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Hypertensive disorders of pregnancy

د.فادية جاسم
Objectives
Define hypertensive disorders of pregnancy.
Classification of this disorder.
Maternal & fetal complications
Managements .

Definition:

Hypertension is defined as changes of BP recorded on at least 2 occasions of either:
Diastolic BP >90 mmHg, or
Systolic BP >140 mmHg, or
A rise (compared to booking) in diastolic BP of at least 15 mmHg, or
A rise (compare to booking) in systolic BP of at least 30 mmHg.
Classification:
Pregnancy-induced hypertension (Gestational hypertension alone): hypertension arising for the first time in the second half of pregnancy &in the absence of proteinuria or any other features of pre-eclampsia.It is not associated with adverse pregnancy outcome.
Chronic hypertension: pre-existing hypertension may be diagnosed before gestation or assumed when a women is found to be hypertensive in early pregnancy. It can predispose to the later development of superimposed pre-eclampsia.
Pre-eclampsia: defined as hypertension of at least 140/90 mmHg recorded on 2 separate occasions at least 4 hours apart & in the presence of at least 300 mg protein in a 24-hour collection of urine, arising de nova after the 20th week of gestation in a previously normotensive women & resolving completely by the sixth postpartum week
Eclampsia: is a serious & life-threatening complication of pre-eclampsia.It is defined as convulsions occurring in a woman with established pre-eclampsia,in the absence of any other neurological or metabolic cause. It is an obstetric emergency.
It may occur:
Antepartum 40%.
Intrapartum 20%.
Postpartum 40%.
Imminent eclampsia (fulminating pre-eclampsia): is the transitional condition characterized by increasing symptoms & signs, it’s the sever form of pre-eclampsia
Pre-eclampsia:
Incidence&Epidmiology:
It complicates approximately 3% of pregnancies.
It is more common in primigravida (effect of fetal and hence paternal genome).
Maternal genetic predispositions (3-4 folds increase in the first-degree relatives of affected women).
Risk factors for pre-eclampsia(predisposing factors):
1. Conditions in which the placenta:-
*multiple gestation.
*diabetes.
*hydrops.
2. Pre-existing hypertension or renal disease.
3. Pre-existing vascular disease (such as in diabetes or autoimmune vasculitis).
Clinical presentation:-
May be asymptomatic.
Headache.
Visual disturbances.
Epigastric& right upper abdominal pain.
Signs of pre-eclampsia:
Elevation of BP.
Fluid retention (non-dependent oedema).
Brisk reflexes.
Ankle clonus (more than 3 beats).
Uterus & fetus may feel small for gestational age.


Etiology:
Trophoblastic tissue provides the stimulus for the disorder, so its only occurs in pregnancy ,but it has been described in pregnancy lacking a fetus(molar pregnancy)& in the absence of the uterus ( abdominal pregnancy) .
Trophoblastic invasion is patchy& the spiral arteries retain their muscular walls which interne prevent the development of a high flow, low-impedance uteroplacental circulation, the reason for that is unknown.
Organ-specific changes associated with pre-eclampsia:
Central nervous system
Cerebral oedema.
Cerebral hemorrhages.
Retinal haemorrhage, exudates &papillodema are characteristic of hypertensive encephalopathy.

Cardiovascular

Generalized vasospasm.
Increased peripheral resistance.
Reduced central Venus/pulmonary wedge pressures.

Haematological

Platelet activation & depletion.
Coagulopathy.
Decreased plasma volume.
Increased blood viscosity.

Renal

Proteinuria
Decreased GFR(oliguria)
Decreased urate excretion (increase serum uric acid).


Hepatic
Periportal necrosis
Sub- capsular haematoma.
Elevation of liver enzymes.

HELLP syndrome: it is sever form of pre-eclampsia, occure in 2-4% of women with pre-eclampsia&is associated with fetal loss rate of up to 60% if occur antenatally& a maternal mortality of up to 24%.
It may be associated with DIC&placental abruption.
H=Haemolysis.
EL=Elevated Liver enzymes.
LP=Low Platelet count.

DIAGNOSIS:

A diagnosis of pre-eclampsia usually requires admission of the patient for more intensive investigations & monitoring of her condition.
1.) Mild form:
BP mildly elevated i.e. diastolic BP of 90-95 mmHg.
Minimal proteinuria.
Normal haematological&biochemical parameters.
Patient can be monitored as an outpatient, attending for regular fetal & maternal assessment.

2.) Moderate (95-105mmHg), it requires admission to the hospital for investigation &follow up.


