hypertensive disorder of pregnancy first year student jivanyog nursing home visnagar first year...
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HYPERTENSIVE DISORDER OF PREGNANCY
HYPERTENSIVE DISORDER OF PREGNANCY
• FIRST YEAR STUDENT
• JIVANYOG NURSING HOME
• VISNAGAR
• FIRST YEAR STUDENT
• JIVANYOG NURSING HOME
• VISNAGAR
DR. SUMAIYA KHARODIA DR. SUMAIYA KHARODIA
IntroductionIntroduction
• Disease of many theories, known from centuries back, PIH is an enigmatic condition of pregnancy, can’t predict, can’t prevent, can’t treat absolutely.
• Disease of many theories, known from centuries back, PIH is an enigmatic condition of pregnancy, can’t predict, can’t prevent, can’t treat absolutely.
IntroductionIntroductionWorld 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• 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
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• 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
IncidenceIncidence• Preelampsia 5 to 10 %
• Eclampsia (Developed countries) 1 : 2000Eclampsia (Developed countries) 1 : 2000 In India 1:30 to 1:500In India 1:30 to 1:500
• Maternal Mortality in US 17.6 % Maternal Mortality in US 17.6 % In India 25.5 %In India 25.5 % Walker JJ, Lancet:2000;356:1260-Walker JJ, Lancet:2000;356:1260-
6565
Sawhney H et al, JOGR 2000
• Three fold increase in Perinatal MortalityThree fold increase in Perinatal Mortality
• Preelampsia 5 to 10 %
• Eclampsia (Developed countries) 1 : 2000Eclampsia (Developed countries) 1 : 2000 In India 1:30 to 1:500In India 1:30 to 1:500
• Maternal Mortality in US 17.6 % Maternal Mortality in US 17.6 % In India 25.5 %In India 25.5 % Walker JJ, Lancet:2000;356:1260-Walker JJ, Lancet:2000;356:1260-
6565
Sawhney H et al, JOGR 2000
• Three fold increase in Perinatal MortalityThree fold increase in Perinatal Mortality
Perinatal OutcomePerinatal OutcomeUK 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 1994 Shah DS, FOGSI Perinatal Survey, 1994 Sardesai Jr Obstet Gynecol 2003
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.
• PIH 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)
• Hypertension that develops de novo as a consequence of pregnancy after 20th week of gestation, returning to normal after 6 weeks of delivery.
• PIH 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)
National High Blood Pressure Education Program Classification ( NHEP) 2000
• Gestational hypertension.
• Preeclampsia (mild, severe).
• Eclampsia.
• Superimposed preeclampsia upon chronic hypertension.
• Chronic hypertension with pregnancy.
Definitions• Gestational hypertension:
– Hypertension for first time after 20 w, without Proteinuria. BP returns to normal before 12 weeks postpartum.
• Chronic hypertension with pregnancy: – Hypertension antedates pregnancy and detected
before 20 w, & lasts more than 12 weeks postpartum.
Definitions– Preeclampsia:
• The development of hypertension and Proteinuria after 20 w
• May occur earlier in vesicular mole or twins.
– Eclampsia (in Greek= Flash of light): • The occurrence of tonic-clonic convulsions (without
any neurological disease) in a woman with pre-eclampsia.
Definitions
• Superimposed pre-eclampsia: ¤ It is the new development of Proteinuria
after 20 weeks gestation in a patient with chronic hypertension
Definitions• Proteinuria:
• ≥ 300mg/24 hours urine.– ≥ +1 dipstick.
• Heavy Proteinuria :–= ≥ 2gm/24 hours
– or ≥ +2 in dipstick.
Preeclampsia
Epidemiology of preeclampsia
Incidence: • Is a disease of humans only.• Is the most common medical disorder complicating
pregnancy 5-15%• Is the most common hypertensive disorder in
pregnancy.• More common in primigravidas and elderly
multipara.• More common in winter.• More in black races.
