therapeutic level 4-6 mEq/L
• Loss of patellar reflex 8-12 mEq/ L
• Feelings of warmth, flushing 9-12 mEq/L
• Somnolence 10-12 mEq/L
• Slurred speech 10-12 mEq/L
• Muscular paralysis 15-17 mEq/L
• Respiratory difficulty 15-17 mEq/L
• Cardiac arrest 30-35 mEq/L
Thinking…..
Delay in MgSo4 treatment-
referred to tertiary hospitals with
no or wrong treatement
13.9% maternal deaths..admitted in moribund state…
Lopez and LleraLopez and LleraLopez and LleraLopez and Llera
Early and –’PROPER” referral
is the is the is the is the cornerstone
in the success of in the success of in the success of in the success of
saving the mother saving the mother saving the mother saving the mother
in eclampsia.in eclampsia.in eclampsia.in eclampsia.
Adetoro reported 14.4% of Adetoro reported 14.4% of Adetoro reported 14.4% of Adetoro reported 14.4% of maternalmortality..referral maternalmortality..referral maternalmortality..referral maternalmortality..referral
without treatmentwithout treatmentwithout treatmentwithout treatment…………....
SEIZURESEIZURESEIZURESEIZURE -FREETRANSPORTATIONTRANSPORTATIONTRANSPORTATIONTRANSPORTATION
‘‘‘‘MgSO4’’’’ before referral’
CONVENTIONAL WESTERN CONVENTIONAL WESTERN CONVENTIONAL WESTERN CONVENTIONAL WESTERN REGIMENS:
• can not be given outside
• ‘‘‘‘obstetric care unitsobstetric care unitsobstetric care unitsobstetric care units’’’’
JOSHI SUYAJNA D.
Longerduration
Cost ineffective
TrainedHealth prof
More sideeffects
RequiresIns.therapy
Costantsupervision
High dose
Conv.mgso4regimen
DIFFERENT MgSO4 REGIMENS DIFFERENT MgSO4 REGIMENS DIFFERENT MgSO4 REGIMENS DIFFERENT MgSO4 REGIMENS …………
� Eastman. Eastman. Eastman. Eastman.
� Pritchard.Pritchard.Pritchard.Pritchard.
� Chesley & Teppers.Chesley & Teppers.Chesley & Teppers.Chesley & Teppers.
� Hall, Anderson, Hall, Anderson, Hall, Anderson, Hall, Anderson, Harbert.Harbert.Harbert.Harbert.
� Flowers.Flowers.Flowers.Flowers.
� Zuspan.Zuspan.Zuspan.Zuspan.
� Cruik Shant.Cruik Shant.Cruik Shant.Cruik Shant.
� Sibai.Sibai.Sibai.Sibai.
� SardesaiSardesaiSardesaiSardesai
� Leens.Leens.Leens.Leens.
etc etc etc etc JOSHI SUYAJNA D.
‘‘‘‘Newer Innovations in the treatment Newer Innovations in the treatment Newer Innovations in the treatment Newer Innovations in the treatment
of of of of …………. . . . ECLAMPSIAECLAMPSIAECLAMPSIAECLAMPSIA……………………SINGLESINGLESINGLESINGLE----DOSEDOSEDOSEDOSE
Joshi Suyajna D.Joshi Suyajna D.Joshi Suyajna D.Joshi Suyajna D.
Professor of OBG,
VIMS- Bellary
MgSOMgSOMgSOMgSO4 4 4 4 DOSAGE SCHEDULEDOSAGE SCHEDULEDOSAGE SCHEDULEDOSAGE SCHEDULE
VIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMEN
4 gm of 50% MgSO4 in 20% dilution 4 gm of 50% MgSO4 in 20% dilution 4 gm of 50% MgSO4 in 20% dilution 4 gm of 50% MgSO4 in 20% dilution
to be given slow iv over to be given slow iv over to be given slow iv over to be given slow iv over
10 10 10 10 –––– 15 min , followed by 4 gm IM 15 min , followed by 4 gm IM 15 min , followed by 4 gm IM 15 min , followed by 4 gm IM
....