3.) Sever pre-eclampsia is identified by
symptoms of sever pre-eclampsia:-

Frontal headache

Visual disturbance
Epigastric pain
General malaise & nausea
Restlessness
Signs of sever pre-eclampsia:

Agitation

Hyper- reflexia(clonus)
Facial &peripheral odema
Right upper quadrant tenderness
Poor urine output

Investigation for pre-eclampsia:

These investigations will be repeated at interval depending on the overall clinical picture.
Urinalysis by dipstick (quantitatively inaccurate).
24-hour urine collection for total protein &creatinine clearance).
Full blood count (platelets &haematocrit).
Blood chemistry (renal function , protein concentration ).
Plasma urate concentration.
Liver function.
Coagulation profile.
Ultrasound assessment :
Fetal size.
Amniotic fluid volume.
Doppler.


Complications:
MATERNAL COMPLICATIONS
Increase maternal morbidity &mortality because of:
Cerebral oedema, cerebral haemorrhage& retinal haemmorrhage.
Heart failure & pulmonary oedema.
Sub-capsular haematoma, periportal necrosis& elevated liver enzymes.
Hematological complications:
Decrease platelets count.
Haemolysis.
Coagulopathy & DIC.
Renal failure.
HELLP syndrome.
Increase risk of thrombosis (DVT, pulmonary embolism).
Increase risk of APH & PPH.
Increase risk of surgical interventions(c/s, instrumental delivery).
Eclampsia.
Adult Respiratory Distress Syndrome (ARDS).
Fetal complications:
Increase perinatal morbidity & mortality.
Preterm delivery (iatrogenic).
IUGR.
IUD.
Birth asphyxia.
Treatment:
The mainstay of treatment is ending the pregnancy by delivering the fetus & placenta; this can be significant problem at 24-32 weeks.
The aim of antihypertensive therapy is to lower the BP & reduce the risk of maternal cerebrovasular accident without reducing uterine blood flow & compromising the fetus.
Antihypertensive drugs are:
Methyldopa: centrally acting antihypertensive agent, safe, can only giving orally ,need at least 24 hours to work, & it is the drug of choice antenatally.
Labetolol: is an alpha & beta- blocking agent ,it can be given orally or IV, safe , can be given antenatally&intrapartum to control BP in sever pre-eclampsia .
Nifedipine : calcium-channel blocker with a rapid onset of action.It can, however , cause sever headache that mimic worsening disease.
Hydralazine : arterial vasodilator , used IV in sever pre-eclampsia.


So sever form of pre-eclampsia , IV infusion of hydralazine/labetolol can be titrated rapidly against changes in the BP.
Management of eclampsia :
Maintain an open air way by mouth piece & oxygen .
maintain an 2 IV line & take blood samples for :
Blood group &Rh.
CBC & Blood film.
LFT
RFT
Serum uric acid.
Coagulation profile.
Control fit by giving magnesium sulphate which is given IV as bolus dose directly & maintenance dose over 24 hours after last fit.
control BP by hydralizin / labetolol IV .
Close observation of vital sign (PR,RR,BP,Temp.), urine output ,patellar reflex&clonus.
Assessment of fetal condition & immediate delivery.

Magnesium sulphate (MgSO4)

*Centrally acting anticonvulsant drug.
* act as membrane stabilizing agent.
* can be given iv or im but preferable iv
* Is the drug of choice (1st drug of choice) in the acute phase treatment of eclamptic fit.
*4-6 g given iv slowly over at least 10 min to arrest fit, then maintain on 1g / hr iv in drip for at least 24 hr from the last fit.
*should be monitored carefully while giving it because of its toxicity by:
1.measuring its level in the blood
2.monitering the following
a) respiratory rate.
b) urine output.
c) patellar reflexes (1st sign to disappear in MgSO4 toxicity).
* antidote of MgSO4 toxicity is calcium gluconate10%, 10 ml over 10 min given iv.


Chronic Hypertension :

Essential hypertension is the underlying cause in 90% of cases.

Before a diagnosis of essential hypertension is made,other causes of chronic hypertension should be excluded which are :
Renal disease:
glomerulonephritis.
Polycystic disease.
Diabetic nephropathy.
Renal artery stenosis.
Collagen vascular disease :
-SLE
- scleroderma.
Coarctation of the aorta.
Endocrine causes:
-phaeochromocytoma.
- conn s syndrome.
Irrespective of the underlying cause , the principal concern is that these women may develop superimposed pre-eclampsia(1/3).

Treatment:

1.mild(BP<150/100): no need for immediate treatment,however , the pregnancy should be monitored carefully to detect any rise in BP or features of pre-eclampsia or IUGR.
2. BP>150/100:antihypertensive medication is recommended which includes:
Methyldopa
Labetolol
Nifedipine.
Aim of treatment is to maintain the BP < 160 mmHg &100-110 mmHg diastolic.
It is reasonable to await spontaneous labour or attempt vaginal delivery by induction at 38 weeks


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