Definition
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Gestational hypertension- new onset of SBP ≥140 mmHg /DBP ≥90 mmHg on at least 2
occasions 4 hours apart after 20 weeks of gestation in a previously normotensive woman &
NO proteinuria/ NO features of preeclampsia followed by normalization of BP post-partum.
Preeclampsia- New onset of SBP ≥140 mmHg or DBP ≥90 mmHg on at least 2 occasions
at least 4 hours apart after 20 weeks of gestation in a previously normotensive
woman or SBP ≥160 mmHg /DBP≥110 mmHg confirmed within a short interval (minutes) to
facilitate timely antihypertensive therapy + proteinuria OR in the absence of proteinuria with
new onset of HTN+ new onset of the following: (thrombocytopenia, renal insufficiency,
elevated liver transaminases, pulmonary edema, persistent cerebral/ visual symptoms)
Chronic HTN- HTN present before pregnancy/20 weeks of gestation OR HTN 1st diagnosed
during pregnancy & persist atleast for12 wks postpartum, SBP ≥140 mmHg, DBP ≥90
mmHg, or both
Superimposed PET on a chronic HTN- sudden increase in BP that was well controlled/
increase in therapy to control BP/ new onset of proteinuria or sudden increase in proteinuria
in pt. with known proteinuria before/ early in pregnancy.
Preeclampsia with severe features- preeclampsia + any of these findings: SBP ≥160
mmHg/ DBP ≥110 mmHg on 2 occasions at least 4 hrs apart while a patient is on bed rest
(unless antihypertensive therapy is initiated before this time), thrombocytopenia, liver
dysfunction, progressive renal insufficiency, pulmonary edema, persistent cerebral/ visual
disturbances.
Eclampsia- preeclampsia+ generalized seizure that cannot be attributed to other causes.
HELLP- variant of preeclampsia suggested by microangiopathic findings (hemolysis,
elevated liver enzymes, low platelets)
Clinical Features
History- GA->before 20 wks-chronic HTN, new onset/worsening HTN after 20 wkspreeclampsia that co-exist with proteinuria/ maternal dysfunction/ uteroplacental dysfunction,
new onset HTN after 20 weeks without co-existing complication-gestational HTN, if dx of severe
HTN/ preeclampsia in 1st/ early 2nd trimester- r/o gestational trophoblastic disease.
Preeclampsia- visual disturbance (scintillations and scotomata), new-onset headache (frontal,
throbbing/ similar to a migraine headache) & GI complaint (sudden, new-onset, constant
epigastric pain), rapidly increasing /nondependent edema, reduced urine output, nausea &
vomiting
Measure BP in sitting position-≥140/≥90mmHg, ophthalmic finding- retinal edema, retinal
vasospasm, impaired vision, RUQ abdominal tenderness, CNS finding- clonus.
Chronic HTN- Signs- Centripetal obesity, buffalo hump/ wide purple abdominal striae
=>glucocorticoid excess/ clinical signs /demonstrating hyperthyroidism, hypothyroidism, /growth
hormone excess. systolic bruit over the abdomen /flanks =>renal artery stenosis, radio femoral
delay /diminished pulses in the lower versus upper extremities =>coarctation of the aorta.
Signs of end-organ damage -presence of S4 on cardiac auscultation =>LVH/ diastolic
dysfunction due to preeclampsia-induced vasospasm. Carotid bruits => atherosclerotic disease
due to longstanding hypertension, and Retinal changes of chronic hypertension.
Investigation- urinalysis, CBC (Thrombocytopenia-<100,000/microL, and serum sodium,
potassium, creatinine, and glucose, creatinine clearance, blood urea nitrogen (BUN), albumin,
24-hour urinary protein, serum calcium, uric acid, glycosylated hemoglobin, TSH, liver enzymes
and bilirubin, and a urine dipstick for protein.
Spot urine for protein- creatinine ratio=> >0.3mg/dl / >300mg/day-> preeclampsia.
Ultrasound assessment of fetal growth, amniotic fluid volume and umbilical artery Doppler
assessment.
Management
-don’t routinely admit to hospital
-Antihypertensive therapy should be initiated for BP ≥ 160/105.
-aim for BP 135/85mmHg or less
-measure BP & dipstick proteinuria once/2x /wk until BP is 135/85 or less
-FBC, LFT, RFT at presentation & then weekly (Assess development of preeclampsia)
-patient education & counselling
-ask mother to monitor fetal movement daily
-timing of delivery at 37+0- 38+6 weeks
Pathophysiology of preeclampsia
Abnormal development of placenta, shallow cytotrophoblast migration toward the uterine spiral
arterioles, defective trophoblast differentiation => placental hypoperfusion & ischemia=> fetal
growth restriction, increased secretion of sFlt-1 & soluble endoglin, decreased availability of
VEGF, PlGF, other mediators of endothelial dysfunction, oligohydramnios => systemic
endothelial dysfunction(vasoconstriction & decreased blood-flow to organs)=> HTN, platelet
activation, CNS changes, edema, glomerular endotheliosis, proteinuria & renal insufficiency,
hemolysis, hepatic ischemia & necrosis.
