OBSTETRICS

DR. Barrot-Gler Topic

 Hypertension + Proteinuria
HYPERTENSION DISORDERS IN PREGNANCY  Hypertension plus
 Thrombocytopenia (100,000μL)
 Renal insufficiency (creatinine >1.1 mg/dl)
Definition of Terms
 Liver involvement (AST levels twice normal)
Hypertension
 Cerebral symptoms (HA, visual disturbances,
 BP> 140-90
convulsion)
Delta Hypertension
 Pulmonary edema
 A sudden rise in MAP later in pregnancy
 May signify preeclmapsia even if < 140/90
Indications of Severity
Proteinuria
 Urinary protein spillage Abnormality Non severe Severe

o Dipstick: +1 SBP <160mmHg 160>mmHg

o > 300 mg/ 24 hrs DBP <110 mmHg >110mmHg
o 1000 mg random taken 6 hours apart Proteinuria None to + None to +
o Protein-to-creatinin ratio >0.3 Headache - +
Pathologic Edema Visual - +
 Pre tibial edema after 12 hour of bed rest disturbances
 Weight gain of 15 lbs/ week Upper abdominal - +
pain
Oliguria - +
CLASSIFICATION OF HYPERTENSIVE DISORDERS
Serum creatinine Normal Elevated
1. Pregnancy- Induced Hypertension
Thrombocytopenia - +
a. Gestational Hypertension
(<100,000 μL)
b. Preeclampsia
Seru Minimal Marked
i. Mild
transaminases
ii. Severe
elevation
c. Eclampsia
Fetal growth - Obvious
2. Pregnancy-Aggravated Hypertension
restriction
a. Superimposed preeclampsia
Pulmonary edema - +
b. Superimposed eclampsia
Convulsions - +
3. Chronic Hypertension

ECLAMPSIA
PREGNANCY- INDUCED HYPERTENSION
 Convulsion in a woman w/ preeclampsia seizure:
GESTATIONAL HYPERTENSION
o Cannot be attributed to other causes
 BP= 140/90 mmHg for the first time during pregnancy
o Tonic-clonic type
 No proteinuria
o May appear before, during or after labor
 May have other signs & symptoms of preeclampsia
o 10%: >48 hours to 10 days postpartum
o Epigastric discomfort
o Thrombocytopenia
 BP returns to normal by 12 weeks postpartum CHRONIC HYPERTENSION
 Final diagnosis made is made only postpartum  Documented BP> 140/90 mmHg before pregnancy
 Transient hypertension  Hypertension detected before 20 weeks gestation
 50% subsequently develop preeclempsia  Persists after 12 weeks postpartum

PREECLAMPSIA SYNDROME
 Pregnancy-specific syndrome
 Affects virtually every organ system
 PREGNANCY-AGGRAVATED HYPERTENSION Preeclampsia ETIOLOGY
Current Plausible Potential Causes:
PREECLAMPSIA SUPERIMPOSED ON CHRONIC 1. Abnormal trophoblastic invasion of uterine vessels

HYPERTENSION 2. Immunological intolerance between material and

fetoplacental tissues
 New onset or worsening baseline hypertension
3. Maternal maladaptation to cardiovascular or
 Accompanied by new-onset proteinuria
inflammatory changes of normal pregnancy
 Develops earlier in pregnancy, after 24 weeks
4. Dietary deficiencies
 25% of patients with chronic HPN
 More severe
Cascade of Events
 Often accompanied by fetal growth restriction
Host of abnormalities
ETIOLOGY???
 Not exactly sure…
 Theories must account for the following:
 Preeclamptic women are more likely: Vascular endothelial
Preeclampsia
o Exposed to chorionic villi for the first time damage
o Exposed to superabundance of chorionic villi
 Twins or hydatidiform mole; have pre-
existing vascular disease
Vasospasm
 Genetically predisposed

