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HYPERTENSIVE DISORDERS IN PREGNANCY

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1 HYPERTENSIVE DISORDERS IN PREGNANCY

2 HYPERTENSION The National High Blood Pressure Education Program (NHBPEP) Working Group defines HYPERTENSION in PREGNANT WOMAN: systolic blood pressure (BP) of 140 mmHg or higher diastolic BP of 90 mmHg or higher on more than 1 occasion

3 Epidemiology Incidence 3% of all pregnancies Etiology Multifactorial

4 Risk Factors Primiparity Immunologic factors BMI
Previous pregnancy complicated by Preeclampsia/Eclampsia/HELLP Family history of Preeclampsia BMI Pregnancy related conditions Primiparity: the risk of preec in 1st pregnancy is 3% whereas 1% in the second Immunologic: immunological tolerance involving cytokines through the tolerance network- TH2 reaction. Preeclampsia caused by failure of trophoblast invasion can be considered as a type of rejection Previous pregnancy-increased risk of recurrence in subsequent pregnancies - recurrence rate is as high as 50% Family history of Preclampsia BMI – relationship between maternal weight and risk of preeclampsia is progressive - increases from 4.3% for women with BMI less than 19.8 kg/m2 to 13.3% to those with BMI >35 kg/m2 Underlying medical condition – related to vaascular, connective and renal implications Pregnancy related conditions – conditions such as hydrops fetalis, multifetal gestation, twin gestation are at increased risk secondary to increased trophoblast mass

5 Risk Factors Socioeconomic status Primipaternity Sexual co-habituation
Maternal infection Gestational age at delivery of 1st Pregnancy Socioeconomic status Smoking Primipaternity – immunogentic factors – immunological habituation to paternal antigens: having new sexual partners will expose the mother to a new paternal antigens – paternal genes in fetus may therefore contribute to woman’s risk of preeclampsia Sexual co-habituation – aka disease of new couples, the longer the duration of co-habituation before conception (w/o barriers to contraception) the lower the risk of preeclampsia <within the first 4 months: the risk is 40% compared to 3-5% over 12 months> Maternal infection – there is a direct relationship, in which a maternal infection increases the risk of preeclampsia, infections such as UTI and periodontal diseases Gestational age at delivery in first pregnancy – risk of recurrent preeclampsia is INVERSELY related to gestational age at the first delivery. <it can be implicated: that a previous preterm delivery and SGA newborn increases rhe risk of preeclampsia in subsequent pregnancies Socioeconomic status – there is a similar risk. Therefore, this disease is NOT associated with poor social status Smoking – IRONICALLY, it is consistently associated with a reduced risk of hypertension during pregnancy

6 Poor Immunoregulation Clinical manifestation
Mechanisms Stage 0 3-8 weeks Stage 1 8-18 weeks Stage 2 20 weeks to birth Poor Immunoregulation Inadequate tolerance to feto-paternal antigens during conception and implantation Poor Placentation Deficient trophoblast invasion and spiral artery remodelling Clinical manifestation Over activation of maternal endothelium and systemic inflammatory network Oxidative Stress Endoplasmic reticulum Stress Inflammatory Stress Abnormal placentation (stage 1), particularly lack of dilatation of the uterine spiral arterioles, is the common starting point in the genesis of pre-eclampsia, which compromises blood flow to the maternal–fetal interface. Reduced placental perfusion activates placental factors and induces systemic hemodynamic changes. The maternal syndrome (stage 2) is a function of the circulatory disturbance caused by systemic maternal endothelial cell dysfunction resulting in vascular reactivity, activation of coagulation cascade and loss of vascular integrity. Pre-eclampsia has effects on most maternal organ systems, but predominantly on the vasculature of the kidneys, liver and brain.