CLOSE MONITORINGCLOSE MONITORINGCLOSE MONITORINGCLOSE MONITORING
No need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levels
Antidote: If patient develops respiratory rate Antidote: If patient develops respiratory rate Antidote: If patient develops respiratory rate Antidote: If patient develops respiratory rate
<16 min administer <16 min administer <16 min administer <16 min administer
Calcium gluconate 1G IV over 10 min. Calcium gluconate 1G IV over 10 min. Calcium gluconate 1G IV over 10 min. Calcium gluconate 1G IV over 10 min.
(10ml of 10 % solution(10ml of 10 % solution(10ml of 10 % solution(10ml of 10 % solution))))
control hypertension
Labetalol - 20 mg i.v., repeated every 30 min & can be doubled maximum
upto 80 mg
Nifedepine : 5 to 10 mg every 15 min maximum upto 30 mg
FLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENT
PE PE PE PE –––– Hypovolaemia Hypovolaemia Hypovolaemia Hypovolaemia –––– Intravascular Intravascular Intravascular Intravascular
with fluid overload with fluid overload with fluid overload with fluid overload ---- Extra vascular Extra vascular Extra vascular Extra vascular
Do not give IV fluids rapidlyDo not give IV fluids rapidlyDo not give IV fluids rapidlyDo not give IV fluids rapidly
Fluid infusionFluid infusionFluid infusionFluid infusion---- Crystalloids 80ml/hrCrystalloids 80ml/hrCrystalloids 80ml/hrCrystalloids 80ml/hr
No colloidsNo colloidsNo colloidsNo colloids
NO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICS
INVESTIGATIONSINVESTIGATIONSINVESTIGATIONSINVESTIGATIONS
FBC FBC FBC FBC ---- peripheral smear peripheral smear peripheral smear peripheral smear
If platelets < 1,00,000 If platelets < 1,00,000 If platelets < 1,00,000 If platelets < 1,00,000 ---- > Coagulation study> Coagulation study> Coagulation study> Coagulation study
LFTLFTLFTLFT----S. bilirubin, SGOT, SGPT, LDHS. bilirubin, SGOT, SGPT, LDHS. bilirubin, SGOT, SGPT, LDHS. bilirubin, SGOT, SGPT, LDH
S. CreatinineS. CreatinineS. CreatinineS. Creatinine
U. albuminU. albuminU. albuminU. albumin
S. Uric acidS. Uric acidS. Uric acidS. Uric acid
Minimum investigationsMinimum investigations-- Hb, platelets, SGOT, SGPT Hb, platelets, SGOT, SGPT UrineUrine--alb alb
Planning the delivery
Delivery is the ultimate cureVaginal.
•LSCS : only for obstetric reasons
•Anesthesia –•General to be avoided, as it increases blood pressure during intubation and extubation.•Epidural is better than spinal.
LABOURLABOURLABOURLABOURLABOURLABOURLABOURLABOUR
Severe / fulminant PE deliver within 24hours
Eclampsia - deliver within 12hours
Precautions during labour
I stage- Close monitoring, avoid fluid overload
II stage- Shorten second stage
III stage- only oxytocin for 3rd Stage Avoid- Ergometrine, PGF2
Route of delivery
• Probability of achieving vaginal delivery after induction through an unripe cervix are below 20%
Hall DR et al, BJOG 2000
Haddad B et al, AJOG 2004
• Prolonged labor can be detrimental for mother and fetus
• Caesarean delivery is preferableSibai BM et al, COG 2005
Status eclampticus
• Phenytoin sodium 0.5gm dissolve in
20mg of 5% dextose iv given slowly
• If no response then complete
anesthesia, muscle relaxant, assisted
ventilation and C. Section is done.