RISK FACTORS Ischemic and

 Maternal RF Transudation of thrombotic sequelae
o Personal RF
plasma
o Medical RF
In a Normal endothelium
 Thrombin inactivation
Personal risk factors
 Non aggregation of platelets
1. Primaparity: 2.4 fold elevated risk
 Fibrin degradation
2. Primipaternity- immunologic habituation to paternal
 Site for
Ags
o Prostacyclin
3. History of preeclampsia: 7-fold risk
o Endothelium derived relaxing factors (EDRF)
4. Obesity
5. Family Hx of Preeclampsia: sisters (37%); daughter
(25%) granddaughter (16%)
In a Normal Pregnancy
 Spiral arterioles in the placental implantation site undergo
6. Ethnicity: Black 2x
morphologic changes which allow a 4-fold rise in the
7. Maternal age: > 40: 2x risk
uteroplacental perfusion
8. Smoking
 Converts the uteroplacental unit into low resistance unit
9. Others
 Interpregnancy interval <2 years or > 10 years
 Previous miscarriage & induced abortion
Normal Pregnancy
In-growth of trophoblastic cells into the tunica media of the
 Environmental RF
spiral arterioles
Medical RF
↓
Underlying medical condition
Denervation and loss of muscular and elastic components of
 DM
the BV
 APAS
↓
 SLE
Thinning of walls dilatation and elongation to a “saw toothed/
 Renal disease
cork screw configuration.
↓
Placental /Fetal Risk Factors
Transforming them from small-caliber resistance vessels to
o Multiple
high-caliber vessels
o Molar pregnancy
↓
Extends to the decidual & myometrial portions of the blood ENDOTHELIAL CELL DYSFUNCTION
vessels  Vasodilators ↓
↓  Vasoconstriction Produced:
Fully established by the 18th-20th weeks gestation o Endothelium derived constriction factor (EDCF)
Prostacyclin (PGI) dependent  ↑sensitivity to pressor agents
In pregnancies complicated with Preeclampsia  Loss of fluid from the intravascular space
Prostacyclin deficient o Thromboxane A2 platelet aggregator
↓  Intravascular coagulation
Uteroplacental development is impaired
↓ Normal Pregnancy vs Preeclampsia
State of relative vasoconstriction Normal Preeclampsia
↓ Pregnancy Characteristics Effects
High resistance to uteroplacental blood flow Endothelium
↓ Site for Prostacyclin Utero-placental
Placental ischemia prostacyclin deficient development is impaired
↓ Release of agents into circulation production
Induce endothelial cell dysfunction Endothelium Endothelium  ↑sensitivity to pressor
derived derived agents
Trophoblastic invasion of Spiral arteries relaxing constriction  Loss of fluid from the
factor (EDRF) factor (EDCF) intravascular space
Thrombic  State of relative
inactivation vasoconstriction
 High resistance to
utero-placental blood
flow
 Placental ischemia
 Release of agents into
circulation
 Endothelial cell
dysfunction
Non Thromboxane A2 Intravascular coagulation
aggregation
of platelets

Pathogenesis
 Vasospasm
 Endothelial cell injury
 Ischemia

Trophoblastic Hypoperfusion
 Earliest and most consistent change
 Believed to be the pivotal insult in this disease
SYSTEMIC EFFECTS  Usually unilateral seldome causes total visual loss
Cardiovascular changes  Usually abate with MgSO4therapy & or lowered BP
 Elevated afterload Blindness
 Cardiac output inversely related to afterload o Occipital blindness or “amaurosis”
Blood o Extensive occipital lobe vasogenic edema
 Reduced BV o Precedes eclamptic convulsions in up to 15%
 Thrombocytopenia o Rare with preeclampsia alone
 ↓clotting factors o May develop up to a week for more following delivery
 Schizocytes- bizarre shaped rbc o Reversible
 DIC o Diffuse cerebral edema from 3 potential areas:
 ↑Fibronectins  Visual cortex of the occipital lobe
Kidney  Lateral geniculate nuclei
 ↓GFR  Retina- Ischemia, infarction, detachment
 ↑uric acid (Purtscher retinopathy)
 Proteinuria
 Glomerular CONVULSIONS
Liver  Diagnostic for eclampsia
 Periportal hemorrhagic necrosis ↓enzymes  liver  Caused by:
rupture  subcapsular hematoma stretching of 1. Excessive release of neurotransmitters- glutamate
Glissons capsule  epigastric pain/ RUQ pain 2. Massie depolarization of network neurons
3. Bursts of action potentials
NEUROLOGIC MANIFESTATION
HEADACHE MENTAL STATUS CHANGES
 Arise from cerebrovascular hyperperfusion  Confusion to coma
 Predilection for the occipital lobes  Results from generalized cerebral edema
 Mild to severe  Dangerous
 Intermittent to constant  Supratentorial herniation may result
 Precedes eclampsia 50-75%
 Usually improves after MgSO4 infusions initiated ECLAMPSIA
Complications
CEREBROVASCULAR PATHOPHYSIOLOGY  Abruptio placenta: 10%
↓ systemic BP  Neurologic deficits: 7%
 Aspiration pneumonia: 7%
Exceeds normal autoregulatory capacity  Pumonary edema: 5%
 ARF: 4%
Forced vasodilatation  Death 1%