7 Mechanisms Normal Pregnancy
invasive cytotrophoblasts of fetal origin invade the maternal spiral arteries transforms them from small-caliber resistance vessels to high-caliber capacitance vessels capable of providing placental perfusion adequate to sustain the growing fetus Normal Pregnancy process of vascular invasion, the cytotrophoblasts differentiate from an epithelial phenotype to an endothelial phenotype, a process referred to as "pseudovasculogenesis" 

8 cytotrophoblasts fail to adopt an invasive endothelial phenotype
Mechanisms Preeclampsia cytotrophoblasts fail to adopt an invasive endothelial phenotype invasion of the spiral arteries is shallow and they remain small caliber, resistance vessels placental ischemia

9 Mechanisms Soluble Flt-1 (sFlt-1) causes endothelial dysfunction by antagonizing vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) In normal pregnancy, the placenta produces modest concentrations of VEGF, PlGF, and soluble Flt-1 In preeclampsia, excess placental soluble Flt-1 binds circulating VEGF and PlGF and prevents their interaction with endothelial cell-surface receptors > release of procoagulant proteins such as von Willebrand factor, endothelin, cellular fibronectin, and thrombomodulin. ENDOTHELIAL DYSFUNCTION decreased prostacyclin nitric oxide production release of procoagulant proteins

10 Reduced Uteroplacental Perfusion
Pathophysiology Faulty placentation Maternal vascular disease Excessive trophoblasts Multiple gestation Hydrops fetalis Genetic/Immunologic/Inflammatory factors Reduced Uteroplacental Perfusion Vasoactive Agents: Prostaglandin Nitric oxide Endothelins Noxious Agents: Cytokines Lipid Peroxidases Endothelial Activation Vasospasm Capillary Leak Activation of Coagulation

11 Pathophysiology Endothelial Activation Vasospasm Capillary Leak
Activation of Coagulation Abruption Edema Oliguria Thrombocytopenia Seizures Proteinuria Liver Ischemia Hypertension Hemoconcentration

12 Definition Gestational HPN Preeclampsia Eclampsia Previously normal BP
Elevated BP without proteinuria Develops after 20 weeks of gestation and BP normalizes 12 weeks postpartum Preeclampsia Elevated BP with proteinuria Eclampsia Hypertension in pregnancy with proteinuria along with convulsions Preeclampsia with occurrence of grand mal seizures

13 Chronic HPN with Superimposed Preeclampsia
Definition Chronic HPN Previously elevated BP Use of antihypertensive medications before pregnancy Develops before 20 weeks of gestation and BP elevation persists longer than 12 weeks postpartum Chronic HPN with Superimposed Preeclampsia Previously elevated BP or persists postpartum with associated signs and symptoms of preeclampsia Develops before 20 weeks of gestation with new-onset proteinuria Development of HELLP syndrome

14 Methods of Indirect Measurement of BP
Ideal: mercury manometer Alternative: aneroid, digital, or other automated devices Cuff should cover: 2/3 of arm or at least 80% of pt’s arm circ Position: seated, supine, or left lateral recumbent position Should be rested at least 5-10 minutes Not smoked or ingested caffeine 30 min. before measurement Bladder is inflated 30 mmHg above point of radial pulse extinction Deflation: 2 mmHg per beat

15 Methods of Indirect Measurement of BP
Systolic BP: 1st clear tapping sound (Korotkoff phase I) Diastolic BP: disappearance of tapping sounds (Korotkoff phase V) OR Present near 0: softening of sounds (Korotkoff phase IV) If BP taken for the 1st time: take BP of both arm, subsequent determination is done on the arm with higher BP Arm with the higher values will be used for all BP measurements For white coat HPN: ambulatory BP monitoring Instruct proper BP monitoring if BP monitoring is done at home

16 Predictive Test for HPN in Pregnancy
Screening maneuvers Mean Arterial Pressure Roll over test MAP-2 with Roll over test 48 hour BP monitoring 24 hours ambulatory BP with heart rate Hyperbaric Index Laboratory Test Doppler Velocimetry Fibronectin Hematocrit Proteinuria Serum uric acid Hemoglobinuria Masternal Serum AFP Hypocalciuria Glucose intolerance Inhibin A MAP= DBP + 1/3 PP where PP= SBP-DBP Inc incidence of preec: MAP-(2nd Tri >90) MAP-3rd Tri >105 Others: biochemical markers