14
Etiology
• Basic concepts– Exposed to chorionic villi for the first time
– Exposed to a superabundance of chorionic villi, as with twins or hydatidiform mole
– Have preexisting vascular disease
– Genetically predisposed to hypertension developing during pregnancy
15
• Vascular endothelial damage with vasospasm, transudation of plasma, and ischemic and thrombotic sequelae.
• Currently plausible potential cause (2003, Sibai)– Abnormal trophoblastic invasion of Uterine vessels
– Immunological intolerance between maternal and fetoplacental tissues
– Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy
– Diatary deficiencies
– Genetic influences
16
Abnormal Trophoblastic Invasion
• In normal implantation, endovascular trophoblasts invade the uterine spiral arteries.
17
18
• In preeclampsia– Incomplete trophoblastic invasion– The magnitude of defective trophoblastic invasion of the
spiral arteries correlated with the severity of the hypertensive disorder (2000, Madazli)
• Using electron micorscopy– Endothelial damage– Insudation of plasma constituents into vessel walls– Proliferation of myointimal cells– Medial necrosis– Lipid and macrophage accumulates in myointimal cells
Abnormal Trophoblastic Invasion
Etiology= theories
• Genetic Predisposition.
• Free Radicals Theory• In pre-eclampsia the levels of free radicals
are higher than normotensive women leading to endothelial damage.
Oxidative stress
Antioxidant capacity
ROS synthesis
O2._
H2O2
ONOO_
Vitamin CSOD
Etiology= theoriesEndothelial injury:
• Endothelin 1(potent vasoconstrictors).
• Nitric Oxide ( vasodilator action).
• Vascular Endothelial Growth Factor (VEGF).
Etiology= theories
Prostaglandins:• There is decrease in prostacyclin
/TX A2 ratio leading to :• vasoconstriction and tendency to
thrombosis.
Etiology= theoriesInflammatory Factors:• Pre-eclampsia is considered an inflammatory
disease due to increased number of activated leukocytes in the maternal circulation.
• Immunological Factor: • primigravidas• Multipara with 1st pregnancy from a
new husband. • Abundant trophoblast ( vesicular mole
and multiple pregnancy.
The Central Players (Hemostats) in PET
1. The Endothelium 2. Neutrophils3. Platelets 4. Coagulation system. Once one is triggeredCo- Workers are released (NO, PGs, ROS,
Homosystein, etc)
The Constant Pathophysiological Changes
IsVascular endothelial:
Damage +Dysfunction + Spasm
PathologyPET is the clinical ice-berg
tip manifestation of the disturbances in the maternal homeostasis, involving many systems and organs.
Multisystem Features Of Preeclampsia
Hypertension Proteinuria
Eclampsia HELLP syndrome
Intra-uterine growth restriction
Multi-organ disease
Cerebral vessels
Fetus
Liver
Systemic blood vessels Kidneys
PATHOPHYSIOLOGY
MULTIPLE ORGAN SYSTEM INVOLVMENT
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
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
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
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
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
3-CVSPlasma 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
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
3-CVS• High systemic vascular resistance &
hyperdynamic ventricular function avoid aggressive fluid adminstration
• Loss of the normal refractoriness to angiotensin II
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
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/mm³Found in 10% of the Pt with severe PET
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
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
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
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
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
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
DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT
OBGYN
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
High Risk FactorsHigh Risk Factors
Primigravida : Extremes of reproductive age (young and elderly) Socio economic (status) : Disadvantaged Ethnicity : African American Family history : Hypertension, pre-eclampsia,
(First degree relatives) eclampsia Placental abnormalities : Molar pregnancy
Hyperplacentosis – multiple pregnancy Placental ischaemia
Associated medical conditions : Obesity, Diabetes, Renal disease, Collagen vascular disease
Thrombophilias : Anti-phospholipid syndrome, Protein C, S deficiency, Factor V LeidenGenetic : History of pre-eclampsia in sister, mother (Multi-factorial inheritance) Immunological
PredictionPrediction Roll-over Test Second Trimester Mean Arterial Pressure Urinary Calcium Uric acid Fibronectin Homocysteine level Cytokines Coagulation factors Placental peptides Doppler Ultrasound Fetal DNA
Roll-over Test Second Trimester Mean Arterial Pressure Urinary Calcium Uric acid Fibronectin Homocysteine level Cytokines Coagulation factors Placental peptides Doppler Ultrasound Fetal DNA
Tests for Prediction
• Roll over test is positive (rise of diastolic blood pressure 20 mmHg or more after turning from left lateral to dorsal position).