Disruption of the end-capillary pressure at the capillary level HELLP SYNDROME

 Acronym created by Louis Weinstein in 1982
↑ hydrostatic pressure o Hemolysis
o Elevated Liver enzymes
Hyperperfusion o Low Platelet
 Describes s subset of severe preeclampsia/ eclampsia with:
Extravasation of plasma & red cells o Mircoangiopathic hemolytic anemia
o Moderate- severe thrombocytopenia
Vasogenic edema o Disrupted/ destroyed RBC or peripheral smear
o Abnormal LFT: RUQ/ epigastric pain; nausea/
VISUAL CHANGES vomiting
 Scotomata, blurred vision, dpiplopia
 Common with severe preeclampsia & eclampsia
 Premonitory symptoms of eclampsia
 Precedes in 20-30%
Pathophysiology PREDISPOSING FACTORS
1st Pregnancy Nulliparity: 6-7 fold prone
Genetic 20-40% for daughters oof
predisposition preeclamptic mothers
(recessive trait) 11-37% for sisters of preeclamptic
placenta shend into women
damage
derived maternal Previous eclampsia 10-15%
hepatic cells
proteins circulation develop
Dietary factors Low protein; calcium diet
SEC Level
Hyperplacentosis Multiple pregnancy; DM; GTD;
 Placenta- instigated liver- targeted acute Hydrops fetalis
inflammatory condition and immunologic process Renovascular disease 15% develop superimposition
Chronic HPN 70% recurrence
Clinical manifestation
 70% antepartum EARLY CLINICAL SIGNS
 30% postpartum  Excessive weight gain
 Ssx:  Edema
o Malaise 90%  Upward trend in BP
o Nausea/ vomiting 50%
o Epigastric/ RUQ pain 90% Weight gain
 Most important sign  Normal weight gain
o First 3 months: 2-4 lbs/ wk
Mortality o Afterward: 1 lb/ week
Causes of Death  Allowable wt gain:
 Subcapsular liver hematoma o Underweight: 28 to 40 lbs
 Eclampsia o Healthy, normal: 25 to 35 lbs
 Placental abruption o Overweight: 15 to 25lbs.
 Acute renal failure o Obese: 15 to 18 lbs
 Pulmonary edema
 Coagulopathy, ARDS, stroke, sepsis Predictors of PIH
Clinical predictors Laboratory predictors
Epidemiology and Risk Factors 1. MAP >90 Hematocrit MS AFP
 5-10% of all pregnancies worldwide 2. Roll over test proteinuria Calcium excretion
 3-10% in: Serum uric acid Doppler
o Healthy nulliparous women velocimtery
o Multiparous women pregnant with a new partner
 Increased risk 1. Mean arterial pressure test (MAP) test
o First degree relative: two-to fourfold  MAP2
o History of preeclamspia in the Father’s mother  MAP3
 Diastolic pressure + 1/3 pulse pressure
PREDILECTION & DETECTION OF PRECLINICAL DISEASE  Pulse pressure (PP)= SP -DP
1. Predisposing factors
2. Early clinical signs’ MAP= DP +
SP- DP
3. Predictors of PIH 3
Ex:140/90 mmHg

140-90
MAP= 90 +
3

= 90 +50/3
=106
MAP 2: 2nd trimester MANAGEMENT
 Lower critical cut off: <90 BASIC OBJECTIVES
 Represents the mid-trimester drop in BP 1. Termination of pregnancy with least possible trauma
 Represents the belief that trophoblastic to mother and fetus
proliferation spiral arteriolar dilatation 2. Birth of an infant who subsequently thrive
3. Complete restoration of health to the mother
rd
MAP 3: 3 trimester
 Lower critical cut-off: <105 Ambulatory treatment
 How management
Interpretation  No worsening of BP (!40/90)
 The absence of a mid-trimester drop in BP despite  Fetal growth retardation not suspected
MAP-2 <90mmHg predict future PIH based on the  Bed rest throughout the greater part of the day
absence of arteriolar vasodilatation  Hospital visits at least 2x weakly

2. Roll over test NON SEVERE PREECLAMPSIA

 At 28 – 32 weeks
 Take the DP in the: “NO GOLD STANDARD DX”
a. Lateral recumbent position
b. Rolled over to supine position MANAGEMENT:
 BP taken immediately & after 5 minutes  Initial hospitalization to obtain baseline date
 Positive: ↑ in DP of 20 mmHg; 3x risk o Discharge after 3 days
o Low salt high Ca diet
PREVENTION o Fetal movement counting by the mother
Low dose aspirin  OPD ff up 2x a week
 Inhibits thromboxane A2  Oral anti-hypertensive, calcium, low dose aspirin
 Prostacyclin level remains unchanged
 Given provided: Antepartum hospital management
o High risk patients identified  Sustained BP >140/90
o No allergy to aspirin o Admitting Hx & PE
o Treatment strated on the 2nd trimester o Daily weight
o Dose: 60-80 mg/day o Baseline proteinuria & check every 2 days
o Monitoring of fetal ductus arteriosus; uterine o BP every 4 hours except midnight & early morning
production, AFV unless elevated
o Other lab exams & ultrasonography
High dose Calcium (2mg/d)
 SEVERE PREECLAMPSIA
Cardinal principles:
1. Control hypertension
2. Control convulsion
Monitor
3. Optimum time and mode of delivery