17 Biochemical Markers Immune factors (such as AT1-AA), oxidative stress, NK cell abnormalities, and other factors may cause placental dysfunction, which in turn leads to the release of anti-angiogenic factors (such as sFlt1 and sEng) and other inflammatory mediators to induce hypertension, proteinuria, and other complications of preeclampsia. Natural killer (NK) cells at the maternal/fetal interface are also thought to play an important role in the pathogenesis of preeclampsia. They are thought to be important in modulating immune tolerance required for normal placental development as well as the induction of angiogenic factors and vascular remodeling 

18 Preeclampsia Prevention
Calcium Supplementation Dose: 1.5 to 2 g per day before 32 weeks AOG until delivery Antiplatelet agents ASA or dipyridamole: reduce risk of preeclampsia by 17% Insufficient evidence on others Antioxidants, nitric oxide, rest, exercise, diuretics, ↓ed salt intake, marine oil, prostaglandin

19 No manifestations of any of severe preeclampsia
MILD No manifestations of any of severe preeclampsia SEVERE BP SBP ≥ 160 or DBP ≥ 110 Laboratories Elevated serum creatinine Thrombocytopenia Hepatocellular dysfunction (↑ed AST and ALT) Pulmonary edema Microangiopathic hemolysis Urine ≥5 g/24h or ≥ 3 in 2 random urine sample (q4h) Oliguria <500ml/24h IUGR or Oligohydramnios Symptoms of End-organ involvement Headache Visual disturbances Epigastric pain or RUQ pain

20 Gestational Hypertension and Mild Preeclampsia
Criteria for home health care Ability to comply with recommendation Diastolic BP <100 mm Hg Systolic BP <140 mm Hg Proteinuria < 1,000 mg/24 hr OR < 2+ on dipstick Platelet count > 120,000/mm Normal fetal growth and testing No indications for delivery

21 DELIVER Timing of Delivery Gestational Age ≥ 40 weeks
Bishop score > 5 Fetal weight < 10th percentile Non-reactive non-stress test (NST) Gestational Age ≥ 37 weeks with: Labor Rupture of membranes Vaginal bleeding Abnormal biophysical profile Criteria for severe preeclampsia Gestational Age ≥ 34 weeks with: DELIVER Timing of Delivery Expectant management: remote from term with mild preeclampsia

22 Monitoring and Medications
Maternal and fetal well-being at least once weekly BP each visit Platelet count and liver enzymes at regular intervals NST at regular interval Fetal growth every 2 to 3 weeks MEDICATIONS Anti-HPN meds will be given only if there is an increase in BP reading. Not recommended: Magnesium sulfate and other anti-convulsants Low-dose aspirin and high dose calcium for prevention of progression to severe preeclampsia

23 Severe Preeclampsia Incidence 5-6% of all pregnancies worldwide
Local incidence: 2-5% 2nd most common cause of maternal death High perinatal mortality and morbidity rate: Iatrogenic prematurity Definitive treatment: Delivery of fetus and placenta

24 Criteria for the diagnosis of Severe Preeclampsia
CNS Dysfunction Blurred vision Scotomata Altered mental status Severe headache Liver capsule distention or rupture Persistence right quadrant pain Epigastric pain Blood pressure criteria Sitting SBP ≥160 mm Hg DBP ≥110 mm Hg * On 2 separate occasions at rest or at least 6 hours apart Eclampsia Generalized seizure Unexplained coma in setting of preeclampsia in absence of neurologic d/o