• Injuries
• Pulmonary edema
• Pneumonia
• Acute LVF
• Cerebral
hemorrhage
• Renal failure
• Pulmonary
embolism
• Hyperpyrexia
• Hepatic necrosis
• DIC
• Postpartum shock
• Puerperal sepsis
• Disturbed vision
• Psychosis
Complications of eclampsia
HELLP syndromeHELLP syndromeHELLP syndromeHELLP syndromeWeinstein, 1982
• Recommended criteria for HELLP syndrome
•
• 1) Hemolysis (at least two of the following)
• a) Peripheral smear(schistocytes,burr cells)
• b) Serum bilirubin (>1.2mg/dL)
• c) Low serum haptoglobin
• d) Severe anemia unrelated to blood loss
• 2) Elevated Liver enzymes
• a) ALT or AST >/= twice upper level of normal
• b) LDH >/= twice upper level of normal
• 3) Low platelets < 100.000/mm3
Pritchard et al in 1954
Hemolysis
Schistocytes in the blood smear
S.Bilirubin > or equal to 1.2 mg%
Absent Plasma hapatoglobin
Elevated Liver Enzymes
SGOT > 72 IU/L
LDH > 600 IU/L
Low Platelet Count
Diagnosis of HELLP Syndrome
Classificationon the basis of platelet
count
class I, less than 50,000 per mm3less than 50,000 per mm3
class II, 50,000 to less than 100,000 per mm350,000 to less than 100,000 per mm3
class III, 100,000 to 150,000 per mm3100,000 to 150,000 per mm3
MISSISSIPPI
ClassificationClassificationClassificationClassification
full HELLP syndrome
partial HELLP syndrome
based on the number of abnormalities
Audibert F, Friedman SA, Frangieh AY, Sibai BM. Am J Obstet Gynecol 1996; 175:460-4.
considered for delivery within 48 hours
candidates for more conservative management
MEMPHIS
HELLP
• Prompt delivery , if it develops beyond 34 weeks.
• Dilemma- Before 34 weeks, administrations of corticosteroid for 48 hrs for both maternal and fetal benefits. But the results are variable in different studies.
• Cerebral haemorrhage
• Anoxia
• Cardiac failure
• Pulmonary oedema
• Aspiration pneumonia
• Pulmonary embolism
• Postpartum shock
• Puerperal sepsis
Causes of maternal mortality
Causes of perinatal mortality :
• Prematurity • Intrauterine asphyxia • Effects of drugs used to control convulsion • Trauma during delivery • Perinatal mortality 30 to 50% •• Sibai BM et al American Journal of Obstet Gynaecol 1983; 146 : 307.
Recurrent PE & EclampsiaRecurrent PE & EclampsiaRecurrent PE & EclampsiaRecurrent PE & Eclampsia
Subsequent to ECLAMPSIA
Chesley Sebai
Eclmapsia 1% 1.9%
Preeclampsia 23% 22%
Post Partum Care
• Over 40% of maternal deaths occur postpartum
• Post delivery a relative oliguria is not uncommon,
occuring in 30% of patients with severe disease
• Continued close monitoring is required in a
suitable environment
• Taper antihypertensive agents
• Contraception Counseling and Follow up
Long term prognosis.
• PE and Eclampsia is a forerunner of later life cardiovascular risk
• It is more in early onset PE.
• Does not affect long term renal function.
• No long term residual hepatic disease.
• Recurrence Risk-20 to 50 %.
• HELLP-2 to 6 %.
LONG TERM SEQUELE
Prevalence of remote hypertension:
� increased in Multiparas who develop pre-eclampsia,
�
�women with severe early onset disease of any parity
Working Group Report on High Blood Pressure in Pregnancy Working Group Report on High Blood Pressure in Pregnancy Working Group Report on High Blood Pressure in Pregnancy Working Group Report on High Blood Pressure in Pregnancy 2001.2001.2001.2001.
Conclusion.
• PE is the leading cause of Maternal and Perinatal Mortality and Morbidity
• Maternal and neonatal outcome is good in gestational hypertension and with antihypertensive drugs they can go up to term.
• But PE is enigmatic, an unique syndrome, dangerous for both mother and fetus, no absolute preventive measure are available and does not respond well to treatment.
• Multidisciplinary approach with close medical supervision, timely delivery and management at tertiary center are the corner stones for good maternal and fetal outcomes.
•Suggested reading;Suggested reading;Suggested reading;Suggested reading;
1) Pregnancy induced hypertension by Harshalal R Seneviratne
and Chandrika by Orient Longman
• 2) Progress in Obstetrics and Gynecology , 17th edition
• 3) Williams Obstetrics 23rd edition
• 4) RCOG guidelines for management of severe preeclampsia/eclampsia
• 5) Critical care Obstetrics by Steven L Clarke et al
• 6) Obstetrics -normal and abnormal pregnancies by Steven G. Gabbe et al
• 7) Management of high risk pregnancy- an evidence based approach by John T.Queenan et al
• 8) Ian Donald’s practical obstetrics problems.