-Systemic endothelial dysfunction of maternal blood vessels=> abnormal systemic arterial
vasoconstriction=> new onset HTN.
-Abnormal systemic arterial vasoconstriction=> blood accumulates in venous system (hepatic
veins) => liver enlargement=> stretches liver capsules & activates liver nociceptors/ hepatic
hematoma or rupture=> abdominal RUQ pain
-Abnormal systemic arterial vasoconstriction=> high pressure in intracranial arteries=> stimulate
vomiting center=> nausea/ vomiting OR liver damage and dysfunction=> abdominal distress=>
nausea/ vomiting.
-Abnormal systemic arterial vasoconstriction=> raised ICP=> headache/ stroke or TIA/ visual
changes
-Vascular dysfunction in brain damages cerebral tissue=> hyperactive, hypersynchronous
electrical activity in the cortex=> eclampsia
-Vascular dysfunction in brain damages cerebral tissue=> damage to UMN=> decrease
inhibition of LMN that mediate reflexes=> hyper-reflexia with clonus.
-Systemic endothelial dysfunction=> abnormal increase in vascular permeability=> rate of fluid
leaking out of vessels> rate of fluid reabsorbed=> pulmonary edema=> SOB.
-Glomerular endothelial dysfunction=> vasoconstriction of afferent arterioles in kidney nephrons/
decreased glomerular filtration=> reduced urine output.
-Placenta under-perfusion and ischemia=> more fragile vascular connection between placenta
& uterus=> easier separation of decidual basalis uterine layer from fetal vessels=>placental
abruption=> uterine tenderness & PV bleeding.
Lab test
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Uric acid- if the kidneys have been damaged by preeclampsia, uric acid levels in the blood
may rise.
Hematocrit- A high hematocrit value can be a sign of preeclampsia; preeclampsia often
causes the body's tissues to absorb blood plasma=> becomes more concentrated=>
abnormally high hematocrit value.
Platelets- Preeclampsia may cause an abnormally low platelet count (<100,000/microL)
Partial thromboplastin time (PTT)-Preeclampsia can cause problems with blood clotting that
increase the partial thromboplastin time.
Electrolytes-eg. sodium, potassium, magnesium, calcium, and chloride, amounts of
electrolytes in the body may change if preeclampsia is causing kidney damage or is causing
fluid to leak out of blood vessels into surrounding tissues (edema).
Urine protein (24-hour urine protein or urine protein to creatinine ratio) – used to look for
elevated protein in the urine
BUN, serum creatinine – kidney function tests used to look for organ damage resulting from
preeclampsia; serum creatinine will be measured frequently to monitor your condition.
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) – elevated levels of
these liver function tests may indicate organ damage from preeclampsia; ALT and AST will
be measured frequently to monitor your condition.
Peripheral blood smear – red blood cells are examined with a microscope for damage or
abnormalities.
Lactate dehydrogenase (LD) – elevated LD levels indicate tissue or cell damage, which
occurs in the breakdown of red blood cells.
Bilirubin – elevated levels of bilirubin are usually an indication of liver damage or red blood
cell destruction (hemolysis).
Principles of management of PET
-Control the BP- Preeclampsia without severe features-> managed with twice-weekly BP
monitoring, antenatal testing for fetal well-being and disease progression, and delivery by 37
weeks' gestation. Preeclampsia with any severe feature ->immediate stabilization and inpatient
treatment with magnesium sulfate, antihypertensive drugs, corticosteroids for fetal lung maturity
if less than 34 weeks' gestation, and delivery plans. monitor as inpatients or closely at home for
72 hours postpartum.