25 Criteria for the diagnosis of Severe Preeclampsia
Pulmonary edema or cyanosis Excessive fluid accumu-lation in the lungs Cerebrovascular accident (CVA) Acute loss of brain function Altered mental status coma Cortical Blindness Partial or total loss of vision in normal appearing eye IUGR EFW < 5 percentile for gestational age EFW <10 percentile for gestational age with evidence of fetal compromise Coagulopathy and Thrombocytopenia Prolonged prothrombin time: >1.4s Low fibrinogen: <300 mg/dl Low platelet: <100,000 mm3 Due to disturbance of vasculature that supplies the brain Damage to the visual region of occipital cortex

26 Criteria for the diagnosis of Severe Preeclampsia
Proteinuria >5 g per 24h or ≥3+ on 2 random urine samples collected at least 4 hours apart Oliguria and/or Renal Failure Urine output <500 ml per 24h Serum creatinine: >1.2 mg/dl HELLP Syndrome Hemolysis: Abnormal peripheral smear total bilirubin >1.2 mg/dl LDH >600 U/L Elevated liver enzyme: ALT > 70 U/L LDH > 600 U/L Low platelet: Platelet <100,000 mm3 Hepatocellular injury Serum transaminase ≥ 2x the normal

27 Hepatocellular damage Uteroplacental insuffieciency
Pathophysiology Multiple factors Endothelial Activation Vasospasm Capillary Leak Activation of Coagulation Hypertension ↓ed kidney perfusion Oliguria ARF Proteinuria Seizures ↓ed liver perfusion Liver Ischemia Eclampsia Edema Hepatocellular damage Oligohydramnios RUQ pain/abd’l pain ↑ed AST Pulmonary edema ↓ed brain perfusion Uteroplacental insuffieciency Thrombocytopenia CNS Dysfunction Occipital cortex damage Hemoconcentration IUGR Blurred vision HELLP SYNDROME Abruption Scotomata Cortical blindness Severe headache Altered mental status Process Signs and symptoms Complications

28 Management Objectives of management
Reduce severity or prevent progression of disease process Prevent convulsions Control severe hypertension Deliver the fetus at the optimum time and with the least trauma Detect and appropriately treat end-organ damage Completely restore the health of the mother

29 Safety of mother and fetus
Management Safety of mother and fetus Main objective Stabilization of mother’s condition Confirmation of gestational age Assessment of fetal well-being Initial

30 Indications for Delivery
Persistent BPP≤ 4 (evaluated 6 hours apart) SOB/chest tightness w/ rales and/or Pulse Oximetry: <94% or Pulm. edema Repetitive late or variable heart rate deceleration Persistent headache, visual change, eclampsia DELIVER Maternal Fetal Epigastric/RUQ pain w/ AST or ALT >2x the normal Severe fetal growth restriction Uncontrolled severe HPN, despite max doses of anti-HPN agents Persistent severe oligo-hydramnios Oliguria or serum creatinine levels ≥1.5 mg/dl Suspected abruption placentae, progressive labor, rupture of membranes Fetal death Umbilical artery Doppler imaging with reverse diastolic blood flow Persistent platelet count <100,000/mm3

31 Non-reassuring fetal status
Complications Maternal HELLP Syndrome % Acute Renal Failure: <1% Eclampsia Pulmonary Edema 0-8.5% Perinatal Perinatal death 0-16.6% Non-reassuring fetal status 26-75% Abruptio placentae %

32 Eclampsia Preeclampsia with generalized tonic-clonic convulsions
Common in the last trimester Other causes excluded, all pregnant women with convulsions Contractions increase in frequency and intensity as convulsion occurs, duration of labor is shortened Complications: (1) Pulmonary edema (2) Blindness

33 Magnesium Sulfate Therapy
Drug of choice for prevention of seizures Drug is considered when women is at risk for eclampsia: moderate to severe preeclampsia (at least BP / mm Hg) (1) continuous intravenous infusions Can be given in 2 ways: (2) intermittent intramuscular injections Urine output Respiratory rate When given, regularly assess: Maternal reflexes Oxygen saturation

