Hypertensive Disorder

The term, “Pregnancy-induced

hypertension (PIH)” is defined as the
hypertension that develops as a direct
result of the gravid state.
It includes—
(i) Gestational hypertension,
(ii) Preeclampsia and
(iii) Eclampsia

1.Gestational HTN –
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 is
called gestational hypertension.
#Hypertension without Proteinuria.

2. Pre-eclampsia –
Preeclampsia is a multisystem disorder of
unknown etiology characterized by
Development of hypertension to the extent
of 140/90 mm Hg or more with proteinuria
after the 20th Week in a previously
normotensive and nonproteinuric woman.

#DIAGNOSTIC CRITERIA OF PREECLAMPSIA –

Hypertension: An absolute rise of blood
pressure of at least 140/90 mm Hg, if the
previous blood Pressure is not known or a rise
in systolic pressure of at least 30 mm Hg, or a
rise in diastolic pressure of At least 15 mm Hg
over the previously known blood pressure is
called pregnancy-induced hypertension.

Calculation based on mean arterial pressure

(MAP) –

Systolic pressure + (diastolic pressure × 2)

3 =MAP

 Normal MAP 93.3 , In pre-eclampsia

105mmHg.

 Edema excluded due to it also present in

normal pregnancy.

 It may seen before <20 pregnancy in

hydatidiform mole and acute poly
hydramnios.
# Clinical Features –
 HTN – 140 /90 mmHg.

 MAP – 105 mmHg.

 Edema – pitting edema over the ankles

after 12 hours bed rest or rapid gain in
Weight 1 lb a week or more than 5 lb a
month in the later months of pregnancy
may be The earliest evidence of
preeclampsia.

 Proteinuria - >0.3 gm /24 hrs.

#types –
1.Mild Pre-eclampsia –
BP >140/90 and <160 /110mmHg.
Proteinuria – 0.5gm/lit.
 2.Severe Pre-eclampsia –
BP >160 /110 mmHg.
Proteinuria – 1gm /lit.
D/t vasoconstriction leads to blurred
vision which resulting in Ratinal
detachment.

#Risk Factor –
 Family history.
 Primigravida (first time exposure to
chorionic villi )
 Obesity.
 Molar pregnancy.
 Gestational DM.
 Imbalance of PG and increased synthesis of
Thromboxane (Vasoconstrictor).
 Kidney ds.
  DM
 Mother younger <20 yrs or older >40yr.
 Twin pregnancy.

#Etiology –
1. Vasospasm – D/t decrease Nitrous oxide
and increase PGI2.
2.Endothelium dysfunction – D/t Free redicals
damage endothelium.
3.
#Alarming sign –
 Headache.
 Disturbed sleep.
 Dimnished Urine O/P (Oliguria) – increase
serum uric acid level (Biological Marker).
 Epigastric pain
 Blurred vision – it may regain within 4 to 6
wks after delivery.
#Investigation –
 BP.
 Urine – Albumin.
 Blood values – serum uric acid level
>4.5mg/dl.

#Management –
 Rest – it increase renal blood flow that lead
to diuresis.

 Diet – High protein diet and less salt intake.

Vit. A, C, E (Antioxident for remove
free redicled).

 Diuretics –
Furosemide 40 mg orally × 5days ABF OD.
  Antihypertensive -
Labetalol – 100 mg TDS or QID.
Avoid in respiratory distress pt.

Methyldopa - 250 to 500 mg TDS or QID.

DOC for pre-eclampsia.

Nifedipine (Ca channel blocker ) – 10 to 20 mg

BD.
Hydralazine – vascular smooth muscle relaxant.
10 to 25 mg BD.
 MgSO4 – As prophylactic in severe pre-
eclampsia.
 Eclampsia
Greek word, meaning “like a flash of
lightening”.

Pre-eclampsia + Grandmal seizure (Tonic

clonic)
Or Coma

#Causes of convulsions –
 Anoxia –
Spasm of cerebral vessels that leads to
increase cerebral vascular resistance.
Resulting in fall in consumption of Oxygen
leads to Anoxia then convulsions may
occur.

 Cerebral edema – cause irritation.

  Cerebral dysrhythmia – excessive releass
of Excitatory neurotransmiter Glutamate.

#ONSET OF FITS:
Fits occur more commonly in the third
trimester (> 50%).
 Antepartum (50%)

 Intrapartum (30%)

 Postpartum (20%):
usually within 48–72 hours of Delivery.
#Clinical Features –
 Premonitory stage: The patient becomes
unconscious. There is twitching of the
 muscles of the face, tongue, and limbs.
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 twitchings start in the face
then involve one side of the extremities
and ultimately the whole body is involved
 in the convulsion. Biting of the tongue
occurs. 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.

# Mortality rate – 2 to 30 %.

#Causes –
 In mother –
(2) Cardiac failure.
(3) Pulmonary edema.
(4) Aspiration and/or septic Pneumonia.
(5) Cerebral hemorrhage.
 (6) Acute renal failure.

#In fetus –
 Prematurity
 Intrauterine asphyxia

#Management –
 Hospitalization.
 Airway clearance.
 Oxygen admn.

 Magnesium sulfate is the drug of choice.

 Induced cerebral vasodilation.

 Thiopental Sodium if seizure not subside.

 Terminate pregnancy.
Therapeutic level – 4 – 7 mEq /lit.
Toxic level - >12 mEq /lit.

#Toxicity –
 Loss of deep tendon reflexes >7 mEq/L;

 Respiratory depression more than 10

mEq/L.

 Cardiac arrest more than 25 mEq/L.

#Nursing officer Role –
 Check The knee jerks are present,
 Check urine output exceeds 30 mL/h
 The respiration rate is more than
12/minute.
 Check Biceps reflex – Strike on ante cubital
fossa If flexion occurs it means therapeutic
dose.

 Injection calcium gluconate 10 mL (10%

solution), IV at bed side.
  To prevent serious maternal injury from
fall

 prevent aspiration,

 To maintain airway.

 To ensure oxygenation,

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