2. INTRODUCTION
Hypertensive disease is used for all forms of
hypertension occurring in pregnancy and may
complicate 5-7% of all pregnancies.
In Africa, it constitutes major threats to maternal
life during pregnancy, labor and immediate post
partum period.
In fact it ranks amongst the four most prominent
contributors to maternal death. The incidence varies
among different regions, countries and hospitals.
3. CLASSIFICATIONS
i. Pre-eclampsia / Eclampsia
ii. Chronic Hypertension (Essential or Secondary)
iii. Pre-eclampsia superimposed on chronic
hypertension
iv. Gestational Hypertension (Pregnancy induced
hypertension – PIH)
4. SIMPLE DEFINITIONS
Hypertension :
It is usually defined as a systolic blood pressure
(SBP) of 140mmHg and above and a diastolic B.P (DBP) of
90mmHg and above.
It can also be defined as an increase of 30mmHg or more
in SBP and increase of 15mmHg or more in DBP. This is
more appropriate in our settings.
A blood pressure at least 2 standard deviations above the
mean or above the 95th
percentile for that gestation.
Increase in mean arterial blood (MAP) pressure of
20mmHg or a MAP of 105mmHg or greater if prior
blood pressure is not known.
MAP = Systolic pressure + Diastolic Pressure x 2
3
5. Significant proteinuria
It is defined as the presence ≥ 300mg/L in a 24hour
urine sample.
Accurate quantification relies on a 24hour collection.
However, a protein measurement of 2+ or greater in at
least two random urine specimen collected 6 or more
hours apart, is also significant.
6. Contamination by vaginal discharge, semen, liquor
amnii or blood
Urinary tract infection
Schistosmiasis in endemic areas
Chronic renal disease
Malaria
Sickle cell disease
Severe anaemia.
Other causes of proteinuria
include: -
7. Oedema
It is non specific generalized accumulation of
fluid which affects more than 50% of pregnant population
thus it is non-discriminatory. Same as unusual rapid weight
gain (>0.5kg/week).
Pre-eclampsia
This is the development of hypertension accompanied by
proteinuria with or without oedema, occurring in the
second half of pregnancy in a previously normotensive,
non-proteinuric woman. It is essentially a disease of
primigravida.
8. Eclampsia
This is the occurrence of generalized convulsions in a
pre-eclamptic patient during pregnancy, labour or in
early puerperium in the absence of coincidental
neurological disease.
Chronic Hypertension
This is hypertension occurring in pregnancy in a woman
known to be hypertensive before the pregnancy, with or
without proteinuria. It usually occurs before 20th
week
gestation and may be essential or secondary.
9. Essential hypertension is usually idiopathic and is the
cause in most cases. Other cases may be secondary to:
1.) Renal disease following:
Chronic glomerulonephritis
Polycystic kidney disease
Diabetic nephropathy
Chronic pyelo-nephritis
Renal artery stenosis
10. Others are secondary to
2.) Coarctation of aorta
3.) Phaechromocytoma, primary aldosteronism,
thyrotoxicosis – Endocrine causes.
4.) Collagen vascular disease e.g. systemic lupus
erythematosus, scleroderma.
Pre-eclampsia superimposed on chronic hypertension:
This is the condition in which a known chronic
hypertensive patient develops proteinuria and/or oedema
during pregnancy.
11. Gestational hypertension (PIH)
This is the development of hypertension in the latter half
of pregnancy or during labour without other evidence of
pre-eclampsia or chronic hypertensive vascular disease
which usually regresses with delivery of the baby (at most
14th
day).
In these patients, there is hypertension but no
proteinuria. It may re-occur and they are predisposed to
essential hypertension later in life. The outcome of
pregnancy is usually good.
12. Definition:
This is the development of hypertension accompanied by
proteinuria with or without oedema, occurring in the
second half of pregnancy in a previously normotensive,
non-proteinuric woman. It is essentially a disease of
primigravida.
# complicates 2 – 3% of pregnancies
PRE - ECLAMPSIA
13. It is a disease of theories. Multiple theories proposed but
to date there is no single satisfactory unifying explanation.
It appears there is an imbalance in factors causing
vasospasm and factors causing vasodilatation in maternal
blood vessels.
It is also attributed to the total or patchy failure of
trophoblast invasion of the myometrial segments of spiral
arteries. It is not clear why the trophoblast invasion fails
but the more complete the failure, the more likely PET will
result.
Aetiology:
14. There is inadequate maternal antibody response to the
fetal allograft resulting in fetal allograft rejection.
Thus, vascular damage from circulating immune
complexes in some pregnant women. Examples of
support for this theory are nulliparous women or
women who have changed their partners in subsequent
pregnancies. These women have limited fetal and
hence paternal antigen exposure resulting in PET.