CONTROL HYPERTENSION
Sympatholytics Hydrazaline Drug of choice RR Patellar reflex Urine output

Methyldopa
Beta blockers Labetalol Not available
Atenolol Adverse effects of fetal
>12 meq/L; Disappearcne ↓DTR:
growth & hemodynamics depression: w. MgSO4 warning sign 30 cc/h or 100
respiratory
Contraindicated for lent tern 12 meq/L paralysis & levels: 8-11 mf MgSO4 cc/4r
cardiac arrest meq/L toxicity
treatment
Calcium Nefidipine
channel Nicardipine Selective
blocker Less placental transport &
OPTIMUM TIME AND MODE OF DELIVERY
fetal exposure
ACE inhibitor Losartan Not recommended due to
adverse fetal effects
Termination of Pregnancy
 Three prime objectives:
Diuretics furosemide For pulmonary edema
1. To forestall convulsion
2. Prevent intracranial hemorrhage and serious damage
CONTROL CONVULSION: MgSO4
to other vital organs
 Arrest & prevent convulsion
3. To deliver a healthy infant
 How:
 Factors which govern on decision
o Inhibit acetylcholine release in response to motor nerve
1. AOG
impulses
2. Severity of disease
o Reduce motor end plate sensitivity to acetylcholine
3. Fetal status
impulses
4. Maternal condition
o Reduce end plate sensitivity to acetylcholine
5. nursery capabilities
o Decrease motor end plate potential
 Immediate
o Calcium influx blocking through glutamate potential
1. Eclampsia regardless of AOG
Maternal Indications Fetal Indications 2. Preeclampsia severe
Gestational age > to 37 weeks Severe fetal growth  At least 34 weeks
restriction o Mature fetal lungs
Platelet count less than 100,00 Non reassuring result o Adequate nursery facilities
from fetal testing  Before 34 weeks
Deterioration liver function Oligohydramnios o Severe maternal disease
Progressive deterioration in o Impending eclampsia
renal function or oliguria o Uncontrolled HPN
Abruptio placenta o Evidence of fetal compromise
Persistent severe headache or  Indications for delivery
visual changes  Mode of delivery
Persistent severe epigastric o Cervical ripening w/ prostaglandin/ or osmotic dilator
pain, nausea or vomiting o Amniotomy
 Loading dose: 4 mg IV o Oxytocin
 Infusion: 20 g in 1L D5W at 100 ml/hr o Cesarean delivery
 Maintain plasma levels: @ 4-7 meq/L to prevent seizure
 Excreted by kidneys
 CHRONIC HYPERTENSION Women who develop hypertension during pregnancy
should be:
 MANAGEMENT  Evaluated during immediate postpartum months
MEDICAL HISTORY PE LABORATORY EXAMS  Counseled about future pregnancies
Duration of Funduscopic CXR: for suspected  Counseled about their cardiovascular risk later in life
hypertension exam heart disease
Use of OGTT for GDM
antihypertensive
meds
Outcome of VMA for
previous pheochromocytoma
pregnancies

 Indications for early delivery

► Superimposed preeclampsia
► Presence of underlying medical problems
 DM; renal insufficiency
► Abnormal antepartal FHT
► SGA
 Complications
► Superimposed preeclampsia:1/3 of cases
► Abruptio placenta
► DIC
► Acute tubular necrosis
► Renal cortical necrosis
► Death: due to CVA (strokes) & heart failure
 Guarded prognosis
► Severe hypertension in the first trimester
► Superimposed preeclampsia before 28 weeks
► Antepartal renal insufficiency
► HCVD
► Congested cardiomyopathy
 Long term consequence
► For women who had preeclampsia

Within 7 years of a At about 1 year

pregnancy
20% develop hypertension
or microalbuminura
 ↑BP total cholesterol, LDL,
TG, BMI, fasting insulin,
urinary microalbuminuria/
creatinine ration
 20% have residual
microalbuminuria
 2x long-term risk for CVD
& cerebrovascular disease

 Increase in long term cardiovascular events may either be

the result of
o Shared risk factors
o The result of subtle vascular damage or persistent
endothelial dysfunction caused by preeclampsia