Hypertension

RCG
Hypertension  Platelet <100,000/ul-thrombocytopenia
 Most common medical complication in pregnancy  Renal insufficiency as evidenced by creatinine of more than 1.1
 5-10% incidence as a whole mg/dl or doubling of the base line
 Deadly triad with HEMORRHAGE and INFECTION  Elevated liver transaminases
 Major cause of maternal and perinatal morbidity world wide  Cerebral symptoms
for it is a part of a part of a deadly triad along with  Visual symptoms
o Hemorrhage and  w/ or w/o Pulmonary edema
o Infection  In the past – subclassified to mild, moderate and severe NOT
 Preeclampsia syndrome (PES) CAUSE OF MATERNAL ANYMORE
DEATH/Mortality rate:
o WHO – 16% (developed countries)
o DOH – 32% (Philippines)

Classification of Hypertensive Disorders of Pregnancy (HDP) accdg

to ACOG 2013:
1. Gestational hypertension
 Evidence for PES does not develop and
 HTN resolves in 12 weeks postpartum also termed as
transient hypertension(temporary).
2. Preeclampsia and eclampsia Syndrome
 Before the 20th week
3. Chronic HTN of any etiology
4. Chronic HTN with superimposed preeclampsia / Preeclampsia
superimposed on chronic HTN

Hypertensive Disorder in Pregnancy

 BP >/= 140mmHg systolic and/or 90 mmHg diastolic.
 Present on atleast 20 occasions at least 6 hours apart but within
a max of 1 week period.
 In the past – (+) 30/15 in SBP/DBP = HTN and requires tx (NOT
TRUE ANYMORE)
 Increased risk for gestational HTN

Gestational HTN
 BP >/= 140 mmHg systolic and or Diastolic BP >/= 90 mmHg
in a PREVIOUSLY NORMOTENSIVE pregnant women who
is >/= 20 weeks AOG and has NO PROTEINURIA
 BP returns to normal within 12 weeks after delivery (Transient
HPN)  Risk factors:
 Increased risk for or possibility of having preeclampsia and o Young and nulliparity
eclampsia syndrome in around 10% of cases. o Older
 Severity will be according to the blood pressure reading. o Environmental
 SEVERE o Socioeconomic
o If it falls on 160 or even higher for systolic and 100 or even o Obesity
higher for diastolic is considered  BMI= 35 high risk
o Presence or absence of proteinuria o Twin gestation
o Presence of maternal symptoms like o Race and ethnicity
 Head ache
 Visual disturbance Eclampsia
 Right upper quadrant pain or epigastric pain  All the severe signs and symptoms of pre eclampsia but this time
 Liver transaminases affectation with severe development of grand mal convulsions or seizures
 Thrombocytopenia in a woman with preeclampsia in the absence of neurologic
 Note: Absence of the following on severe criteria will be disease that could account for Seizure before during and after
considered mild. delivery or labor.

Preeclampsia Syndrome Preeclampsia superimposed on chronic hypertension/ Chronic HTN

 Gestational HTN that happened >20 weeks BP >/= 140 mmHg
systolic and or Diastolic BP >/= 90 mmHg or 160/110 but this
time with PROTEINURIA
 Pregnancy-specific syndrome that can affect every organ
 PROTEINURIA is the most impt diagnostic criterion
 >/= 300 mg or .3g in 24 hour urine sample
 Urine Protein:Creatinine ratio
o >/= 0.3 grams
 Persistent 30 mg/dl (1+ or 2+ dipstick) protein in random urine-
pre eclampsia
with superimposed preeclampsia
 BP >/= 140/90mmHg before pregnancy or is present before the
20th week AOG of pregnancy or both
 Atleast 2 occasions or persist longer than 12th week post partum
 Accompanied by new onset proteinuria or other findings listed in
subclassification to characterize severity of superimposed PES