Immunologic theory:
15. The basis is on the damage to the placenta which can
cause release of thromboplastin. Thromboplastin then
cause DIC and fibrin deposition in the kidney and
placenta resulting in development of hypertension and
placental insufficiency.
This is evidenced by decrease in number of circulating
platelets, increase in fibrin degradation products,
reduction in fibrinolytic activity observed in some cases
of pre-eclampsia.
# molar pregnancy, abdominal pregnancy
Disseminated intravascular coagulation (DIC)
theory:
16. Nulliparity
Multiparous with PET in previous pregnancy and/or >10
years subfertility
Extremes of age i.e. more common in <20years and
>35years
Very obese women - BMI > 35kgm2
Family history of pre-eclampsia
Risk factors:
17. Pre-existing hypertension, renal disease
Pre-existing vascular disease e.g. Collagen vascular
disease
Enlarged placenta as in Diabetes mellitus, multiple
gestation, hydropic pregnancy and molar gestation.
Prolonged exposure to paternal antigens thus can reoccur
with the same partner at a later gestation. A new partner
increases risk of re-occurrence.
Risk factors contd:
18. Classification:
Based on Diastolic blood pressure measurements
Mild: B.P ≥ 140/90mmHg (90-100)
Moderate: Diastolic of 100 – 110mmHg
Severe: ≥110mmHg i.e. 160/110mmHg
19. Clinical features:-
May have no symptoms especially in mild cases.
Increased blood pressure.
Proteinuria
Fluid retention causing oedema ( especially non
dependent oedema )
Brisk reflexes
Uterus and fetus small for gestational age.
Cerebral manifestation in severe cases include
headaches, dizziness, tinnitus, drowsiness, change in
respiration, hypereflexia; tachycardia and fever.
Visual changes: blurred vision, diplopia
Gastrointestinal symptoms: epigastric pains, nausea and
vomiting
Renal symptoms: oliguria, anuria, haematuria &
haemoglobinuria.
Signs of HELLP syndrome
20. Haemoglobin / packed cell volume. Elevated due to
haemoconcentration
Platelet count. If <150,000/L or falling, show severity
Serum electrolyte, urea and creatinine
Liver functions tests
Clotting profile – prothrombin time, partial thromboplastin
time
Full blood count
Urinalysis, microscopy culture and sensitivity
Ultrasound scans – obstetric for fetal monitoring
Investigations:
21. Uric acid
Uric acid levels are particularly useful in diagnosing and
monitoring the patient because increased levels occur
early and reflect the severity of the disease.
Renal scan
24 hour urinary protein / creatinine clearance
ECG and echocardiography
Investigations Cont.
22. In the management, the following principles are applied:-
Control hypertension to stop further progression of the
disease.
Prevent fits
Safe mother followed by delivery of a life mature baby.
The ultimate aim of management of pre-eclampsia is safety
of the mother first. In severe cases the fetus is
sacrificed in the interest of the mother. The ultimate cure
for pre-eclampsia is delivery and a decision needs to be
taken as to when to deliver.
Management:
23. The decision between expectant management and immediate
delivery will depend on the severity of the disease process,
maternal condition and gestational age. If a decision is taken
for immediate delivery, mode of delivery will depend on the
condition of the fetus and cervical effacement.
For mild cases, bed rest is good therapy for fetal survival
because it reduces blood pressure, improves utero placental
flow and aids fetal growth such that the fetus is matured
enough to decrease prolonged neonatal intensive care admission.
Management Cont...
24. For moderate to severe cases, anti-hypertensive agents
are needed and also sedatives. A wide variety of
antihypertensives are used.
The ideal hypertensive should:-
Lower BP effectively, predictably and permanently
Ensure fetal growth and well being by increasing utero
placental blood flow.
Reverse renal vascular spasm and prevent pathological
changes.
Be safe and free from side effects to mothers and
babies
Be convenient to use with reasonable margin of safety
Management Cont...
25. Labetalol: This is the first line drug used. It is an alpha
and beta blocker. Can be given intravenously in acute
cases. It reduces blood pressure, proteinuria and helps
in lung maturation
Hydralazine: Causes peripheral and central vasodilation
because it has direct action on vascular smooth muscle.
It increases cardiac output so causes reflex tachycardia.
It improves renal and uteroplacental blood flow.
26. Methyl dopa: Is another drug which acts on hypothalamus. Its
side effects are sedation, depression, nightmares.
Nifedipine: a calcium channel blocker
Magnesium Sulphate: Is very useful in severe cases for
prevention of fits
Diazepam: a sedative
Fetal assessment:
Measure symphysiofundal height daily
Daily fetal kick chart
Non stress antenatal cardiotocogram done daily where
available.
