HYPERTENSION CHRONIC HYPERTENSION POST HYPERTENSION

 Diagnosed empirically when appropriately taken blood pressure:  High BP known before pregnancy or elevation before 20 weeks of  Not recommended in this classification
 >140 mmHg systolic gestation or both  Women with normotensive gestation who develop hypertension (usually
 > 90 mmHg diastolic.  >140/90 mmHg mild) in a period of 2 weeks to 6 months postpartum
 Incremental increases of 30 mmHg systolic or 15 mmHg diastolic above  Proteinuria may or may not be present  BP usually normalizes by the end of the 1st year
blood pressure values taken at midpregnancy – no longer used to define  If patient has taken antihypertensives before pregnancy, you can  Frequently diagnosed when:
hypertension surmise that the patient has chronic HPN  Women in postpartum period remain hospitalized for as long as 2
 These incremental changes are no longer used to define  Usual causes: CKD (most common), primary aldosteronism or weeks
hypertension, but it is recommended that such women be observed pheochromocytoma  Preeclampsia complicates about 3% of pregnancies, and all hypertensive
more closely because eclamptic seizures develop in some whose blood disorders affect about 5-10% of pregnancies.
pressures have stayed below 140/90 mm Hg.  An estimated value of 50,000 – 60,000 preeclampsia related deaths per
year occur worldwide.
 In the Philippines, preeclampsia is the 2nd leading cause of maternal
morbidity and mortality.
DELTA HYPERTENSION CHRONIC HYPERTENSION WITH SUPERIMPOSED PREECLAMPSIA ETIOLOGY OF PREECLAMPSIA
 Sudden rise in mean arterial pressure but still in a normal range (<  Patients with chronic hypertension who develop  Young and nulliparous women – preeclampsia (3-10%)
140/90 mm Hg) later in pregnancy preeclampsia  Primipaternity
 BP is in the 25th percentile until about 36 weeks when blood pressure  Includes patients with hypertension in early gestation with  Obesity – BMI ≥ 30
begins to increase. By term (36 weeks), it is the following findings:  History of preeclampsia
substantively higher and in the 75th percentile, but is still  Proteinuria develops before or even after 20 weeks  Family history of pregnancy induced HPN (PIH)
considered “normotensive” (<140/90). with:  Age more than 40 years old, race and ethnicity - and thus by
GESTATIONAL HYPERTENSION 1. Sudden exacerbation of Hypertension genetic predisposition
 New-onset elevations of BP 2. RUQ pain and severe headache, increase in liver  Smoking
o After 20 weeks of gestation enzymes  Twin gestation, molar disease
o Absent proteinuria 3. Pulmonary congestion/edema  Metabolic syndrome
4. Renal insufficiency (Creatinine doubling or increasing to or above 
 Reclassified by some as transient hypertension if evidence for Chronic hypertension
1.1 mg/dl in women without renal disease. Hypertensive disorders
preeclampsia does not develop and the blood pressure returns to normal  Chronic renal disease – infection
can create diFFicult problems with diagnosis and management in
by 12 weeks postpartum  Anti-phospholipid syndrome
women who are not first seen until after midpregnancy. This is
o Failure to normalize after postpartum, change to chronic
because blood pressure normally drops during the second and early  Angiotensin gene – Homozygous, heterozygous
hypertension
third trimesters in both normotensive and chronically hypertensive  Hyperhomocysteinemia
 Almost half of these women subsequently develop preeclampsia
syndrome.
women. ETHIOPATHOGENESIS
 10 % of eclamptic seizures develop before overt proteinuria
Thus, a woman with previously undiagnosed chronic vascular  Gestational hypertensive disorders are more likely to develop in women
disease who is seen before 20 weeks frequently has blood with the following characteristics:
can be detected pressures within normal range. During the third trimester, however, o Are exposed to chorionic villi for the first time
as blood pressures return to their originally hypertensive o Are exposed to a superabundance of chorionic villi, as with
ECLAMPSIA SYNDROME levels, it may be diicult to determine whether hypertension is twins or hydatidiform mole
 Convulsive phase of preeclampsia and among the severe manifestation chronic or induced by pregnancy. o Have preexisting conditions associated with endothelial cell
of the disease 5. Platelet below 100,000/µL activation or inflammation, such as diabetes, obesity,
6. Sudden, substantial and sustained increase in cardiovascular or renal disease, immunological disorders, or
 Often preceded by premonitory event:
protein excretion hereditary influences
o Headache
o Epigastric pain o Are genetically predisposed to hypertension developing during
o Hyperreflexia pregnancy.