34 Magnesium Sulfate Therapy
Continuous intravenous infusion Loading dose: 4-6 g dose of MgSO4 diluted in 100 ml of IVF administered over min Begin 2 g/h in 50 ml of IV maintenance infusion Measure serum Mg level at 4-6 h and adjust infusion to maintain levels between 4 and 7 mEq/L MgSO4 is discontinued 24 h after delivery Intermittent intramuscular injections Give 4 g MgSO4 as 20% solution of intravenous at a rate not to exceed 1 g/min Follow with 10 g of 50% MgSO4 solution: 5 g (one-half) injected deep in the upper outer quadrant of both buttocks through a 3-inch-long, 20 gauge needle. If convulsion persists after 15 min, give up to 2 g more IV as 20% solution at a rate not to exceed 1 g/min. (if the woman is large up to 4 g may be given slowly) Every 4 h thereafter: 5 g of 50% solution of MgSO4 deep IM upper outer quadrant of alternate buttocks, assuring that: Patellar reflex is present Respirations are not depressed Urine output during the previous 4 h exceeded 100 ml

35 Magnesium Sulfate Therapy
PHARMACOLOGY TOXICOLOGY Clearance: renal excretion 10 mEq/L (12 mg/dl) Therapeutic level: 4-7 mEq/L ( mg/dl) Loss of patellar reflexes Avoid toxicity by ensuring: >10 mEq/L (>12 mg/dl) Patellar/biceps reflex present Respiratory depression Urine output is adequate 4-7 meq/l or mg/dl or mmol/L No respiratory depression UO below 20 ml/hr STOP giving MgSO4 Calcium gluconate 1 g (10 ml) over 10 minutes

36 Control of Blood Pressure
ANTI-HPN Treatment BP≥160/110 mm Hg Start if: BP below 160/110 mm Hg but with markers of severe disease SBP: mm Hg DBP: mm Hg Aim DRUGS Urgent control of Severe HPN Gestational OR Chronic HPN Contraindicated/Avoided Postpartum HPN Given if BP >150/100 mm Hg PP: Drugs used during antepartum Diuretics Avoid NSAIDs PP Labetolol Hydralazine Nifedipine IV Nicardipine Methyldopa Second line agent: Labetolol Nifedipine Hydralazine Beta-receptor blocker Hydrochlothiazide ACE-I ARB Diuretics

37 Precautions and Adverse Effects
DRUG Dose and Route Precautions and Adverse Effects Labetalol (C) > 10 to 20 mg IV, then 20 to 80 mg every 20 to 30 minutes > maximum of 300 mg; > for infusion: 1 to 2 mg/min > Lower incidence of maternal hypotension and other adverse effects, displaces hydralazine; > Avoid in women with asthma or congestive failure. > Not available locally Hydralazine (C) > 5 mg IV or IM, then 5 to 10 mg every 20 to 40 minutes; once BP controlled repeat every 3 hours; > for infusion: 0.5 to 10.0 mg/hr; if no success with 20 mg IV or 30 mg IM, consider another drug A drug of choice according to NHBEP; long experience of safety and efficacy Nifedipine (C) > Tablets recommended only: 10 to 30 mg PO, repeat in 45 minutes if needed Should be used with caution if concomitantly used with MgSO4 IV Nicardipine > D5W 90 mL + Nicardipine 10 mg in soluset Concentration = 0.1 mg/mL > Start drip at 10 ugtts/min (equivalent to 1 mg/hr). > Maximum dose 10mg/hr *Note: The IV infusion site must be changed every 12 horus Should be used with caution if concomitantly used MgSO4 Pharmacology

38 Drugs: Gestational HPN or Chronic HPN
Dose Concerns Methyldopa (B) Preferred agent: 0.5 to 3.0 g in 2 divided dosage Drug of choice (NHBEP) Safety after 1st trimester Labetolol (C) May be assoc. with fetal growth restriction 200 to 1200 mg/d in 2-3 divided dose Nifedipine (C) May inhibit labor and synergistic action with MgSO4 in lowering BP 30 to 120 mg/d slow release prep Second line agents Useful in combination with sympatholytic agents May cause neonatal thrombocytopenia Hydralazine (C) 50 to 300 mg/d in 2-4 divided doses May ↓ uteroplacental blood flow May impair fetal response to hypoxia Risk of IUGR when start 1st or 2nd Tri (Atenolol) Associcated with neonatal hypoglycemia Beta Blockers (C) Depends on specific agent

