HYPERTENSIVE DISORDERS IN PREGNANCY

Classification of hypertensive disorders in pregnancy.

Preeclampsia, eclampsia,

Chronic hypertension- presence of hypertension of any cause antedating or before the 20th week
of pregnancy and its presence beyond the 12 weeks after delivery.

Gestational hypertension -A sustained rise of blood pressure to 140/90 mm Hg or more on at

least two occasions 4 or more hours apart beyond the 20th week of pregnancy or within the first
48 hours of delivery in a previously normotensive woman

i) Pre-eclampsia- multisystem disorder of unknown etiology characterized by

development of hypertension to the extent of 140/90 mm Hg or more after the 20th
week in a previously normotensive woman. It can either be pre-eclampsia with or
without severe features.
 The severe features include;
 decreased urine output < 400ml in 24hrs.
 severe headache
 disturbed sleep
 blurring of vision ( regained after 4-6 wks
after delivery)
 pulmonary edema
 pain not responding to analgesics
 epigastric pain associated with vomiting
(coffee colour) due to subcapular
hemorrhage in liver
 Bp of 160/110 mmHg
 platelet count less than 100*10^3/ul
 liver transaminase levels elevated 3 times
upper limit of normal( significant).
 Doubling of serum creatinine levels or >
1.1mg/dl
 Diagnostic criteria for PET (OBS BY DUTTA).
a) Hypertension: An absolute rise of blood pressure of at least 140/90 mmHg,
rise in systolic pressure of at least 30mmHg or diastolic of at least 15mmHg
over the previously known Bp is called *pregnancy induced hypertension. A
rise of 20mmHg over previous reading or when MAP > 105mmHg is
considered significant. Rise of Bp should be evident on at least 2 occasions at
least 6 hrs. apart.
 b) Edema; Demonstration of pitting edema over the ankles after 12hrs bed rest
or rapid gain in weight over 1lb a week or more than 5lb a month in the later
months of pregnancy.
c) Proteinuria; Presence of total protein in 24 hours urine of more than 0.3 g or
more than or equal to 2+ (1.0 g/L) on at least two random clean-catch urine
samples tested more than or equal to 4 hours apart in the absence of urinary
tract infection is considered significant.
Dipstick results can either be;
 Trace = 0.1g/l
 1+ =0,3g/l
 2+= 1.0g/l
 3+ = 3.0g/l
 4+ = 10g/l

Risk Factors for Preeclampsia

i. Primigravida- young or elderly{ first time exposure to chorionic villi)

ii. Family history of hypertension, preeclampsia
iii. Obesity ; BMI > 35kg/m^2, insulin resistance
iv. New paternity
v. Thrombophilia
vi. Preexisting vascular disease
vii. Multiple pregnancy
 HELLP syndrome- a rare complication of preeclampsia. Denotes hemolysis,
elevated liver enzymes and low platelet count < 100,000/mm^3.

Investigations in PET

i. FHG- (platelets) may show decreased Hb level due to hemolysis. Can cause jaundice
ii. LFTs- AST three times upper limit significant, bilirubin levels
iii. KFTs- baseline serum creatinine levels can predict the risk for mild and severe
preeclampsia.
iv. Urinalysis- acute tubular necrosis and proteinuria
v. Bedside clotting time- normal 8-15 minutes
vi. Radiological; obstetric ultrasound request for restrictive index level > 0.8 in mean
cerebral artery. What other values are requested in an obs ultrasound???
vii. Fetal monitoring; CTG , bpp, NST.
viii. Blood biochemistry- Lactate dehydrogenase values. Elevated values indicate cell death
and thus a sign of end organ damage.
ix. Ophthalmic examination to detect any retinal edema.

