Transcript
Presenter : Sumit Gupta
Moderator : Prof. Anjan Trikha
IntroductionIncidence : 5-7% of all pregnancies.
Maternal and perinatal mortality & morbidity:
50-60,000 deaths/year
Developed countries: Leading cause of prematurity
Pregnancy Induced Hypertension
Hypertensive disorders of pregnancy
ClassificationIst classified in 1972 by ACOG
National High Blood Pressure Education Program: 2000
Recent: ACOG 2013.
Preeclampsia & Eclampsia:
Chronic Hypertension.
Chronic Hypertension with superimposed Preeclampsia
Gestational Hypertension
Preeclampsia: Not a triadHypertension:
After 20 wks, MC near term
SBP> 140 or DBP>90
SBP>160 or DBP>110 → Initiate treatment
Proteinuria: 24 hour excretion>300mg in 24 hours.
Single sample: Urine protein: Creatinine >3.0 As good as 24 hr sample.
Dipstick test: +1 reading. False +ve Used only when other tests aren’t available.
EdemaNon specific. “Physiological in pregnancy”
Korotkoff 5
2 readings 4
hours apart
PreeclampsiaPreeclampsia without Proteinuria,
Hypertension with
Thrombocytopenia (<100000).
S. Cr>1.1 or 2X of previous value w/o any renal disease
Pulmonary edema
Elevated AST/ALT (2X the normal value).
S/s of intracranial or visual abnormalities.
Severe preeclampsia
Severe preeclampsia SBP>160 or DBP>110.
Thrombocytopenia (<100000).
S. Cr>1.1 or 2X previous value w/o any renal disease
Pulmonary edema
Rt upper quadrant pain, Elevated AST/ALT (2X the normal).
S/s intracranial or visual abnormalities.
Mild preeclampsia “Preeclampsia without severe features”.
Chronic HypertensionChronic Hypertension
Hypertension diagnosed either before conception or before 20 weeks pregnancy
Gestational hypertension persisting 12 weeks postpartum.
Chronic hypertension with superimposed preeclampsia Preeclampsia
Incidence 4-5 times more in Hypertensive.
Worse prognosis
Both mother and child.
Chronic HypertensionChronic hypertension with superimposed
preeclampsia
New onset Proteinuria
After 20 weeks in known hypertensive (<20 weeks).
No Proteinuria
Thrombocytopenia (<100000).
S. Cr>1.1 or 2X previous value.
Pulmonary edema
Rt upper quadrant pain or Elevated AST/ALT (2X the normal)
Sudden worsening of hypertension or need to ↑ t/t in previously controlled patient.
Gestational HypertensionGestational Hypertension
New onset ↑BP after 20 weeks
No proteinuria
Transient nature (if not→?? Chr. HTN)
Enhanced surveillance : Risk of HTN ↑ ↑.
“Late” or post partum hypertensionNormotensive during gestation.
Mild HTN post partum (2weeks-6months)
Labile BP
Normalizes upto 1 year.
Risk FactorsDemographic factors
Age>35 years(2X than 20-29 years).
Ethnicity: African Americans, Hispanic
Severe hypertension→ require intense therapy.
Genetic factors
Previous history of Preeclampsia(7X more likely)
Multiple affected pregnancies.
Family history for Preeclampsia(2-4X more)
History of placental abruption, IUGR or IUD
Risk FactorsMedical Conditions
Obesity ↑BMI 5-7kg/m2 ↑ 2X risk
Chronic Hypertension
Diabetes Mellitus
Chronic renal disease, APLA syndrome, SLE
ObstetricMultiple Gestation, H. mole
BehavioralCigarette smoking protective
↓ 30-40%. Dose related effect.
Physical activity protective
Partner related risk factorsNulliparity.