39 Drugs: Gestational HPN or Chronic HPN
Dose Concerns Can cause volume contraction and electrolyte d/o Useful in combination with Methyldopa and vasodilator to mitigate fluid retention Second line agents: 12.5 to 25.0 mg/d Hydrochlothiazide (C) ACE-I Leads to fetal loss in animals Human use is associated with: Cardiac defects oligohydramnios Fetopathy Growth restriction Renal agenesis Neonatal anuric renal failure Contraindicated ARB

40 Drugs: Eclampsia Control of seizures Anti-HPN Therapy MgSO4 Diazepam
For prevention and reduction of recurrence Diazepam Loading dose: 10 mg IV over 2 min Followed by: IV infusion 40 mg in 500 ml Normal saline for 24 h After 24 h: 20 mg in 500 ml NS, slowly reduced Phenytoin Only for seizure prevention Dose: initial - 1 g slow IV d by 100 mg every 6 hours for the next 24 hours Anti-HPN Therapy Hydralazine Drug of choice IV boluses of 5 to 10 mg at min interval until desired BP attained Clonidine Next recommended drug IM: mcg Nifedipine 5-10 mg orally NOT sublingual Labetalol Initial dose: 20 mg IV bolus If desired BP not attained w/in 10 min, give 40 mg then 80 mg every 10 minutes

41 Delivery Corticosteroids
> 34 weeks Deliver Mode: vaginal delivery < 34 weeks Defer delivery Give corticosteroids (24-34 weeks) <32 weeks: CS Eclampsia Deliver after seizure is controlled CS is done if: Anticonvulsant therapy continued atleast 24 hours after deliver Vaginal delivery is not easy and imminent Failure of progress after induction Fetal compromise Betamethasone: 12 mg IM every 24 h for 2 doses Corticosteroids Dexamethasone: 6 mg IM every 12 h for 4 doses Given between weeks for fetal lung maturity

42 Oligohydramnios DEFINITION: Amniotic fluid index < 5cm
Uteroplacental insufficiency Chromosomal Abnormalities Hypertension Congenital anomalies Maternal Fetal Preeclampsia Growth restriction Diabetes Demise Postterm pregnancy Prostaglandin synthase inhibitors Drugs Ruptured membranes AFI – calculated by dividing the pregnant uterus into 4 quadrants and placing the transducer on the maternal abdomen along the longitudinal axis Vertical diameter of largest amniotic of in each quadrant is measured with the transducer held perpendicular to the floor. Several factors may modulate amniotic fluid index: Attitude Maternal fluid restriction dehydration ACE Inhibitors Abruption Placental Twin-twin transfusion Idiopathic

43 Fetal well-being studies
Non-stress test Biophysical profile Doppler velocimetry

44 Non-stress test Most widely used for assessment of fetal well being
Hypothesis: HR of non-acidotic fetus temporarily increase in response to movement Normal or reactive: ≥2 accelerations of ≥15 bpm lasting for ≥15 sec within 20 min Nonreactive: Does not contain at least 2 accelerations Uteroplacental insufficiency: Absent acceleration during 80-min period with variability or late deceleration following spontaneous uterine contractions

45 5 biophysical variables
Biophysical Profile 5 biophysical variables Fetal mov’t Nonstress test Fetal Tone Highest score: 10 Fetal Breathing Amniotic fluid volume