•
•
THANK YOU
• Joint Secretary FOGSI - 2009
• Consultant Obstet. & Gynecologist, Mumbai
• Ex. Associate Professor, GMC, Mumbai
• Member Managing Council, MOGS
• Chairperson Medico-legal committee, MOGS
DR. (MRS.) MADHURI A. PATEL
TO CONTACT ME
[email protected]@[email protected]@yahoo.com
www.suyajna.comwww.suyajna.comwww.suyajna.comwww.suyajna.com
Why prediction is important:
1. The risk for recurrent PE can be as high as 65% (Barton& Sibai, 2008).
2. PE is associated with substantial
maternal& perinatal
complications
Prediction� Roll-over Test
� Second Trimester Mean Arterial Pressure
� Urinary Calcium
� Uric acid
� Fibronectin
� Homocysteine level
� Cytokines
� Coagulation factors
� Placental peptides
� Doppler Ultrasound
� Fetal DNA
SCREENING TESTS FOR PE (WHO, 2004)
I. Placental perfusion & vascular resistance dysfunctionMean arterial blood pressureRoll over test Doppler ultrasound Isometric exercise test Intravenous infusion of angiotensin II Platelet angiotensin II binding Platelet calcium response to arginine vasopressin Renin 24-hour ambulatory blood pressure monitoring II. Fetoplacental unit dysfunctionHuman chorionic gonadotropin Alpha fetoprotein Estriol Inhibin A Pregnancy-associated plasma protein A Activin A Corticotropin release hormone
Roll-Over Test
• GANT… ‘Roll – Over test’
Position of BP cuff….Nisell et al 1985
Gant NF, Daley GL, Chand S, Whalley PJ, MacDonald PC. A study of angiotensin II pressor responsiveness throughout primigravid pregnancy. J Clin Invest.1973;52:2682–2689
III. Renal dysfunction Serum uric acid Microalbuminuria Urinary calcium excretion Urinary kallikrein Microtransferrinuria N-acetyl- glucosarninidase
Platelet countPlatelet activation and endothelial cell adhesion moleculesProstacyclinCytokinesIsoprostanes, Antiphospholipid antibodies, Placenta growth factorHematocritAntithrombin IllCalciumTransferrinAtrial natriuretic peptide
Fibronectin Endothelin Thromboxane Homocysteine Serum lipids Insulin resistance Plasminogen activator inhibitor Leptin Total proteins Magnesium Ferritin Haptoglobin microglobulin Genetic markers
IV. Endothelial& oxidant stress dysfunction
II. Biochemical Markers
Angiogenic factors before & after the onset of PE(Barton& Sibai, 2008).
Serum placental growth factor: reducedSoluble fms-like tyrosine kinase: elevatedEndoglin: elevated
‘Angiotension-II infusion…’Gant…1973
Gant NF, Chand S, Worley RJ, Whalley PJ, Crosby VD, MacDonald PC. A clinical test useful for predicting the development of acute hypertension in pregnancy. Am J Obstet Gynecol. 1974;120:1–7
MDP
2nd trimester MD BP ≥ 90 mm Hg
Chesley LC, Sibai BM.
Clinical significance of elevated mean arterial pressure in the second trimester.
Am J Obstet Gynecol. 1988;159:275–279.[
Biophysical
Mean arterial pressure(2DBP+SBP)/3
•Better predictor of PE than S& DBP(BMJ 200817;336:111; Meta-analysis of 34 RCT)
•BP remains the cornerstone of early diagnosisalthough it has limitations:
….measurement errors associated with sphygmomanometer..(effect of maternal posture on BP in pregnant women).
Uterine artery Doppler ultrasound
‘Diastolic Notch’
�Impaired trophoblastic invasion of the spiral arteries: reduction in uteroplacental blood flow.
�High pulsatility index and/or Notch in 1st & 2nd
trimesters: poor predictor of PE(Papgeorghiou & Leslie, 2007)
Repeated routine urinalysis
throughout pregnancy NOT useful for predicting PE
(JAMA 2003: 12;289(10):1220)
Prevention
Aspirin-19% reduction in risk of PE.
-16 % reduction in fetal and neonatal death.
- 8 % reduction in the incidence of small for gestational age infants.
Updated chrochane review-2000. Systemic review 2003.
The controversy is when to start treatment.
Prevention
Calcium• Protective effect in women with low calcium intake.