Trans by: TIMMY Edited by: RCGonzales,Dedeem,Caraveo #1

Incidence of Preeclampsia Genetic factors
 Young and nulliparity – risk for PES  Familial history
 Older – risk for chronic HPN w/ superimposed PES o HTN
 Environmental o Gestational HTN
 Socioeconomic influence o Preeclampsia
 Obesity BMI 35 vs 20 o Eclampsia
 Twin gestation – 13 vs 6%  Concordance in monozygotic female twin pairs
 Race and ethnicity (African Americans > Caucasian or whites,
Asian middle) Pathogenesis
 Spiral arterioles(1st to be affected) go to Vasospasm resulted by
Etiopathogenesis of Preeclampsia endothelial activation
 First time exposure to chorionic villi  Endothelial activation and constriction inc vascular resistance
 Exposure to superabundance of chorionic villi (twins and Molar hyper tension
Pregnancy H- mole)  Endothelial cell damage causes:
 Pre-existing conditions of endothelial cell activation and/or o Interstitial leakage – platelets and fibrinogen
inflammation (DM, renal, CVD) o Disruption of endothelial junction protein
 Genetics o Diminished blood flow ischemia of surrounding tissues
TAKE NOTE: ectopic and H-mole predispose to hypertension which causes:
disorder  Necrosis
**meaning, fetus is not a prerequisite for preeclampsia to develop.  Hemorrhage
Although chorionic villi are essential, they need not be uterine as  Disruption of end organs
in ectopic and molar pregnancy o The above is also caused by loss of anticoagulant property
and loss of intact endothelium.
Etiology- occurrence of HTN
 Two-stage disease Endothelial Cell injury
 Increase pressor response
 Stage 1: asymptomatic placental stage
o Loss of normal refractoriness to vasopressor
o No signs and symptoms
o Increase sensitivity to NE and angiotensin II
o MainReason: Faultyendovascular trophoblastic
remodelling  Prostaglandin mediated decrease in vascular responsiveness
o How the body would react to the invasion of the chorionic  Inhibition of nitrous oxide synthesis (potent vasodilator)
villi/ trophoblast  Increase production of endothelin (vasoconstrictor)
 Stage 2: symptomatic maternal stage  Angiogenic and anti-angiogenicprotein imbalance endothelial
o Invasion and development already hence symptoms already dysfunction
occur  Multi-organ involvement
o Endothelial cell activation  Pathology develops progressively at the AOG until delivery is
considered
Mechanism:  Ultimate management – Deliver the baby or the fetus
 Normal trophoblastic invasion
o Arterioles coiling at the end of cycle, penetrates PATHOPHYSIOLOGY
remodelling (endovascular trophoblast) lining arteriolar Cardiovascular System
endothelium reactive to vasoactive agents 1. Increase cardiac afterload caused by HTN
vasodilation, Large caliber blood vessels 2. Cardiac preload affected by hypovolemia of pregnancy (d/t
 Abnormal trophoblastic invasion constricted vessels, interstitial extravasation of fluid) and increase
o Endovascular trophoblast(incomplete penetration)does not by IV crystalloid or oncotic solutions.
line the endothelium do not react to vasoactive agents 3. Endothelial activation with inter-endothelial extravasation of
do not cause vasodilation hypertension develops intravascular fluid into extracellular space  pulmonary edema
Immunologic factors:
 Loss of maternal immune tolerance or dysregulation to paternally A. HEMODYNAMIC CHANGES AND CARDIAC FUNCTION
derived placental and fetal antigenAcute graft rejection (should  Decreased cardiac output- d/t increased peripheral resistance
be recognized by mother as its own)  Myocardial dysfunction
 Presence of antibodies like antiangiogenic factors  Hyperdynamic ventricular function
 Blood volume- hemoconcentration of intravascular content
Endothelial cell activation or inflammatory changes which is a severely diminished hypervolemia
continuation of stage 1 (assymptomatic placental stage)
 Maternal signs and symptoms B. HEMATOLOGICAL CHANGES
o Increase leukocytesreleases cytokines and IL  Thrombocytopenia
(IL8)oxidative stresspreeclampsia o Severe diseases assoc with <100,000/uL(OVERT)
o Leads to HELLP syndrome
Nutritional factors o Increase morbidity and mortality if
 Fruits and vegetables with antioxidants  decrease in blood decrease in function or lower count of
pressure platelet
 Not beneficial supplementation and will not protect from o Indication of delivery
hypertensive crisis  Platelet surface alteration
o Vitamin C and E  Neonatal thrombocytopenia
o Calcium o Nonsevere
o Not indication for CS
 Hemolysis
o RBC displays abnormal morphology resulting like
spherocytes reticulocytosis resulting from
microangiopathic hemolysis