46 Biophysical Profile 2 2 2 Fetal mov’t Fetal tone NST AF volume
≥3 discrete or body limb movement w/in 30 min <3 discrete movements Fetal tone ≥1 ep of ext and flex of extremity OR opening/closing of hand w/in 30 min No movement or no extension/felxion NST 2 ≥2 accelerations of ≥15 bpm lasting for ≥15 sec within 20 min 0 or 1 acceleration in min Fetal Breathing ≥1 ep rhythmic breathing lasting ≥30 sec w/in 30 min <30 sec of breathing in 30 min AF volume 2 Single vertical pocket >2cm Largest single vertical pocket <2cm

47 Modified Biophysical Profile
Modified BPP NST UTZ assessment of AF Requires less time Excellent method of fetal surveillance

48 Recommended management
Biophysical Score Interpretation Recommended management 10 Normal, nonasphyxiated No fetal indication for intervention Repeat test weekly Repeat 2x weekly for postterm and diabetic 8 Normal fluid Normal, nonasphyxiated fetus Repeat test per protocol 8 oligohydramnios Chronic fetal asphyxia suspected Deliver if ≥37 weeks, otherwise repeat test 6 Possible fetal asphyxia IF: AF is abnormal: deliver Norma AF >36 weeks w/ favourable cervix: deliver Repeat test <6: deliver Repeat test >6: observe and repeat per protocol 4 Probable fetal asphyxia Repeat test on same day: if ≤6 - deliver 0-2 Almost certain fetal asphyxia Deliver

49 Doppler Velocimetry Non-invasive way to assess blood flow characterizing downstream impedance Umbilical artery systolic/diastolic ratio is commonly used Doppler index Ratio compares max systolic flow with end-diastolic flow: evaluate downstream impedance to flow Consider abnormal if elevated above 95th percentile OR if diastolic flow is absent or reversed Doppler of the uterine and uteroplacental arteries at 24 weeks is an effective test to predict Preeclampsia

50 Doppler Velocimetry This vessel normally has forward flow throughout the cardiac cycle, and the amount of flow during diastole increases as gestation advances. Thus the S/D ratio decreases, from about 4.0 at 20 weeks to 2.0 at term. The S/D ratio is generally less than 3.0 after 30 weeks (Fleischer and associates, 1986). Umbilical artery Doppler may be a useful adjunct in the management of pregnancies complicated by fetal growth restriction.

51 ABSENCE OF END-DIASTOLIC FLOW
NORMAL DIASTOLIC FLOW ABSENCE OF END-DIASTOLIC FLOW Umbilical artery Doppler is considered abnormal if the S/D ratio is above the 95th percentile for gestational age. In extreme cases of growth restriction, end-diastolic flow may become absent or even reversed (Fig. 16–20). These are ominous findings and should prompt a complete fetal evaluation—almost half of cases are due to fetal aneuploidy or a major anomaly (Wenstrom and associates, 1991). In the absence of a reversible maternal complication or a fetal anomaly, reversed end-diastolic flow suggests severe fetal circulatory compromise and usually prompts immediate delivery. Sezik and colleagues (2004) recently reported that fetuses of preeclamptic women who had absent or reversed end-diastolic flow were more likely to have hypoglycemia and polycythemia. REVERSED END-DIASTOLIC FLOW

52 DOPPLER ABNORMALITY AND FREQUENCY OF BPS
BPS FREQUENCY DECISION TO DELIVER (FETAL) Elevated Indices Only Weekly Abnormal BPS or Term or >36 weeks with no fetal growth AEDV Twice weekly Abnormal BPS or >34 weeks proven maturity or conversion to REDV REDV Daily Any BPS < 10/10 or >32 weeks dexamethasone given REDV-UVP Three times daily Any BPS < 10/10 or >28 weeks dexamethasone given AEDV is not stable and will progress to REDV over time •AEDV is not stable and will progress to REDV over time • Many fetuses with AEDV also have altered brain blood flow with increased diastolic velocities-”brain-sparing phenomenon” • Indication to prepare for delivery, appropriate referral, administartion of antenatal steroids, and detailed maternal evaluation • 20% of fetuses with AEDV have malformations or overt aneuploidy so a congenital anomaly scan is indicated and in some cases, even fetal karyotyping. (


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