• Increased pressor response.
• Uric acid: is elevated.
• Hypercalciuria.
• Doppler velocimetry to detect Uteroplacental hypo perfusion.
Diagnosis Of PET
Hypertension + Proteinuria =
Two facets of a complex pathophysiological process
A): Signs: :
it is a disease of signs :
2 cardinal signs + or - Edema:
• Hypertension: – usually precedes Proteinuria,
• Proteinuria: detected by – Boiling test.– Quantitative assay.– Dipstick test.
+ or - Edema• occult or manifest:
» The lower extremities.
» Abdominal wall, vulva or may be generalized anasarca.
• usually after hypertension.
Peripheral edema is not a useful diagnostic criterion
1) it is common in normal pregnancy.
2) PET can occur without edema (dry type).
so its presence does not ensure a poor prognosis and its absence not ensure a favorable outcome.
B) Symptoms (non specific):
• Headache.
• Blurring of vision.
• Nausea and vomiting.
• Epigastric pain (distension of the liver capsule)
• Oliguria or anuria
Severity Of Pre-eclampsia
• The severity of pre-eclampsia is assessed by:
–The frequency and intensity of the signs and symptoms.
–The more the severity of PET, the more likely is the need to terminate pregnancy.
DD ,mild & severe PET
Abnormality Mild SevereDiastolic blood pressure < 100 mg Hg 110 mm Hg or higher
Proteinuria Trace to 1+ Persistent 2+ or more
Headache Absent Present
Visual disturbances Absent Present
Upper abdominal pain Absent Present
Oliguria Absent Present
Convulsion Absent Present (eclampsia)
Serum creatinine Normal Elevated
Thrombocytopenia Absent Present
Liver enzyme elevation Minimal Marked
Fetal growth restriction Absent Obvious
Pulmonary edema Absent Present
4) Diagnosis Of Eclampsia:
• Eclamptic fit stages ( 4 stages):– Premonitory stage (1/2 minute):
» Eye rolled up.» Twitches of the face and hands.
– Tonic stage (1/2 minute): » Generalized tonic spasm with
episthotonus.» Cyanosis.» Tongue may be bitten between the
clenched teeth.
4) Diagnosis Of Eclampsia:
• Clonic stage (1-2 minutes): » Convulsions .
» Tongue may be bitten.
» face is congested and cyanosed.
» conjunctival congestion.
» blood stained froth from the mouth,
» Stertorous breathing,
» temperature may rise.
» involuntary passage of urine or stool.
» Gradually convulsions stop.
4) Diagnosis Of Eclampsia:
• Coma: – Variable duration due to respiratory and
metabolic acidosis.– Deep coma may occurs (cerebral hemorrhage). – Labor usually starts shortly after the fit.– Sometimes labor does not start and convulsions
recur again the so called ‘intercurrent eclampsia’ and carries a bad prognosis.
Classifications of Eclampsia
–Intercurrent Eclampsia: eclampsia in which the eclamptic fits recur in the same pregnancy.
–Recurrent Eclampsia: eclampsia that recurs in subsequent pregnancy.
Classifications of Eclampsia 1)Mild
2) Severe (Eden's criteria):• Coma > 6 hours.• Temperature > 39 (pneumonia or pontine
hge)• Systolic Bp > 200 (risk of cerebral hge)• Pulse > 120/min ( acute heart failure).• Anuria or Oliguria( renal failure).• Respiratory rate > 40/min( pneumonia)• More than 10 fits (status eclampticus).