Cochrane data base 2005
• Supplementation with 1.5 gm calcium /day did not result in statistically significant decrease in the overall incidence of PE, but there is significant decrease risk of the more serious complications which included maternal and neonatal morbidity and mortality and preterm delivery .
WHO-2006
Prevention
• Antioxidants • Antioxidants like Vit C, E, and lycopene found to be effective in smaller trials but VIP Trial demonstrated no decrease in risk of PE.
Lancet-2006, 367,1145-54.
• In the other large multicentric trial, the supplementation did not decrease the incidence of preeclampsia, IUGR or the risk of death or other serious outcomes.
N. Eng. J .of Med. 2006, 354, 1796-806
II. Pregnancy-Related FactorsRegular antenatal care is mandatory for the prevention & early detection of PE.
�Risk factors: Magnitude of risk depends on the number of factors
�Hydrops/hydropic degeneration of the placenta
�Multifetal gestation�Unexplained FGR�Gestational hypertension�UTI�Periodontal infection�Markers�Biophysical�Biochemical
Conclusion•BP remains the cornerstone of early diagnosis•MarkersReliability is inconsistentMany suffer from poor specificity & predictive values.None provided a cutoff value that could be clinically useful for the prediction of PE (Widmer et al, 2007).
Secondary•Breaking off the disease process before emergence of obvious clinical disease•{Etiology of the disease is unknown} •To correct theoretical pathophysiology
I. Non pharmacologicalII. Nutritional III. Pharmacological
Primary prevention•Avoiding occurrence of the disease•Obese:achieve an ideal b wt before conception (Villamor& Cnattingius, 2006)
No RCT•Ch hypertension:Control BP before conception. No RCT
I. Non pharmacological1. Daily Bed restRest for 4Rest for 4Rest for 4Rest for 4----6 h/d6 h/d6 h/d6 h/d
May reduce risk of PE for women with normal BP (level 2 evidence)(Cochrane Library 2006 Issue 2:CD005939)
2. Life-style changes •High job stress: greater risk of PE(Sharma& Mittal, 2006)
•Reducing job stress may be beneficial in the prevention of PE
•Stretching exercises are more effective at reducing the risk of PE than walking(University of North Carolina,2008)
3. Regular prenatal exercise•May prevent or oppose progression (Weissgerber et al, 2004)
•{Stimulation of placental growthReduction of oxidative stressReversal of maternal endothelial dysfunction}. •Insufficient evidenceModerate intensity regular aerobic exercise(Cochrane Library 2006 Issue 2:CD005942) Aerobic exercise =cardiovascular exercise=any sustained rhythmic activity that involves large muscle groups: makes the lungs work harder as the body's need for oxygen is increased.
�Smoking: Reduced risk for PE (Sibai et al, 2005).
{Nicotine inhibition of interleukin-2 & tumor necrosis factorEffects of nicotine on angiogenic proteins}. Smoking: abnormal fetal growthpreterm birthAbruptionAdverse effects on maternal health.
II. Nutritional1. Higher total dietary fiber intake in early pregnancymay reduce risk for PE(level 2 evidence)Prospective cohort study Am J Hypertens 2008 Aug;21(8):903
2. Increasing dietary protein & energy intake RCT: no benefit
•5 or more servings of chocolate/w in 3rd trimester:40% reduction(Triche, 2008; Epidemiology .19:459-464), Yale University
{Chocolate, especially dark chocolate, is rich in theobromine: stimulates the heart, relaxes smooth muscle & dilates blood vessels, and has been used to treat chest pain, high blood pressure}
3. Garlic Insufficient evidence to recommend for preventing PECochrane Library 2006
)Issue3:CD006065
5. Weight Reduction •Although obesity is a known risk factor, there is no evidence that limiting wt gain during pregnancy; reduces its occurrence.•Wt reduction is not recommended during pregnancy even in obese women (Kramer, 2004)
6. Fish Oil Supplementation •Observational studies: beneficial effects •{inhibition of platelet thromboxane A2 without affecting prostacyclin: shifting the balance toward a reduced platelet aggregation and increased VD}. •RCT: No benefit (Olsen et al, 2000)
•High doses: increase the risk of PIH(Olafasdottir et al, 2006).
