4. Introduction
Hypertensive disease in pregnancy is a major
cause of maternal and fetal morbidity and
mortality in the developing countries as well
as in the developed countries. It is one of the
most common causes of perinatal morbidity
and mortality, resulting in an estimated 35-
300 deaths per 1000 births/year worldwide,
depending on neonatal support capabilities of
the hospital delivering care. This mortality
rate is almost double that of normotensive
pregnancies.
5. Hypertensive disorders account for about 50,000
maternal death worldwide/year (Duley et al 1992) and
majority of these death occurs in the developing
countries.
In Tanzania about 15% of pregnant mothers die every
year due to PIH, and in MNH about 22% of maternal
death are caused by the PIH.
6. Prevalence
In the US: Preeclampsia is a complication
in approximately 12-22% of all
pregnancies.
In the general population prevalence is
about 6%, but this varies with the
geographical location, eg along the EA
cost the prevalence of PIH is higher
compared to highlands in the same
location. Duringcold season there is
peaking of the prevalence of PIH both in
coast areas of Africa and in mountain
areas of Latin America.
7. Classification of HDP.
Pt are considered to have hypertension if they have
either of the following
Systolic BP>140mmhg and DBP>90mmhg.Rise in
SBP>30mmhg and /rise in the DBP>15mmhg from
preconception or 1st trimester reading confirmed by
reading 6hrs apart
8. Gestational hypertension
Transient PIH if preeclampsia is present at the time of
delivery and BP is normal 12/52 after delivery.
Chronic PIH if BP persist 12/52 after delivery.
9. Preeclampsia- this is a syndrome xterised by HTN,Protinuria,
oedema,epigastic pain,visual disturbance and headache.
Eclampsia –the same as in preeclampsia but with the presence of fits.
10. Chronic hypertension
Essential
Sec to renal disease ,endocrine disease,
vascular abnormalities.
Chronic HTN with superimposed preeclampsia
11. Etiology and predisposing
factors
Age:PIH/ Preeclampsia usually occurs in women at both
extremes of reproductive age; however, the risk of
preeclampsia is greatest in women younger than 18
years and older than 35years.
12. Maternal risk factors for
preeclampsia
First pregnancy
New partner/paternity
History of preeclampsia
Family history of preeclampsia in a first-degree relative
13. Black race, Black women have higher
rates of preeclampsia complicating their
pregnancies compared to other racial
groups, mainly because they have a
greater prevalence of underlying chronic
hypertension. Among women aged 30-39
years, chronic hypertension is present in
22.3% of black people, 4.6% of white
people, and 6.2% of Mexican Americans.
Hispanic women generally have blood
pressure levels that are the same as or
lower than those of non-Hispanic white
women.
14. Medical risk factors for
preeclampsia
Chronic hypertension
Secondary causes of chronic hypertension
such as hypercortisolism,
hyperaldosteronism, pheochromocytoma,
or renal artery stenosis
Preexisting diabetes (type 1 or type 2),
especially with microvascular disease
Renal disease
Systemic lupus erythematosus
Obesity
Thrombophilia
16. Pathophysiology of
preeclampsia.
Although the exact pathophysiologic
mechanism is not clearly understood,
preeclampsia can be thought of as a
disorder of:
Endothelial dysfunction with vasospasm.
Rejection phenomenon(insufficient
production of blocking abs)
Imbalance between prostacyclin and
thromboxane A
Membrane fluidity.
Others like genetic predisposition
17. Rejection
phenomenon(insufficient
production of blocking abs)
The presence of the placenta is thought to be the
primary in the causation of PIH.During placenta
development the trophoblastic tissues invade both
myometrium and decidual cells in 2 ways:
Interstitial invasion - anchoring the placenta
18. Endovascular invasion- invades the maternal spiral
arteries and replaces the endothelium by
destroying the medial elastic tissues and muscular
tissues of the arterial wall. The arterial wall is
replaced by the fibrinoid material and form a
saclike structure. Fraction of spiral uterine
arterioles fails to dilate in the same way as in
normal pregnancy, thus decreasing the blood
supply to fetus (Khong et al, 1986). Electron
microscopic studies have shown characteristic
damage to endothelial cells that is somewhat
similar to that of vessels in transplanted but
rejected kidney. This observation has led to
suggestion that immunological mechanisms i.e.,
rejection of the fetus by maternal immune
system, may be operative in preeclampsia
(Kitzmiller and Benirschke, 1973).