PreventionPrevention
• 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.
• 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.
PreventionPrevention
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
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
PreventionPrevention
• 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
• 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
Criteria for diagnosis of Preeclampsia
Criteria for diagnosis of Preeclampsia
• Blood pressure of 140 mm Hg systolic or higher or 90 mm Hg diastolic or higher that occurs after 20 wks of pregnancy in a woman with previously normal BP
• Proteinuria as urinary excretion of 0.3 g protein or higher in a 24 hrs specimen
Am J Obstet Gynecol 2000;183:S1-S22
• Blood pressure of 140 mm Hg systolic or higher or 90 mm Hg diastolic or higher that occurs after 20 wks of pregnancy in a woman with previously normal BP
• Proteinuria as urinary excretion of 0.3 g protein or higher in a 24 hrs specimen
Am J Obstet Gynecol 2000;183:S1-S22
PROTEINURIAPROTEINURIA
Develops late in the disease processInfluenced by exercise and posture24 hour estimation is better than randomHypertension with proteinuria is a reliable indicator of fetal jeopardy
Proteinuria alone PNM unchangedHT alone PNM 3 fold riseHT + proteinuria PNM 8 fold rise(PNM: perinatal mortality rate)
EDEMAEDEMA
• Early but non specific sign• Rapid weight gain• Edema of PIH 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
• Early but non specific sign• Rapid weight gain• Edema of PIH 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
ManagementManagement
AIMS• Control of hypertension• Prevention of eclampsia• Prevention of accidental hemorrhage
and DIC• Prevention of renal damage• Maintenance of placental perfusion• Monitoring of fetal growth and well-
being• Planning timely delivery• Care in puerperium• Follow up.
AIMS• Control of hypertension• Prevention of eclampsia• Prevention of accidental hemorrhage
and DIC• Prevention of renal damage• Maintenance of placental perfusion• Monitoring of fetal growth and well-
being• Planning timely delivery• Care in puerperium• Follow up.
Out Patient ManagementOut Patient Management
Gestational Hypertension less than160/100 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
Gestational Hypertension less than160/100 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.
• 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 (Severe
Preeclampsia)
Indications for Hospitalization from Day Care Unit (Severe
Preeclampsia)
• 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
• 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 SURVEILLANCEMaternal SURVEILLANCE
Bed restVital parametersBP measurement 6 hourly Daily weightInput /output chartingUrine protein estimation dailyPremonitory symptomsDeep tendon reflexesFundoscopy
BIOCHEMICAL MONITORINGBIOCHEMICAL MONITORING
CBCUrine routine and microscopy24 hour urineRFT, BUN, Creatinine, uric acid, creatinine cleareanceLFT: enzymes, bilirubin, proteinsPlatelet countCoagulation profile
Fetal Well-beingFetal 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 HypertensionControl 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
• 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
Indications for Antihypertensive Therapy
• Role of antihypertensive therapy in Mild to Moderate Hypertension is unclear.
Drugs and therapy Perceptive 2001,17(18),11-15
• Persistent rise of BP in mild to moderate cases
• Severe preeclampsia• Hypertensive crisis• Chronic hypertension
• Role of antihypertensive therapy in Mild to Moderate Hypertension is unclear.