Management of PET
 i. Control hypertension- use antihypertensive in pregnancy. 1st line labetalol 100mg TDS,
methyldopa (aldomet)250-500mg tds, nifedipine 10-20 mg bd or hydralazine 10-25 mg
bd (in diastolic htn). Hydralazine used cautiously due to its addictive effect. On
nifedipine S/E may be headache due to its vasodilation effect.
ii. Monitor htn to achieve Bp of 120-140/60-90 and to cont. pregnancy till 37 completed
weeks. Delivery either induction of labour or CS.
iii. Bed rest- it increases renal blood flow hence diuresis, increases uterine blood flow hence
improve placental perfusion and reduces blood pressure.
iv. Administer dexamethasone. Role is for lung maturity, neurodevelopment, preventing
necrotizing enterocolitis and hemorrhage.
v. Prevent convulsions- administer Magnesium sulphate, phenotyn, *diazepam – reduces
GCS score.
vi. Monitor urine output.
vii. Deliver at 34 completed weeks?
viii. Prophylactic low dose aspirin (81mg/day) – recommended in women at high risk of PET.
Administered at 12-28 wks and cont. till delivery. It improves blood flow across the
placenta by dilating uterine arteries. It also inhibits thromboxane known to raise Bp and
know to be elevated in PET.
ix. Antioxidants vitamin C and E plays a role in protective development of PET by reducing
the oxidative stress and endothelial dysfunction.
x. Regular antenatal checkup for early detection of rapid weight gain or tendency of rising
diastolic bp.
xi. Heparin or LMWH in women with thrombophilia and with high risk pregnancy.
xii. Calcium supplementation (2g/day) reduces risk of gestational htn.
xiii. Balanced diet rich in proteins.

Complications of PET

A. Maternal – eclampsia, CVA, abruption placenta, DIC, oliguria, anuria, renal failure,
pulmonary edema, HELLP syndrome, Hepatic failure, Blurring of vision and blindness,
preterm labour, PPH, death.
B. Fetal- IUGR, preterm delivery and prematurity, asphyxia, IUFD, oligohydromnios,
increased perinatal death.

Worrisome signs for PET development.

 Rapid increase in weight during the latter half of pregnancy

 Upward trend in diastolic bp. even while in normal range
 Tachycardia
 Restlessness
 HELLP syndrome
 SPO2 < 95%
  Headache, blurring vision

Prediction screening tests for PET

 Doppler ultrasound of high resistance index in the uterine artery in second trimester.
 Development of renal dysfunction: Rise in the level of serum uric acid and appearance of
microalbuinuria are observed to be the predictors of preeclampsia.
 Average mean arterial pressure (MAP) in second trimester > 90 mm Hg may predict the
onset.
 Maternal serum level of SFlt-1 is increased in women with preeclampsia
 Fetal DNA—Detection of free fetal DNA (ff DNA) in maternal plasma in early
pregnancy may be predictive of preeclampsia.
 Roll over test: This screening test is done between 28 and 32 weeks. Blood pressure is
measured with the patient on her side first and then the patient is asked to roll on her back
to check the blood pressure once again. An increase of 20 mm Hg in diastolic pressure
from side to back position indicates a positive “rollover test”.

Indications of delivery without delay in severe PET.

 Persistent symptoms of severe PET

 Pulmonary edema/hypoxia < 95%
 Hepatocellular injury ; increased AST/ALT twice the normal
 Oliguria , 500ml/24hr
 Abnormal coagulation profile
 FGR with non-reassuring status
 Eclampsia

Monitoring a patient with severe PET on magnesium sulphate.

 Vital signs every 10-30 minutes

 Lung sounds every 2 hrs.
 Deep tendon reflexes, level of consciousness, headaches, visual disturbances,
epigastric pain every 4 hrs.
 Intake and output record ( intake iv crystalloids, colloids total <125 ,l/h)
 Fetal well-being ( anti and intrapartum) continuous EFM

ECLAMPSIA- Woman with pre-eclampsia when complicated with convulsions and/or coma.

Types of Eclampsia-

 Antepartum (majority 50%)

 Intrapartum (30%)
 Postpartum (20%).
Stages of convulsion in eclampsia;

Premonitory stage: The patient becomes unconscious. There is twitching of the muscles of the
face, tongue, and limbs. Eyeballs roll or are turned to one side and become fixed. This stage lasts
for about 30 seconds.

Tonic stage: The whole body goes into a tonic spasm — the trunk-opisthotonus, limbs are flexed
and hands clenched. Respiration ceases and the tongue protrudes between the teeth. Cyanosis
appears. Eyeballs become fixed. This stage lasts for about 30 seconds.

Clonic stage: All the voluntary muscles undergo alternate contraction and relaxation. The
twitching start in the face then involves one side of the extremities and ultimately the whole body
is involved in the convulsion. Biting of the tongue occurs. Breathing is stertorous and blood
stained frothy secretions fill the mouth; cyanosis gradually disappears. This stage lasts for 1–4
minutes.

Stage of coma: Following the fit, the patient passes on to the stage of coma. It may last for a
brief period or in others deep coma persists till another convulsion. On occasion, the patient
appears to be in a confused state following the fit and fails to remember the happenings.

DDX in Eclampsia; epilepsy, hysteria, encephalitis, meningitis, peurperal cerebral thrombosis,

poisoning, cerebral malaria in tropics and intracranial tumors.