Trans by: TIMMY Edited by: RCGonzales,Dedeem,Caraveo #2

  HELLP syndrome Brain
o Hemolysis  Neuroanatomic lesions
o Elevated liver enzymes o Intracerebral haemorrhage 60%(not as fatal as
o Low platelet pulmoedema)
 Cerebral blood flow
C. COAGULATION CHANGES o Loss of autoregulation to maintain the decrease CBF by
 Increase factor 8 consumption 20% in normal pregnancysignificant hyperperfusion in
 Increase fibrinopeptides PES
o A &B and D-dimers
 Decrease regulatory proteins Other Neurological Manifestations
o Antithrombin 3 1. OCCIPITAL HEADACHE AND SCOTOMA – M/C
o Protein C & S  Occipital lobe predilection
 FIBRINOGEN – UNAFFECTED (only increased in 2. CONVULSIONS caused by:
ABRUPTIO PLACENTA)  Excessive release of excitatory NT (GLUTAMATE)
 Increase fibronectin  Massive depolarization of network neurons
 Burst of action potential – result to GRANDMAL SEIZURES
D. VOLUME HOMEOSTASIS 3. BLINDNESS – rare with preeclampsia alone
 Endocrine changes 4. GENERALIZED CEREBRAL EDEMA – Increased ICP , mental
o Increase renin status changefatal Transtentorial herniation may result
o Increase Angiotensin II
o Increase aldosterone Visual changes and Blindness
o Electrolye imbalance due to sodium  Amaurosis-(temporary blindness)
retention o Occipital blindness d/t extensive occipital lobe edema
o Increase Vasopressin o Lasting only for 4 hours to a few days but resolves
o Increase ANP completely
o ALL seen in Normal px but more on  Purtscher retinopathy
preeclamptic women o Caused by retinal detachment or infarction
 Deoxycortisone Predictive test to indicate severity of Preeclampsia:
o increased in normal and preeclampsia(more on preec) 1. Vascular resistance testing and placental perfusion
o due to sodium retention 2. Proactive pressor test/ roll over test
 Fluid and electrolytes 3. Uterine artery Doppler velocimetry – good test for impending
o Increase ECF complication diminished placental perfusion; accurate
o Decrease plasma oncotic pressure / colloid osmotic 4. Pulse wave analysis
pressure resulting to 5. Fetal placental unit endocrine dysfunstion
 Very low intravascular volume 6. Test of renal function like serum uric acid
o Electrolyte cons do not differ 7. Micro albuminuria, Endothelial dysfunction and oxidative stress
o After seizure: dec pH and HCO3 d/t lactic acidosis and
compensatory respiratory loss of CO2 Prevention:
 Diet low in salt- ineffective in preventing hpn
Kidneys  Calcium supplementation- unless Ca deficit then it has no benefit
 Decrease renal blood flow and GFR (due to decreased IV volume)  Fish oil supplement- no benefit
 Glomerular endotheliosis blocking filtration barrier  Exercise
 Increase serum creatinine  Antihypertensive drugs
 Increase urine sodiumconc o Diuretics
 Proteinuria  No value except pulmonary hypertension – depletes
o >/= 0.3g protein in a 24 hour urine specimen or persistent Intravascular space that is already depleted
+1(30 mg/dl) on dipstick  Antioxidants “statins”
o Random protein: crea ratio is >30 mg/mmol o May prevent hypertensive d/o of pregnancy
 Acute kidney injury (ATN)  Antithrombotic agents
o Result from preeclampsia with a coexistent hemorrhage o Neo aspilet 80-130mg is beneficial
with hypovolemia and hypotension o Low dose aspirin
o Does not happen with HTN alone only if it is accompanied  50 -150 mg/day
by hypovolemia as a result of hemorrhage by abruption  Inhibits thromboxane A2 biosynthesis
placenta for example o Low dose aspirin + heparin

Liver DIAGNOSIS OF PREECLAMPSIA

 Periportal haemorrhage in liver periphery  Frequent visits for suspected early developing preeclampsia in the
 Involvement relates to severity of disease 3rd trimester
 Development of HELLP syndrome o Maintain DBP 80-90 mmHg
o Hemolysis o Sudden weight gain of >/= 2lbs per week
o Elevated Liver transaminases or Liver function  Complete history and PE
o Low Platelet  BP reading in sitting position
 Has worse outcome  CBC with platelet
 Serum crea and liver transaminases
Pancreas  Sonography- fetalwell being and AFV
 Severe hemoconcentration predisposes to pancreatic
inflammation