Pathophysiology Normal pregnancy
Cytotrophoblast of embryo invade the spiral arteries of pregnant uterus
Remodeling of smooth muscle of uterine arteries S Spiral artery diameter ↑
Intervillous space has very low resistance to blood flow and remodeled arteries Nonresponsive to vasoconstrictors
PathophysiologyPreeclampsia
Asymptomatic First stageAbnormal placental implantation
Symptomatic Second stage
Release of angiogenic factors into
Maternal circulation
Asymptomatic first stageAbnormal placental implantation
Cytotrophoblast of embryo invade the spiral arteries of pregnant uterus
Remodeling of smooth muscle of uterine arteries S spiral artery diameter ↑
Intervillous space has very low resistance to blood flow and remodeled arteries Nonresponsive to vasoconstrictors
Incomplete cytotrophoblastic
invasion
of spiral arteries
No remodeling of spiral
arteries and diameter
remains small . Exaggerated
response to vasopressors
Superficial Placentation
↓ placental perfusion,
placental infarcts, IUGR
Placental ischemia gradually
worsens
Abnormal placental implantation Complex interplay of vascular, environmental, genetic
and immune factors.
Immune factors.
↓ NK cells &↑ macrophages and chemokines in placenta.
NK cells facilitate trophoblastic invasion.
Macrophages
↑ ↑ inflammation: inhibits placentation.
HLA C and HLA DR are associated with ↑ risk.
Abnormal placental implantation
Angiotensin receptor-1 Antibodies.
Act as agonist and ↑ sensitivity to angiotensin II
Defective remodeling of placenta vasculature
Block trophoblastic invasion.
↑production of reactive oxygen species.
↑ Sflt-1 (Receptor for VEGF)
Hypertension and proteinuria.
Oxidative stress
Cause atherosclerosis and atherosis
Symptomatic second stageRelease of angiogenic factors intoMaternal circulation
Symptomatic second stage Endothelial dysfunction:
Key event
Placental hypoxia → antiangiogenic substances released into maternal circulation.
Soluble fms like tyrosine kinase-1(sFlt-1) and Soluble endoglin (sEng)
Antagonize angiogenesis
Bind to and ↓ VEGF and PIGF.
Symptomatic second stage
Maternal Syndrome Preeclampsia: multisystem disorder
•AIRWAY
•Pharyngolayngeal edema
•Tracheal diameter ↓ ↓
•Difficulty in direct
laryngoscopy
•Subglottic edema
• Airway obstruction
PULMONARY
•Pulmonary edema
•3% of preeclampsia.
•More in elderly
multigravida, superimposed
Chr. HTN or oliguria
↓ Plasma oncotic
pressure
↑ Vascular permeability.
•Excess iv fluids.
CVS
•Vasospasm
•SVR and BP ↑ ↑
•↑ Sensitivity to
catecholamines
•Hyper dynamic circulation
↑ C.O
•Misleading CVP
measurement
•High risk: ↓ LV
function, ↓ ↓SVR
•Severe form plasma vol. ↓
HEPATIC
•Rt hypochondrium and epigastric
pain.
•D/t sub capsular hematoma
•Periportal hemorrhage and
sinusoidal
fibrin deposits.
•HELLP syndrome
• Spont. Hepatic rupture
•Rare but fatal(32% mortality)
Maternal Syndrome Preeclampsia.CNS
•Severe headache, hyper
excitability,
•Loss of cerebral auto
regulation, vasogenic
edema
•Cerebral hemorrhage and
edema
•PRES: Posterior
Reversible
Encephalopathy
Syndrome.
•Eclampsia: Seizures
OPTHALMOLOGICAL
•Scotoma, blurred vision
and amaurosis
•Retinal arteriolar spasm
•Bilateral retinal
detachmentRENAL
•“Glomerular capillary
endotheliosis”
Most Characteristic lesion.
•GFR ↓ (↑ in N pregnancy).
•Proteinuria( ∆stic criteria)
•Uric acid ↑ ( early detection).
•Oliguria
Occurs late & correlates with
severity.
•Renal failure
•With DIC, APH and IUFD.
HEMATOLOGICAL
•Thrombocytopenia: MC
hematological abn
•Severe disease or HELLP.
•Severe disease:
Hypercoagulable.
(↓ Blood Volume & ↑
Viscosity)
•Mild disease: hypocoagulable
•DIC
Fetal Syndrome PreeclampsiaLeading cause of IUGR
Preterm labor
NICU admission
IUD → DIC & PPH in mother
Prophylaxis
Prevents imbalance b/w thromboxane & prostacyclin.
Modest risk reduction (15-20%) but no S/E.
No. Needed To Treat
Low risk 500 Vs High risk NNT: 50
Started in late Ist trimester
H/o Preeclampsia causing preterm delivery<34 weeks.
Preeclampsia in > 1 pregnancy.