Drugs and therapy Perceptive 2001,17(18),11-15
• Persistent rise of BP in mild to moderate cases
• Severe preeclampsia• Hypertensive crisis• Chronic hypertension
Oral Antihypertensive for Control of Mild to Moderate Hypertension in
Pregnancy
Oral Antihypertensive for Control of Mild to Moderate Hypertension in
Pregnancy
• 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
• 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
Antihypertensive for Control of Acute or Severe Hypertension in
Pregnancy
Antihypertensive for Control of Acute or Severe Hypertension in
PregnancyShort Acting Antihypertensive agents :• Hydralazine : 5 mg IV repeated after 20 min• 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 mgOther Antihypertensive agents :Diazoxide : 30 to 50 mg IV, repeated every 10to 15 min or by continuous infusion.Sodium Nitroprusside : IV infusion 0.5 to 10 mg/kg/min
Short Acting Antihypertensive agents :• Hydralazine : 5 mg IV repeated after 20 min• 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 mgOther Antihypertensive agents :Diazoxide : 30 to 50 mg IV, repeated every 10to 15 min or by continuous infusion.Sodium Nitroprusside : IV infusion 0.5 to 10 mg/kg/min
Drugs used to lower blood pressure during pregnancyDrugs used to lower blood pressure during pregnancy
Planning DeliveryPlanning Delivery
PlaceMultidisciplinary team and high dependency care availableNeonatal care facilities
RouteAim for vaginal deliveryLSCS required for obstetric indication or maternal or fetal compromiseTo avoid general anaesthesia
TimeConservative v/s Early intervention
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
Criteria for delivering patient with Severe Preeclampsia
Criteria for delivering patient with Severe Preeclampsia
• 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
• 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
Labour Management• IV access
• Repeat haematological investigations
• Fluid management
• Seizure prophylaxis and anti
hypertensives
• Electronic fetal monitoring
• Analgesia and Anaesthesia
• No ergometrine
Period of gestation convulsions occur
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.
• Eclampsia • Epilepsy • Cerebral malaria in tropics • Encephalitis • Meningitis • Intracranial tumors • Peripheral cerebral
thrombosis • Poisoning • Hysteria
Differential Diagnosis
• 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
• Cerebral haemorrhage
• Anoxia
• Cardiac failure
• Pulmonary oedema
• Aspiration pneumonia
• Pulmonary embolism
• Postpartum shock
• Puerperal sepsis
Causes of maternal / Perinatal 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.
• General management
• To control convulsions using MgSO4
• To control Hypertension
• To avoid Diuretics
• To limit IV fluids unless excessive fluid loss
• To investigate
• To terminate the 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
Specific managementTo control seizures and to prevent its recurrenceMagnesium sulfate: the drug of choice
Regimens Loading dose Maintenance dose
Pritchard 4gm IV over 3 to 4 min 5gm buttock 4 hrly 10gm 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%
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%
Phenytoin therapy
10mg/kg IV followed by 5mg/kg 2 hrs later
Sedatives can be used with above regimen
To control hypertensionInspite of sedative if BP >160/110mg then antihypertensive drugs are administered
Hydralazine
- 5mg iv slowly
- rate 10mg every 20 minutes
-Monitoring BP every 5 minutes
- Repeat the dose when diastolic BP >110mmHg labetalol - 20 mg i.v., repeated every 30 min & can be doubled maximum upto 80 mgNifedepine : 5 to 10 mg every 15 min to maximum upto 30 mg
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.
Planning the delivery
• Delivery is the ultimate cure
•Vaginal.
•LSCS is done for obstetric reasons, or before 32 weeks of gestation.•Anesthesia – •General to be avoided, as it increases blood pressure during intubation and extubation.•Epidural is better than spinal.
Route of delivery• Probability of achieving vaginal
delivery after induction through an unripe cervix are below 20%
Hall DR et al, BJOG 2000Haddad B et al, AJOG 2004
• Prolonged labor can be detrimental for mother and fetus
• Caesarean delivery is preferableSibai BM et al, COG 2005
HemolysisSchistocytes in the blood smearS.Bilirubin > or equal to 1.2 mg%Absent Plasma hapatoglobinElevated Liver EnzymesSGOT > 72 IU/LLDH > 600 IU/LLow Platelet Count
Diagnosis of HELLP Syndrome
HELLP Syndrome.
• 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.
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 %.
Conclusion.• PIH 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.
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Motherhood … .
.. A dream of every woman