Trans by: TIMMY Edited by: RCGonzales,Dedeem,Caraveo #3

Management Management Protocol for severe preeclampsia and eclampsia
 Consideration for delivery (160/110
 Dictum is to diagnose early 1. Control convulsions(NOT HTN) with IV MgSO4 given 2 doses
 Aim is delivery of baby that will be able to thrive loading dose and maintenance dose
 Patient with BP of 80 -90 mmhg diastolic are the ones to be 2. Intermittent antihypertensive drugs to lower BP if dangerously high
monitored,specially with weight gain of 2lbs per week which 3. Avoid diuretics unless PULMONARY EDEMA is present. Avoid
should be normally 1 lb per week hyperosmotic agents
 Termination of pregnancy 4. Delivery of fetus
o Only cure for preeclampsia
 Ominous signs of impending eclampsia are: Magnesium Sulfate – for seizure and as tocolytics
o Headache  Continuous IV infusion
o Visual disturbance  IV Loading dose: 4-6 gms diluted in 100 ml IVF given over 15-
o Epigastric pain 20mins
o Oliguria  Maintain 1-2 gm/hr in 100 ml of IVF
 Preterm fetus: less severe disease  Monitor for toxicity- Assess DTR
o Temporize to reduce risk of neonatal death or morbidity from  Maintenance level: Mg 4-7 meq/L
prematurity  Discontinued 24 hours after delivery
o Assess fetal well-being by NST or biophysical profile scoring  IV – 4 gms 20% solution not to exceed 1gm/min
o L/S ratio to assess lung maturity o Follow with 10gm of 50% soln5 gm on each buttock deep
**only thing to hold back immediate delivery = PRETERM/ AOG IM
o 5 g of 50% soln deep IM every 4 hrs after
Severe preeclampsia at 20 -32 weeks AOGwith no HELLP  Decrease uterine contraction
syndrome: o d/t its effect on intracellular calcium
 Aggressive management o MgSO4 is considered as uterolytic agent
o Glucocorticoid administration  Fetal effects
 Dexamethasone o Decrease beat-to-beat variability
 Betamethasone o Lower APGAR score
o Deliver in 48 hours o Higher intubation rate
 Expectant management o Neuroprotective against cerebral palsy
o Bed rest and oral antihypertensive if responded may prolong o Neonatal osteopenia – long term
pregnancy.
o Prolonged pregnancy by 2 weeks(34wks AOG nasya nun so Management of Severe Hypertension
mature na lungs) then deliver.  Antihypertensive drugs
o check lung maturity by use of LS ratio o Hydralazine – prevents cerebral haemorrhage
(satisfactory response: DBP of 90-110 mmHg) TAKE
NOTE OF THIS
o Labetalol- a1 and nonselective beta blocker; not readily
available
o Nifedipine
 Calcium channel blocker
 Oral never sublingual
 Quicker reduction of BP (take note of this)
 Diuretics does not lower BP TAKE NOTE OF THIS
 Fluid therapy- use of controlled, conservative LR soln

Delivery
 Vaginal
o Less morbidity
Eclampsia: Goal and management o Preferred mode of delivery
1. Forestall convulsion o Minimal blood loss = d/themoconcentration
2. Prevent ICH and organ damage  Anesthesia/ anlagesia
3. Delivery of a healthy new born o Epidural – ideal\

Diff Diagnosis of Eclampsia Long term consequence

1. Epilepsy  Increase risk chronic HTN
2. Encephalitis  Ischemic cardiac disease
3. Meningitis  Stroke
4. Brain tumor  Incidence of chronic renal dse
5. Neurocysticercosis  Findings of cerebral infarct
6. AFE **early and judicious monitoring antenatally is the best way to address
7. Postdural puncture cephalgia the dreaded complication of pregnancy
8. Ruptured cerebral aneurysm **prevention is better than treatment
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Trans by: TIMMY Edited by: RCGonzales,Dedeem,Caraveo #4