o But can occur without warning signs or symptoms
 Convulsion is generalized and may occur before, during, or after labor
 Generally occuring within 48hours of delivery
 PATHOGENESIS IMMUNOLOGIC FACTORS GENETIC FACTORS
An imposing number of mechanisms have been proposed to  Immunological maladaptive tolerance between maternal, Hereditary predisposition for preeclampsia likely stems from interactions of
explain the cause of preeclampsia. Those currently considered paternal (placental) and fetal tissues literally hundreds of inherited genes both maternal and paternal-that control
important include:  Loss of tolerance or dysregulation of paternally derived myriad enzymatic and metabolic functions throughout every organ system.
 Placental implantation with abnormal trophoblastic invasion of placental and fetal antigens PRIMIPATERNITY
uterine vessels  Immune maladaptation – extravillous trophoblasts early in
 Immunological maladaptive tolerance between maternal, pregnancy expressed reduced amounts of immunosuppressive non-
paternal (placental), and fetal tissues classic HLA G → defective placental vascularization
 Maternal maladaptation to cardiovascular or inflammatory  Women with 1597ΔC allele are predisposed to develop
changes of normal pregnancy preeclampsia
 Genetic factors including inherited predisposing genes and
epigenetic influences
TROPHOBLASTIC INVASION: ENDOTHELIAL CELL ACTIVATION
 Proliferation of extravillous trophoblasts from the anchoring villous  In response to ischemia or other inciting causes
 Trophoblasts invade the deciduas and the walls of the spiral arteriole to  Results as continuation of defective placentation that leads to
replace the endothelium and muscular wall to create a dilated low inflammatory and ischemic changes that provokes endothelial cell
resistance vessel injury
 Preeclampsia - implantation characterized by incomplete invasion  Results from extreme activated state of leukocytes in the maternal
of spiral arteriolar wall by extravillous trophoblasts circulation
 Early preeclamptic changes included:  Oxidative stress generates toxic radicals that injure
 endothelial damage endothelial cells
 insudation of plasma constituents into vessel wall  Placental factors are released and begin a cascade of event
 proliferation of myointimal cells  Antiangiogenic and metabolic factors and other inflammatory leukocyte
mediators are thought to provoke systemic endothelial cell injury
 medial necrosis
 lipid accumulation first in myointimal cells and then within
macrophages (atherosis – lipid-laden cells)
ANGIOGENIC FACTORS PREECLAMPSIA HELLP SYNDROME
Soluble FMS-like tyrosine kinase-1 (sFIT-1)  Inadequate maternal vascular remodeling that leads to high  Acronym for the following presentation : H-hemolysis, EL-elevated liver
 An endogenous anti-angiogenic protein that enters the maternal resistance, high pressure, low flow system then to placental enzymes, LP-low platelet
circulation after being produced in the placenta ischemia.  Recognized as complications of preeclampsia and eclampsia
 Inhibitor of placental growth factor (PIGF) and vascular  Endothelial damage promotes vasospasm which will lead to three  Often characterized by progressive and sudden deterioration in maternal
endothelial growth factor (VEGF) events: increased platelet activation with increased and fetal condition
microvasculature consumption, increased endothelial fibronectin  With its presence consider immediate delivery
levels, and decreased antithrombin III (the decrease facilitates clot o Prompt delivery is indicated if the syndrome develops beyond
formation) and anti-plasmin 34 weeks of gestation or earlier if there is disseminated
 Imbalance of prostacyclin (PGI2)-dilator and thromboxane (TXA2)- intravascular coagulation, liver infarction or hemorrhage, renal
constrictor; balance shifts to favour thromboxane. failure, pulmonary edema, suspected abruptio placenta, or
 Increased endothelin-constrictor, decreased nitric nonreassuring fetal status
oxide-dilator and decreased PGI2
PREECLAMPSIA WITH SEVERE FEATURES
Characterized by the certain findings in women meeting the basic criteria
for diagnosing preeclampsia, along with the evidence of
thrombocytopenia, impaired liver function, renal insufficiency, pulmonary
edema, visual loss or cerebral disturbance
 MANAGEMENT
Antepartum Management
 History and physical examination BASIC MANAGEMENT OBJECTIVES OF PREECLAMPSIA WITH SEVERE FEATURES
 Detection of pregnancy associated hypertensive disorder • To reduce its severity or progression of the disease process
 Review of obstetrical records • To control severe hypertension
• To prevent convulsion
 Past and current – changes and progression