Serial ultrasound scans.
If fetus is in jeopardy, it is always best to deliver.
27. Bed rest with constant fetal and maternal monitoring is
key to success till pregnancy reaches term.
However, with worsening fetal and maternal condition e.g
uncontrollable blood pressure, worsening proteinuria,
IUGR, decreased fetal kick, then delivery must be
accomplished.
28. Should be supervised in a tertiary institution
Induce labour anytime after 38weeks because vaginal
route will provide least haemodynamically stressful
outcome if no contraindication.
Elective C/S on purely obstetric grounds or if patient is
remote from term and cervix is unfavourable for induction.
Labour should be as short as possible and second stage
shortened with use of vacuum or forceps.
Avoid use of ergometrine
Paediatrican needed.
Labour and Delivery:
29. Intra uterine growth restriction
Oligohydramnios
Abruption
Placental infarcts
Uteroplacental insufficiency leading to still births
or
neonatal deaths.
Prematurity
Complications – Fetal
31. Tends to complicate first pregnancies. When it occurs
in multipara, look for associated conditions.
Reoccurrence can occur especially in patients with
chronic hypertension. Complications correlate with age of
patient and severity of disease.
Women with chronic hypertension especially with end
organ damage should avoid pregnancy.
Prognosis:
32. Difficult because, etiology is diverse.
However, low dose aspirin known to help if given to women
at high risk of pre-eclampsia after 12weeks of gestation.
It is not useful once the disease has developed.
Calcium supplementation
Fish Oils
Anti-oxidants Vitamins C and E (reduced anti-oxidant
status)
Prevention
33. Introduction
This is derived from a Greek word, “To shine forth”
or “like a Bolt from the blue”. It is a multi
systemic disorder which results in tonic-clonic fits
and loss of consciousness.
It tends to occur more often in low socio-economic
groups. It is one of the serious obstetric
emergencies seen in our sub region and requires
active management to prevent maternal mortality
or morbidity.
ECLAMPSIA
34. Defined as occurrence of fits or seizures in a patient with
signs and symptoms of pre-eclampsia in the absence of
underlying neurologic disease.
Pathophysiology:
Major cause of the pathological changes seen in eclampsia
is cerebral vasospasm leading to ischaemia, disruption of
the blood brain barrier and cerebral oedema. This
vasospasm occurs in all the vessels leading to ischaemic
changes in most organs.
Also, the release of micro thrombi following endothelial
damage.
Definition
35. Brain
Irregular excitation impulses and rapid neurological damage lead to
convulsions.
Kidney:
Glomeruli capillaries became oedematous and cause swelling of the
basement membrane.
Decreased renal blood flow to capillaries cause arterial spasm which
leads to renal ischaemia causing decreased renal perfusion and
decreased glomerulo filtration rate (GFR). This will cause selective loss
of proteins e.g albumin causing proteinuria
Acute tubular necrosis or if more severe cortical necrosis results in
oliguria and haematuria. The pathologic damage to the kidneys in
eclampsia is termed Glomeruloendotheliosis
36. Retina:
Retinal oedema, haemorrhage and exudates lead to retinal
detachment causing partial or total blindness.
Liver:
Subcapsular oedema and hepatic necrosis. Seen more on the right lobe
than left. Due to deposition of fibrin thrombi in liver capillaries. This
Will lead to increased liver enzymes which usually resolves.
However, a rare complication is rupture of the liver and is of bad
prognosis. It causes up to 60% fetal loss and 24% maternal loss
Lungs:
Pulmonary oedema. Alveolar haemorrhages and fibrin deposition
leads to bronchopneumonic changes which cause aspiration pneumonitis.
Fluid overload worsens the pulmonary oedema.
37. Heart
Generalized vasospasm, increased peripheral
resistance, increased left ventricular work index.
Subendocardial haemorrhages may involve muscles leading to
cardiac conduction aberration.
Adrenals
Haemorrhage into adrenal glands can cause
abdominal pains and shock.
38. Blood System:
Haemoconcentration leads to increased haematocrit
and packed cell volume. The intravascular space is
reduced.
Increased haemolysis of red blood cells resulting in
decreased platelet count.
A fall in plasma colloid osmotic pressure leads to
generalized oedema. Blood coagulation state increases
due to higher blood viscosity.
Micro thrombi formation will lead to increased fibrin
degradation products, increased fibrinolysis and DIC
ultimately.
39. Placenta:
Red infarction of placental bed because of intravascular
obstruction or thrombi deposition. Sizes and number of
infarcts said to determine degree of hypertension.