19. PIH develops followings partial process of
placentation, the invaded arteries in the
1st phase is complete where as the 2nd
phase is partial and the myometrial
portion of the spiral arteries retain their
reactive musculoelastic walls.There is
development of acute atherosis in the
spiral arteries and this lesion is xterised
by fibrinoid necrosis of the arterial wall
and obliteration with corresponding area
of placental infarction.
20. Endothelial dysfunction
with vasospasm
Endothelin 1,2&3 are strong
vasoconstrictors released by endothelium
of blood vessels,kidney and CNS tissues.Its
fns is to cause vasoconstriction in the
control of placental blood vessel after
delivery and closure of the ductus
arteriousus in the new born.
Disruption of endothelial integrity caused
by the hypoxic condition created by the
placental insufficient would also be
associated with a general loss of
vasodilator capacity, which could account
for the enhanced pressor response to
angiotensin II and noradrenaline.
21. Imbalance between
prostacyclin and
thromboxane A
Prostacyclin is synthesized by the cell of endothelium
with the aid of cyclooxygense enzyme . Prostacyclin,
one of the prostaglandins, is a very potent vasodilatator
produced by the endothelium. Vessels of preeclamptic
women and umbilical veins of their fetuses produce far
less prostacyclin as compared with normal pregnancy
(Dadak et al., 1982).
22. Nitric oxide is another vasodilator produced by
endothelium (EDRF, endothelium-releasing factor)
which acts synergistically with prostacyclin (Moncada et
al., 1991). Nitric oxide production is also decreased
because of endothelial cell injury. Therefore it seems
clear that endothelial injury and decreased production
of vasodilatators play a major role in pathogenesis of
PIH
23. TA is generated by the platelets with the aid of
cyclooxygenase enzyme and is a strong vasoconstrictor.
Therefore imbalance btn PI&TA due to damage of
endothelium will favor vasoconstriction and platelets
aggregation hence worsen PIH.
24. MEMBRANE FLUIDITY
Changes in the cell membrane that affect the
functioning of receptors may also be
important in pregnancy induced hypertension
and pre-eclampsia. In studies using platelets
as models of vascular smooth muscle, the
density of binding sites for angiotensin II was
lower in women during a normal pregnancy
than in those who were not pregnant but was
unchanged in women with established
disease. A prospective study showed that
although primigravidas who remained
normotensive showed a very rapid fall in
binding site density during the first few weeks
of pregnancy, nulliparous women who
developed pregnancy induced hypertension
never showed such a fall. Membrane fluidity
is altered in established pregnancy induced
hypertension and pre-eclampsia
25. Pathogenesis of the disease
PIH is a mult-organ disease; therefore the
clinical presentation will involve several
organs as follows:
CNS
Brain tissues have a wide range of
autoregulation of BP and have a constant
cerebral perfusion at 55ml/min in the same
wide range (60-140 MAP).
When the BP rise and the autoregulation fails
then the endothelial tight junction open and
cause leakage of plasma and RBC to the
extravascular space (petechial h’ge or
intracranial h’ge
26. Pathology
Fibrinoid necrosis
Thrombosis of arteriole
Microinfarct and petechial h’ge
The brain stem and basal ganglia are
more affected compared to the other
parts of the brain.
Other parts include in the watershed area
–occipital and parietal areas where
anterior, middle and posterior meningeal
arteries meet.
Brain edema is common in prolonged
coma.
27. R/S
Pulmonary oedema which may be
cardiogenic or non-cardiogenic
It is very common after delivery either
due to over infusion of fluid in the
treatment of ARF or blood loss, or due to
delayed mobilization of intravascular fluid
to the intravascular compartment.
It may occur in the pt with underlying
heart disease, systolic dysfunction or in
aspiration of gastric content following
eclamptic fits and this may lead to
chemical pneumonitis or airways
obstruction from particulate matters.
28. CVS
Contracted intravascular compartment due to
generalized vasoconstriction and extravasations of fluid
to the extravascular compartment due to reduced
oncotic pressure (low albumin).
29. LIVER
HELLP syndrome
Subscapular h’ge
Elevated total bilirubin>1.2mg/dl
Decreased protein synthesis
33. ENDOCRINE
Estrogen increases production of rennin substrate,
rennin activity as well as AII
Plasma Aldosterone is also increased .
34. Clinical presentation &
diagnosis
History: Mild preeclampsia does not involve clinical
evidence of end-organ pathology, except for minimal
proteinuria. Severe preeclampsia is characterized by
end-organ damage due to systemic vasoconstriction.