Features of organ dysfunction in PET and eclampsia.

Cardiovascular – generalized vasospasms, increased peripheral resistance, decreased CVP,

decreased pulmonary wedge pressure.

Hematological- decreased plasma volume, hemoconcentration, coagulation disorder, increased

blood viscosity.

Renal- decreased GFR, decreased renal plasma flow, and increased serum uric acid.

CNS- cerebral edema, cerebral hemorrhage,

Hepatic –liver damage, periportal necrosis, subcapsular hematoma.

Maternal complications of eclampsia

 Injuries- tongue bite, injuries due to fall, bed sores

 Pulmonary complications- edema (due to leaky capillaries), pneumonia (aspiration),
embolism, adult RDS.
 Hyperpyrexia
 Cardiac- acute left ventricular failure
 Cardiomyopathy
  Renal failure
 Hepatic- necrosis, subcapsular hematoma,
 Neurological deficits
 Disturbed vision
 Hematological – thrombocytopenia, DIC
 Postpartum- shock, sepsis, psychosis

Principles of management in eclampsia

Supportive care
a. Patient is kept in a railed cot and a tongue blade is inserted between the teeth. She is kept
in the lateral decubitus position to avoid aspiration. Vomitus and oral secretions are
removed by frequent suctioning; oxygenation is maintained through a face mask (8–10
L/minute) to prevent respiratory acidosis.
b. Detailed history is to be taken from the relatives, relevant to the diagnosis of eclampsia,
duration of pregnancy, number of fits and nature of medication administered outside.
c. Examination: Once the patient is stabilized, a thorough but quick general, abdominal
and vaginal examination is made. A self-retaining catheter is introduced and the urine is
tested for protein.
d. Monitoring: Half hourly pulse, respiration rate and blood pressure are recorded.
Hourly urinary output is to be noted. If undelivered, the uterus should be palpated at
regular intervals to detect the progress of labour and the fetal heart rate is to be
monitored.
e. Fluid balance: Crystalloid solution (Ringers solution) is started as a first choice. Total
fluids should not exceed the previous 24 hours urinary output plus 1000 mL. Normally, it
should not exceed 2 litres in 24 hours.
f. Antibiotic: To prevent infection, Ceftriaxone 1 g IV twice daily is given

Specific management

a. Anticonvulsant regime: The aim is to control the fits and to prevent its recurrence.
Magnesium sulfate is the drug of choice. It acts as a membrane stabilizer and
neuroprotector. It reduces motor endplate sensitivity to acetylcholine. Magnesium also
blocks neuronal calcium influx. It induces cerebral vasodilatation, dilates uterine arteries,
increases production of endothelial prostacyclin and inhibits platelet activation
Dosage; loading dose IM 4g( 20%) solution over 3-5 minutes followed by 10g(50%)
deep IM(5g in each buttock).Maintenance dose 5g(50%) IM 4hrly in alternate buttock.
Or loading dose 4-6g IV slow over 15-20 mins and maintenance 1-2g IV infusion.
b. Antihypertensives and diuretics: if BP remains more than 160/110 mm Hg, First line of
antihypertensive drugs are: labetalol and hydralazine
c. Status eclampticus: Thiopentone sodium 0.5 g dissolved in 20 mL of 5% dextrose is
given intravenously very slowly.
Magnesium sulphate toxicity signs.

 Loss of deep tendon reflexes

 Decreased respiratory rate (<12 per minute)
 Urine output (< 30 mL/h)
 Chest pain, heart block
 Management of toxicity involves; stopping magnesium therapy, estimation of
serum magnesium and creatinine levels, injecting calcium gluconate 10ml
(10% sol) IV.

Medical Management of Eclampsia—Immediate Measures

 Call for extra help (Communication)

 To put patient in left lateral recumbent position
 Maintain oral airway
 O2 inhalation – nonbreather mask; 10 L/minute
 Commence IV lines; 1 or 2 wide bore cannulas
 Foley catheter with urometer
 To monitor O2 saturation; pulse oximeter (SPO2 > 95%)
 Control of seizures: MgSO4, (IV/IM regimens)
 To monitor vitals; fetal status and magnesium toxicity
 Control of hypertension: Labetalol, Hydralazine
 Fluids: Crystalloids (saline) or colloids (albumin/blood) ≤ 125 mL/h
 Suction: oropharyngeal
 Diuretics: pulmonary edema
 Investigations to organize: Blood: CBC, AST, ALT, LDH, Creatinine, Uric
Acid, Urine analysis - protein