Low dose Aspirin 60-80 mg
Prophylaxis
Believed to reduce oxidative stress.
No benefit in multicentre trials
Benefit in females with calcium deficiency 1.5-2g in patients with low base line intake or high risk.
No benefit in females with adq. calcium intake.
No Benefit.
Diuretics: no benefit
Vitamin C(1000mg) and E(400 IU)
Calcium supplementation.
Dietary salt restriction
Prophylaxis
No benefit in pregnant patients
Risk of DVT ↑
Exercise : 30 min or more
Protective
Improves uterine blood flow, placental angiogenesis and endothelial function
Bed rest and no physical activity
InvestigationsInitial evaluation:
CBC with Plt. Count
S. Creatinine level
LFT (AST, ALT, and S.bil.)
Uric acid
Marker of severity
Detects disease early.
Urine analysis
24 hr Urine protein
Urine protein to creatinine ratio.
Danger signs → Headache, Unusual change in vision, ↓Urine,
epigastric/ labor pain Hospitalize
Severe Preeclampsiarepeated daily Mild Preeclampsia:Repeated weekly
Proteinuria Not evaluated again if +ve for preeclampsia
InvestigationsFetal evaluation
USG evaluation for fetal weight
Amniotic fluid index(AFI)
Daily fetal movement count(DFMC)
NST & BPP
Gestational Hypertension: Weekly NST
Preeclampsia: Bi Weekly NST
Umbilical artery Doppler:
Screening: no benefit
Indicates severity of IUGR
↓ DFMC /Fundal Ht<3cm (Prompt NST & AFI)
Investigations.Coagulation profile
Platelet count >100,000: Not needed.
Plt. Count<100,000: PT and aPTT.
Additional studies
DIC Risk: Abruptio, liver disease, HELLP
Induction of labor: platelets repeated 6 hrly.
ManagementAnti HTN drugs
Only if BP>160/110mmHg
No benefit if BP>140/90 but<160/110
↓progression to severe HTN.
Risk of fetal growth retardation
No change in maternal or fetal mortality or prematurity.
First line drugs: Methyldopa, Labetalol
Second line drugs: Hydralazine, Nifedipine,.
C/I: Ace inhibitors or ARBS
Anti Hypertensive drugs
Labetalol
• 100mg BD
• S/E: CHF, Asthma
• Discontinue :liver dysfunction
Methyldopa
• 250 mg TDS
• S/E: dry mouth, somnolence, sedation
Nifedipine
• 10-30 TDS
• S/E: Edema,
• headache, allergic hepatitis
Atenolol
• 50-100mg OD
• S/E: Heart Block, IUGR
Anti Hypertensive drugs.For Emergency Control.
Management. Observe for 24-48 hours
Corticosteroids if gestational age <34 weeks.
Monitor: USG, FHR, investigations and danger signs daily.
MgSO4 for severe preeclampsia.
Oral anti HTN drugs
C/I to expectant management → delivery
Eclampsia DIC Pulmonary edema Uncontrolled HTN
Non Viable fetusAbnormal fetal test resultsAbruptio placentaeIUD
Management. Deliver after 48 hrs with corticosteroids
Persistent symptoms
HELLP
IUGR, Severe oligohydramnios
USG Doppler: Reversal of flow
Labor
Significant Renal dysfunction
ManagementRoute of delivery
Vaginal delivery in all Unless Cesarean is indicated.
CorticosteroidsAll patients between 24- 34 weeks of gestation
Beneficial in HELLP syndrome
Fetal lung maturity.
Dexamethasone or Betamethasone
Seizure prophylaxisSevere Preeclampsia & Eclampsia
MgSO4
Long term outcome
↑ Risk of
Chronic Hypertension
DM
Ischemic Heart disease.
AHA: Preeclampsia risk factor for cardiovascular disease.
Renal failure.
↑ Risk for
Recurrent Preeclampsia
Preeclampsia with IUGR or Preterm Birth
ADVICE
BP, FBS, Lipids and
BMI yearly
Aerobic Exercise
5 days/ week -30min.
Avoid Tobacco
ComplicationsCerebrovascular accident
↑ risk of intracerebral and subarachnoid hemorrhage.