-Control and prevention of eclampsia- Elevate bed side rails, place patient in the lateral
decubitus position (physical restraints may be necessary), suction oropharyngeal secretions and
vomitus, maintain airway, adequate oxygenation, and IV access, Fetal resuscitation involving
maternal oxygenation, left lateral positioning, and continuous fetal heart rate monitoring is
needed. Magnesium sulphate (IV or IM) ->Used as prevention if sustained SBP >160, DBP
>110; proteinuria > 1g/24h or ≥ 3+ on dipstick; liver and/or renal impairment; coagulopathy.
loading doses of 4 to 6 g intravenously over 20 to 30 minutes and maintenance doses of 1 to 2
g/hour (and up to 3 g/hour)
-presence/surveillance of severe features of PET- Hospitalize until delivery, review findings from
frequent maternal and fetal assessment throughout the day, monitor blood pressure every 4
hours, frequently assess maternal symptoms (eg, headache, vision changes, epigastric or
abdominal pain, decreased fetal activity, vaginal bleeding). Symptoms of preeclampsia with
severe features would warrant delivery, accurately record fluid intake and urine output to identify
oliguria (defined as <500 mL over 24 hours), deteriorating kidney function (rising creatinine to
above 1.1 mg/dL [0.1 mmol/L]) and persistent oliguria over 24 to 48 hours would warrant
delivery, repeat lab test (CBC, serum creatinine, liver chemistry 2x weekly.
-Fetal surveillance- Monitor with monthly ultrasounds to assess fetal growth after viability and
fetal surveillance by biophysical profile weekly or non-stress test twice weekly.
--Timing of delivery- Mild preeclampsia should be delivered at 37 weeks, Severe preeclampsia
should be delivered after 34 weeks & Corticosteroids are given for fetal lung maturity where
appropriate (IM Dexamethasone 6 mg 6 hourly 4 doses or 12 mg 12 hourly 2 doses.
-Mode of delivery- cesarean delivery to a nulliparous woman with preeclampsia with severe
features of <32 weeks of gestation having unfavorable cervix, given the relatively high
frequency of abnormal intrapartum fetal heart rate tracings and low likelihood of a successful
vaginal delivery. preeclampsia with features of severe disease, does not mandate immediate
cesarean birth.
-Counselling patient/ spouse- patient education on signs and symptoms & severity of disease &
advice to monitor fetal movement daily, instruct correct procedure for woman who self-monitor,
recommend lifestyle modification & follow prescribed medications regularly, advice spouse/
family members to provide intervention/ notify health-care provider immediately if severe
symptoms occur, counsel for informed choice of post-partum family planning & next pregnancy
should attend ANC services early to prevent and identify and appropriate management of preeclampsia.
Induced labor
maternal complications- uterine tachysystole, uterine hypertonus, caesarean section, uterine
rupture, instrumental vaginal delivery, severe hypertension, worsening of pre-eclampsia,
development of seizures and eclampsia and HELLP Syndrome, maternal vomiting, maternal
diarrhea, fever, antibiotic use, and postpartum hemorrhage.
fetal-neonatal complications -meconium-stained liquor, Apgar score <7 at 5 minutes, NICU
admission, seizures, birth asphyxia, and stillbirth.
C-section
Risk baby to breathing problems and surgical injury, risk mother to infection, PPH, reaction to
anesthesia, blood clots, wound infection, surgery injury, increase risk during future pregnancy &
problems in future pregnancies, such as low-lying placenta, placenta accreta and damage to the
wall of the womb.
possible complications associated with this condition (and if left untreated)
-liver, kidney and brain damage
-bleeding problems
-eclampsia
-stroke
-PPH
-baby=> premature birth/ placental abruption
Management of eclampsia
Ensure airway, breathing and circulation (keep airway patent, establish IV line, monitor SaO2,
insert catheter), protect airway & minimize risk of aspiration, place pt. on her left side & suction
her mouth, immediately called skilled person for intubation, prevent maternal injury- close
observation & use of soft padding & side rails on bed, administer magnesium sulphate-If the
patient has already received a prophylactic loading dose and is receiving a continuous infusion
when the seizure occurs, an additional 2 g should be given intravenously. Otherwise, a 4- to 6-g
loading dose IV over 15 to 20 minutes, followed by a continuous infusion of 2 g per hour.
Lorazepam and phenytoin may be used as second-line agents for refractory seizures
Discharge advice
-Post-partum mx of HTN- Monitor BP for 72hrs in hosp., equivalent outpt. surveillance, repeat
BP assessment 7-10days postpartum & repeat BP earlier if symptoms, BP >160/100mmHg=>
high dependency care & invasive monitoring, sustained BP≥150/100mmHg-start/ increase antiHTN drugs, sustained BP≥140/90mmHg-start anti-HTN drugs (labetalol/atenolol,
nifedipine/amlodipine, ACEI)
Methyldopa Should be discontinued postnatally due to its maternal side effect (sedation,
postural hypotension, postnatal depression)
-Family planning- POPs & levonorgestrel-releasing intrauterine system (Mirena) are appropriate
options in women with hypertension.
-Her future health & next pregnancy- counsel on the risk of recurrence, recurrence risk for
gestational HTN-16-47%, recurrence risk for preeclampsia-2-7%