Features of the history may include the following:
35. Headache
RUQ abdominal pain
Decreased urine output
Shortness of breath or dyspnea on
exertion
Hand and facial edema
Visual disturbances
Confusion and apprehension
Nausea and vomiting.
36. Physical: Findings at physical
examination may include
thefollowing Sustained systolic BP increases by 30 mm Hg, and diastolic
BP increases by 15 mm Hg, or absolute BP higher than 140
mm Hg/90 mm Hg.
Severe preeclampsia (sustained systolic BP >160 mm Hg or
diastolic BP >110 mm Hg with end-organ damage)
Tachycardia
Tachypnea
Pulmonary edema
Alteration of mental status
Hyperreflexia, clonus
Localizing neurologic deficits
Cerebrovascular accident
Generalized edema
Small fundal height for estimated gestational age
Intrauterine growth retardation
37. Management
Investigation
Laboratory
FBP may reveal the following:
Anemia due to the microangiopathic hemolytic
anemia and dilution of pregnancy
Thrombocytopenia (platelet count <100,000) due
to HELLP syndrome
The serum creatinine is elevated due to
decreased intravascular volume and a
decreased glomerular filtration rate (GFR).
Liver function test (LFT) results may reveal
the following:
38. Aspartate aminotransferase (SGOT) level higher than
72IU/L, total bilirubin levels higher than 1.2 mg/dL,
lactate dehydrogenase (LDH) levels higher than 600
IU/L
Elevated levels due to HELLP syndrome
The coagulation profile may reveal a normal
prothrombin time (PT) and a normal activated
partial thromboplastin time (aPTT), fibrin split
products, and fibrinogen levels
Rule out associated disseminated intravascular
coagulopathy (DIC).
Urinalysis may reveal the following findings:
Proteinuria
Positive human chorionic gonadotropin (HCG) result
39. Imaging Studies:
CT scan of the head
Obtain a head CT scan in patients with severe
preeclampsia and associated neurologic
deficits.
This is used to assess intracranial hemorrhage
or cerebrovascular accident.
MRI
Transabdominal sonogram
This is used to estimate gestational age.
It also is used to rule out abruptio placentae,
which can complicate severe preeclampsia.
40. TREATMENT
This will involve pharmacological and non
pharmacological mgn.
In case the pt has mild pre-eclampsia
Admit for bed rest
Assess the GA
Do Lab and Radiological investigation.
Administer steroid in the premature baby
and plan for delivery if BP is not
responding
41. In case the pt has severe
pre-eclampsia./eclampsia
The aim should be at:
Prevention of convulsion
Control of BP
Induce labor and deliver
Prevent more organ damage
Monitor i/o of fluid .
42. Pharmacological mgn
Magnesium sulphate is the drug of choice. It is given in
several regimens depending on the availability of the
equipment for monitoring serum magnesium level.
Prevention of convulsion
In MNH we use I/V regime of 4g given as a bolus then
maintance dose of 1g/hr. (98%are below the therapeutic
level)
Other center use I/M regime of 14g as a bolus given as 4g
i/v then 10g i/m in @ buttock then maintenance of 4g
i/v./hr
Loading dose of 6gi/v then maintenance dose of 2g/hr(50%
are below the therapeutic level) and the maintanence
dose of 3g i/v /hr non will be below the therapeutic level).
The therapeutic level of mg sulphate is 2-3.5mmo/l (4.8-
8.4mg/dl).
43. Magnesium toxicity
Serum mgso4 symptoms
4mmol/l loss of DTR
5-6mmol/l respiratory
paralysis
15mmol/l cadiac arrest
Action of mgso4: it cause vasodilatation of
blood vessel, block ca entry into neuron
and decrease amount of acetylcholine
released at neuromuscular junction.
45. Control of BP
Sympatholytic agent- Methyldopa
Ca chanel blockers- Nifedipine
Vasodilators - Hydralazine
Loop diuretics indicated only when there is sign of
pulmonary oedema
46. Prevention of
preeclampsia/eclampsia
Health education to the pregnant mothers
and the society about the danger sign.
Frequent ANC visit will be insuffient to
reduce the incidence of eclampsia, rather
drs and nurses should have life saving
skill available when the unforeseeable
preeclampsia occurs
Early referral of the pt
Equipped with anticonvulsant drug .
Use of ASA prophylactically in high risk
patient .
47. Reference
Williams textbook of obstetrics 20th edition
Current OBS & GYN internation edition
Dewhurt’s OBS &GYN for postgraduates6th edition
Maternity care in developing countries by Lawson
ACOG practice bulletin no 33, 2002
Online