↑ ↑ risk with DIC or HELLP
Loss of cerebral autoregulation → Vasogenic edema
Systolic BP better than DBP or MAP at predicting adverse events
Majority are Hemorrhagic (93%) and occur in post partum
ComplicationsPulmonary edema
3% cases of preeclampsia
More in elderly multigravida or women with superimposed preeclampsia
Presents in 2-3 days after delivery
T/t underlying cause (sepsis, cardiac failure)
O2, Fluid restriction, diuretics
Rapid Resolution
ComplicationsRenal Failure
Rare complication
HELLP and severe preeclampsia
Majority Pre-renal or Intra-renal (ATN) Resolution completely
B/L cortical necrosis High maternal mortality and morbidity
DIC, HELLP, Abruptio placentae, IUD, Sepsis etc
Abruptio placentae:2% of preeclampsia (3X risk);
Chronic Hypertension.
EclampsiaNew onset seizures or unexplained coma in a
Preeclamptic patient
During pregnancy or postpartum.
No preexisting neurological disorder.
0.1-5.9/10,000 pregnancies
Most Commonly
Intrapartum or 48Hrs after delivery
Late Eclampsia: 48Hrs after delivery to 4 wks postpartum
EclampsiaRisk factors
Young nullipara
Multifetal & Molar pregnancy
Preexisting Hypertension, renal or cardiac disease.
SLE or non immune hydrops
Maternal Complications:
Pulmonary aspiration, pulmonary edema, Cerebrovascular accident, venous thromboembolism, ARF or death
Fetus
IUGR, Prematurity
EclampsiaSigns or symptoms
80% premonitory symptoms. MC Headache or Visual disturbances.
Photophobia, Right upper quadrant pain, Hyperreflexia
Seizures abrupt onset Facial twitching →Tonic phase (15-20 seconds).
Generalized clonic phase →apnea for 1 minute.
Postictal state with variable period of coma .
Poor neurocognitive outcomeUsually temporary ( focal motor deficit, blindness etc).
Can be permanent as well
HELLP syndromeVariant of severe preeclampsia
Maternal mortality ↑↑ (DIC, pulmonary edema, APH, Liver failure etc.)
Sibai’s criteria
Hemolysis•Abn Periph. Blood smear MAHA(Schistocytes&BURR cells)•↑ S. bilirubin>1.2mg%
•↑S. LDH>600IU/L
Low platelets•Platelet count
<100,000/cumm
Elevated liver enzymes
•↑AST>70IU/L•↑LDH>600IU/L
HELLP syndromeNot candidates for expectant management
Seizures: IV magnesium
Anti HTN: BP>160/110 mmHg.
Corticosteroids for fetal lung maturity.
Platelets:
Spontaneous bleeding or platelet count <20,000.
Sub capsular hematoma d/t liver rupture
Serial USG/MRI
Surgery/ Embolization.
Thank YOU
Seizure prophylaxisMgSO4
↓ Risk for Eclampsia Maternal death Abruptio placentae.
No benefit Maternal morbidity Fetal/neonatal outcome. Preeclampsia w/o severe disease.
↑ Risk Hypotension Muscle weakness Respiratory depression.
Seizure prophylaxisMOA
↓peripheral vascular resistance
NMDA agonist ↑ seizure threshold
Protects blood brain barrier
Dose:
4-6gm over ½ hour f/b infusion of 1-2gm/hr
For caesarean
2hr before procedure.
Continued till 12 hrs postpartum.
MgSO4 toxicity1.5-2.0 meq/l : normal plasma level
4.0-8.0 meq/l :therapeutic range
5.0-10.0 meq/l: p-q interval prolong, wide QRS
10.0 meq/l : loss of deep tendon reflexes
15.0 meq/l :Respiratory paralysis
25.0 meq/l : cardiac arrest
ANTIDOTE – CALCIUM Gluconate
Eclampsia
Airway
• Left lateral position, jaw thrust.
• Bag and mask ventilation.
• Avoid Oropharyngeal airway,
• Nasopharyngeal airway
Breathing
• Continue Bag and mask ventilation.
• Apply pulse oximeter and monitor SpO2
Circulation
• Secure IV access
• Monitor BP and ECG
Stop convulsions
MgSO4
4-6g IV over 20 min
1-2g/hr IV maintenance
2g iv over 10 min for recurrent seizures
Antihypertensive therapy
Labetalol or Hydralazine
Induction of labor
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