•Not recommended for the prevention of PE
III. Pharmacological
1. Low-dose Aspirin•{inhibits biosynthesis of platelet thromboxane A2 with little effect on vascular prostacyclin production: altering the balance in favor of prostacyclin}. •(50-150 mg/day) For women with a previous history of hypertension or PE (n=6,107):Small to moderate benefits, safe. level 2 evidence(Cochrane Library 2007 Issue 2:CD004659)
2. Low-dose Aspirin/Heparin•History of severe preterm PE & LBW infants.(Sergio et al, 2006)
•Lower incidence of PE (3Vs 30%) Greater gestational age at deliveryHigher birth wt
3. Calcium Supplementation •Reduces the risk of PIH, particularly in populations that have diets deficient in calcium level 1 evidence (Cochrane Syt review , 2006)
•The relationship between cal & risk of PIH is inconsistent& inconclusiveThe relationship between cal & the risk of PE is highly unlikely.Evidence-based review by FDA (2007)
4. Antihypertensive Drugs •Mild to moderate hypertension: Halving in the risk of developing severe hypertensionNo difference in the risk of developing PE or proteinuria (Cochrane syst review, 2007)
5. Diuretics •No reduction in the incidence of PE or perinatal mortality•May have deleterious effects: reduced renal & placental perfusion. (Cochrane Library 2007 Issue 1:CD004451)
6. Antioxidant supplementation may not affect risk of PE or clinical outcomes level 2 evidence
)1:CD004227Cochrane Library 2008 Issue (
7. Concomitant Vit C& E supplementation•{PET: imbalance of oxidant & antioxidant activity: multiorgan endothelial dysfunction}. •Vit C (1,000 mg/d) plus vit E (400 IU/ d)•Did not prevent PElevel 2 evidence (Obstet Gynecol 2007 Dec;110(6):1311)•May increases rate of LBW infants& might be associated with higher rate of SBlevel 2 evidence (Lancet 2006 Apr 8;367(9517):1145
8. Magnesium •{Mg is beneficial for the prevention & tt of severe PE & EDecreased intracellular Mg in PE} •No effect•(365 mg& 500 mg).Cochrane syst review, 2004
9. Folic acid& other B-vits •{Deficiency of vit B2 may cause biochemical changes simulating abnormalities of PE}•No evidence that any of B vits can prevent PE (Shrama& Mittal, 2006).
10. Zinc supplementation •{Zinc concentrations are reduced in PE}•RCT: No benefit(Jonsson et al, 1996)
MCQ
1. Predictive tests for PIH are considered as positive when there is increase in all except
a) Maternal Serum Inhibin A level
b) Fibronectin level
c) Maternal Plasma Endothelium I level
d) Calcium / Creatinine ratio
Answer: d)Answer: d)Answer: d)Answer: d)
Explanation : This is considered a predictor test, with a lower calcium excretion in PIH. It has a sensitivity of 70% and specificity of 95%. Calcium – creatinine ratio of less than 0.04 is significant.
MCQ2. Maternal complications due to severe preeclampsia
includes all except
a) Convulsions
b)HELLP Syndrome
c) Abruptio Placenta
d) Placenta Previa
Ans. :Ans. :Ans. :Ans. : d)d)d)d)
Explanation : Vascular constriction in results in hypoperfusion in brain, liver and placenta and causes convulsion, HELLP Syndrome and abruptio placenta respectively but not placenta previa
MCQ3. PIH causes decrease in followings except :
a) Antithrombin III
b) Tissue Plasminogen activator
c) Protein S
d) Platelet count
Answer: bAnswer: bAnswer: bAnswer: b
Explanation : PIH is associated with altered coagulation, fibrinolysis, platelet and vascular endothelial function . The fall in the platelet count is most common , probably due to increased consumption (low grade DIC). Platelets are in an activated state. There is also reduction in anticoagulants .
MCQ4. Antihypertensives usually recommended in pregnancy
are all except
a) Methyldopa
b) Labetalol
c) Atenolol
d)Nifedipine
Ans. :Ans. :Ans. :Ans. : c)c)c)c)
Explanation : use of Antenolol, a β adrenergic blocker in pregnant women with chronic hypertension resulted in significantly lower birth-weight compared with other antihypertensive agents. Many studies also indicated that treatment with atenolol associated IUGR was dose and duration related, hence, should be avoided throughout pregnancy.