Arteriospasm in placenta leads to reduction in placental
perfusion rate thus will influence metabolic
equilibrium of fetus.
Most of the complications of Eclampsia are as a result
of the pathological damage to the organs which may be
reversible in some cases.
40. Clinical features
Basically those of pre-eclampsia except that they
are worsening.
Severe hypertension (>160/110mmHg),
Severe proteinuria,(> 5g in 24hours , ++ or more with
dipstick urinalysis)
In addition, headaches, visual symptoms e.g. flashes of
light, epigastric pain, vomiting, increased tendon reflexes,
oliguria (<400mls in 24hours), overt hemolysis.
It may present with few warning signs especially in those
with mild disease.
Most times the patients are unbooked rushed to the
hospital in an unconscious state after having fitted at
home with injuries sustained during the convulsion (bitten
tongue, mouth injuries).
41. Principles of Management
Resuscitation
Abort fits and prevent further fits
Effect delivery after resuscitation
Post delivery management of complications
First Aid Measures
Nurse as an unconscious patient.
Position on left side to reduce risk of aspiration of
secretions.
Management:
42. Airway should be protected so insert a padded tongue
blade or an airway. Suction to clear secretions. Give
oxygen to maintain adequate oxygenation.
Breathing should be maintained. Monitor vital signs and
auscultate lung bases to rule out pulmonary oedema.
Circulation: Establish an intravenous line to hydrate
patient and administer the necessary drugs especially anti
convulsants.
Also, pass a self retaining urethral catheter to monitor
urinary output.
Drugs given include antihypertensives, anticonvulsants and
antibiotic prophylaxis especially for pulmonary oedema and
in those with aspiration pnemonitis.
Early delivery
43. Blood, urea and electrolytes
Serum creatinine
Uric acid
Full blood count, blood film and platelets, group &
crossmatch blood
Liver function tests
Urine analysis microscopy, culture and sensitivity
Retinoscopy
Clotting profile
Investigations
44. Diazepam
Phenytoin
Magnesium sulphate is the drug of choice. It is a
safe and effective agent to prevent and treat
convulsion however, it can cause somnolence, respiratory
depression, absence of deep tendon reflexes, oliguria and
cardiac arrest in extreme cases.
Therapeutic levels are 4 – 8 mEq/l
Lytic cocktail which is a mixture of chlorpromazine
(largactil), promethazine (phenergan) and pethidine
Anticonvulsants
45. Chlormethiazole – obsolete
Bromethol contraindicated in pulmonary oedema
Barbiturates e.g thiopentone good anti convulsants but
depress fetal respiration.
Paraldehyde causes injection abscess
Morphine and Chloral hydrate no longer used
Antihypertensives are as in Pre-eclampsia
46. Delivery should be done after maternal condition is
stabilized.
The aim is usually for delivery by the fastest possible
means within 6hours of the first eclamptic fit. Aim for
a vaginal delivery unless there are contraindications.
Give adequate analgesia,
Shorten second stage,
Avoid ergometrine in third stage.
There should be increased vigilance in the first 48 hours
of the peurperium because failure to recognize a
deteriorating condition will result in death commonly
from DIC, renal failure and Adult respiratory distress
syndrome (ARDS)
Delivery
48. Maternal:
Cerebral haemorrhage - cerebral accidents
Blindness
Acute pulmonary oedema
Aspiration of vomit during convulsions - Aspiration pneumonitis
Cardiovascular accidents - congestive cardiac failure (left
ventricular failure)
Acute renal failure
Acidaemia - hyperventilation from acidosis due to several fits or
prolonged coma.
Hyperpyrexia: Damage to temperature regulating centre in mid
brain by anoxia which causes strain on the heart. Can cause
death from circulatory failure.
Rupture of liver capsule
DIC
HELLP syndrome
Complications:
50. Loading dose:
4g of 20% IV over 5 minutes.
10g of 50% solution, 5g in each buttock as deep IM
injection with 1ml of 2% lignocaine to dilute.
If still convulsing after 15minutes give 2g of 50% IV over
5 minutes.
It causes a feeling of warmth.
Magnesium Sulphate regime
51. Maintenance dose:
5g of 5% solution with 1ml of 2% lignocaine by deep
IM injection into alternate buttocks every 4 hours.
Continue for 24hrs after delivery or last convulsion.
You can give 1g of 20% solution every hour by
continuous IV infusion if above not available.
If respiratory rate is < 16/min, absent patellar
reflexes or urine output < 30mls/hr over preceding 4
hours stop MgSO4 and give antidote which is Calcium
gluconate 1g (10ml of 10%) IV slowly until it
antagonizes and respiration normalizes.