• To deliver the mother of a fetus at the optimum time with the least trauma
 Signs and Symptoms • To detect and appropriately treat end organ damage
 Visual disturbance, persistent headaches, loss of consciousness, seizures, RUQ pain, edema, oliguria, • To completely restore the health of the mother.
preeclampsia with or without severe features COMMON ANTIHYPERTENSIVE AGENTS FOR URGENT CONTROL OF BP
 Diagnosis of hypertensive disorder • Labetalol – 10-20mg IV then 20-80mg q20-30min to a maximum dose of 300mg
 Hypertension: most dependable finding • Hydralazine – 5mg IV or IM then 5-10mg IV q 15-20min or constant infusion of 5-10mg, monitor again then if it
 Sudden increase in weight and significant edema of the hands and face - >2lbs/week or 6lbs/month remained constant give another dose of 5-10mg, you can give a maximum of 20mg. Take note not to exceed
 Persistent edema unresponsive to resting in supine 20mg.
 Other S/sx: headache, epigastric pain, blurry vision and shortness of breathing • Nifedipine – 10-20mg orally, repeat in 30 mins if needed then 10-20mg q 2-6h
ANTIHYPERTENSIVE AGENTS IN PREGNANCY FOR THOSE WITH CONTROLLED BP
 Laboratory
• Labetalol – 200-2400 mg/day orally in 2-3 divided doses
 CBC with platelet • Nifedipine – 30-120 mg/day orally TID, IV slow release preparation
 Serum creatinine • Methyldopa – 0.5-3g/day orally in 2-3 divided doses
 Lactic dehydrogenase MANAGEMENT OF ECLAMPSIA
 Liver enzymes • Watch out for premonitory signs
 24-hour urine protein or protein/creatinine ratio • Magnesium Sulfate Prophylaxis
 Assess for symptoms of severe preeclampsia • Given as an continuous IV or intermittent IM
 Abnormal labs • Should be given up to 24 hours after delivery
• Loading dose: 4g IV diluted in 100 ml IVF given for 15min
 Thrombocytopenia
• Continuous infusion: 10g IM (5g per buttock) : 2g/hr
 Elevated serum uric acid levels • Maintenance: 5g every 4h : 1g IV
 Elevated aminotransferase levels • If available, serum magnesium levels should be monitored at intervals for possible toxicity
 Hypertension plus presence of significant proteinuria If MgSO4 is Contraindicated
Predictive tests for hypertensive complications of pregnancy: • Diazepam – Loading dose: 10mg slow IV over 2 min, repeated if convulsion recur
○ Mean Arterial Pressure (MAP) • Maintenance dose: IV infusion of 40 mg in 500ml saline for first 24 hours
o MAP value in the second trimester of >90mmHg and a MAP value in the 3rd trimester of • Next 24 hours: IV infusion of 20mg in 500 ml normal saline
>105-110 mmHg has resulted in an increase incidence of preeclampsia (Level 1 Grade B) • May be used with phenytoin in absence of MgSO4
o Combination of MAP • Phenytoin
 2 and roll over test • After giving diazepam 10mg IV: initial loading dose of phenytoin (1g slow IV over 20 minutes) must be
 prediction rate increased to 78% given with continuous cardiac monitoring
o Supine pressor test or roll over test • Followed by succeeding doses of 100mg every 6 hours for the next 24 hours
 Done at 28-32 weeks due to increased plasma volume at this time DELIVERY:
 How it is done: • Termination of the pregnancy is the only cure for preeclampsia
○ AOG – preterm, term (deliver the baby)
- Let the patient lie on her left lateral recumbent position
○ Presence or absence of severe features
- Stabilize for a while ○ Presence of eclampsia, HELLP syndrome
- Get the diastolic pressure of the superior arm ○ Presence of maternal or fetal compromise – placental abruption, IUGR
- After 5 min, let the patient lie flat MODE OF DELIVERY
- Immediately take the BP after 5 min. Interpret the result • Vaginal delivery – induced or spontaneous if
Fetal evaluation o Cervix is ripe or
o Sonographic estimated fetal weight (Check for growth restriction and fetal state, and amniotic o Fetal demise
fluid) • Cesarian delivery – if the cervix is
o Amniotic fluid - to check for oligohydramnios o Unfavorable for vaginal birth, not yet effaced. Obstetrical indications like in Cpd, fetal malposition,
o Non stress test abruptio placenta, nonreassuring fetal heart rate, oligohydramnios with variable deceleration showed
o Biophysical profile In the tracing, IUGR, and those with late deceleration tracing.
o Doppler velocimetry – to check for presence of IUGR Glucocorticoids for Lung Maturation
o Fetal weight – to check for presence of IUGR • Betamethasone – 12 mg, 2 doses for 24 hours
• Dexamethasone – 6 mg, every 12 hours for 4 doses
• Hospitalization: Recommendation for immediate hospitalization (gestational
hypertension and preeclampsia without severe features)

o New s/sx of severe preeclampsia

o Evidence of fetal growth restriction

o Elevation of liver enzymes Thrombocytopenia

Severe Hypertension ≥160 SBP or ≥ 110mmHg DBP