Hypertensive Disorders in Pregnancy

Hypertensive Disorders in Pregnancy

Hypertension is one of commonest complications of pregnancy and it is a common cause of fetal and maternal morbidity and mortality.
It complicates 8-11% of all pregnancies.

Classification of hypertension:

Pre-existing (chronic) hypertension:
Hypertension is present before pregnancy, detected in early pregnancy (before 20 weeks in absence of vesicular mole) and postpartum.

Examples:

Essential hypertension.
Secondary to chronic renal disorders e.g. (pyelonephritis and renal artery stenosis).
Coarctation of the aorta.
Systemic lupus erythematosus.
Pheochromocytoma.

Classification:

Pregnancy-induced hypertension (PIH):
Transient hypertension:
Late onset hypertension, without proteinuria or pathologic oedema.
Pre-eclampsia:
Hypertension with proteinuria and / or oedema after 20 weeks of pregnancy, but may be earlier in vesicular mole.
Eclampsia:
Pre-eclampsia + convulsions.


Classification
Superimposed pre-eclampsia or eclampsia:
Development of pre-eclampsia or eclampsia in pre-existing hypertension detected by a further increase of 30 mmHg or more in systolic blood pressure or 15 mmHg or more in diastolic blood pressure.

Pre-eclampsia:

Incidence:
5-10%.

Aetiology:

Although eclampsia had been described since 200 years, no definite aetiology is found for PIH and it is still a disease of theories.

Predisposing factors:

• Primigravidae more than multigravidae.
• Pre-existing hypertension.
• Previous history of pre-eclampsia.
• Family history of pre-eclampsia.
• Hyperplacentosis i.e. excessive chorionic tissue as in hydatidiform mole, multiple pregnancy, uncontrolled diabetes mellitus and foetal haemolytic diseases.
• Obesity.
• Climatic variations.

Theories:

The uteroplacental bed:
In early pregnancy, the cytotrophoblasts invade the decidual arteries making their musculature more flaccid and dilated. During the second trimester of normal pregnancy, a second wave of invasion occurs into the myometrial segments of the spiral arteries. If the second invasion does not occur pre-eclampsia develops.

Theories:

Immunological factor:
Stimulation of the maternal immune system by the early conceptus is essential for production of the blocking factors that prevent rejection of the foetus and placenta. Hypo immune response results in damage of the placenta and subsequent pre-eclampsia.

Theories:

Genetic factor:
A maternal autosomal recessive gene or a foetal genetic component could be responsible. An increase in HLA-DR4 (subtype of human leucocyte antigen) has been noted in pre-eclamptic women.

Theories:

Renin- angiotensin system:
It was found that the vascular sensitivity to angiotensin II is reduced in normal pregnancy while it increases in PIH.
Angiotensin II-binding sites on platelets increase in women with PIH in comparison with normal pregnancy. This can identify the women in risk of developing PIH and hence prophylaxis against it can be achieved by anti-platelets as aspirin.


Theories:
Atrial natriuretic peptide (ANP):
It’s release is stimulated by volume expansion and increase in atrial pressure. It is increased in normal pregnancy to ameliorate the effect of the increased angiotensin II. Actually, there is no evidence that there is decrease in ANP in PIH, but in contrast, it may be increased as a response to increased blood pressure.

Theories:

Prostaglandins:
Prostacyclin is a vasodilator and an inhibitor for platelets aggregation while thromboxane is a vasoconstrictor and platelets aggregator. In PIH, there is imbalance towards an increase in thromboxane production.

Theories:

Neutrophils:
Neutrophils activation causes damage and dysfunction of the vascular endothelium leading to platelets aggregation, coagulation activation, hypertension and proteinuria.

Pathological Changes:

Vasospasm
The vascular changes and local hypoxia of the surrounding tissues lead to haemorrhage, necrosis and others.
Central nervous system: ischaemia, haemorrhages and oedema.
Liver: subcapsular haemorrhage, periportal necrosis and infarctions.

Pathological changes:

Endocrine glands: necrosis and haemorrhage in pituitary, pancreas and adrenal glands.
Heart and lungs: myocardial and endocardial haemorrhage and necrosis.
Lungs show haemorrhage and secondary bronchopneumonia.


Pathological Changes:

Kidney: decrease in renal blood flow glomerular damage (glomerular endotheliosis) leading to:

• Decrease glomerular filtration rate by about 50%,

• Loss of protein in urine (albuminuria),
• Elevated serum levels of uric acid, urea and creatinine. Serum uric acid level is diagnostic and prognostic for severe pre-eclampsia.

Pathological changes:

Placenta:
• Reduced utero-placental blood flow leading to intrauterine growth retardation (IUGR) and even death.
• Placental thrombosis, infarction and abruptio placentae.
• Retina: Vascular spasm, haemorrhage, exudate and rarely retinal detachment in severe cases.

Pathological Changes:

• Coagulation status
• Fibrin production is increased.
• Fibrinolytic activity is decreased.
• Factor VII, factor VIII- related antigen and fibrin/ fibrinogen degradation products (FDP) concentrations in the plasma are all increased.

• Fibrin and platelet deposition is increased particularly in the placental arteries.

• Thrombocytopenia.
• Platelets are activated in the microcirculation of the placenta, kidney and liver, release their products as 5-hydroxytryptamine and re-enter the circulation in an exhausted state, unable to respond normally to aggregating agents.


Pathological Changes:
The end result of these changes is hypercoagulability and disseminated intravascular coagulation in severe pre-eclampsia and eclampsia.

Pathological Changes:

Sodium and water retention
There is haemoconcentration with fluid shift from the intravascular to the extravascular compartment.
HELLP syndrome is described in PIH which consists of: H = Haemolysis, EL= Elevated Liver enzymes, LP= Low Platelet count.

Diagnosis:

Signs
Hypertension:
Blood pressure of 140/90 mmHg or more or an increase of 30 mmHg in systolic and/ or 15 mmHg in diastolic blood pressure over the pre- or early pregnancy level.

Diagnosis:

• How to measure the blood pressure in pregnancy?
• The patient should rest for at least 30 min. after arriving to the clinic.
• Remove any tight clothing from the right arm.

Diagnosis:

• The patient lies comfortably on the left side that her back makes an angle of about 30o with the bed. The right arm is supported to be with the sphygmomanometer at the same level with the patient’s sternum i.e. her heart. Each cm above or below the level of the heart induces a difference of 0.7mmHg in blood pressure reading. She should lie undisturbed in this position for 2-3 min. before blood pressure is measured.


Diagnosis:
• The cuff should be applied to the right upper arm with the connecting tubes pointing downwards, the centre of the rubber bag in the cuff is directly over the brachial artery leaving ante-cubital fossa free.
• Apply cuff firmly but not tightly around the arm.

Diagnosis:

• Feel the brachial artery and apply the stethoscope directly over it without undue pressure.
• Pump up cuff rapidly to 20-30 mmHg above the point at which the pulse sound disappears, and take blood pressure reading without delay.
• Let air out slowly so that mercury falls steadily by 2-3 mm/sec.

Diagnosis:

Blood pressure measurement phases (Korotkoff):
• Korotkoff I Appearance of the sound systolic reading.
• Korotkoff II Accentuation of the sound.
• Korotkoff III Sound becomes harsh.
• Korotkoff IV Sound becomes muffled diastolic reading.
• Korotkoff V Disappearance of the sound.

Diagnosis:

• Korotkoff I and IV is the reading for systolic and diastolic blood pressure respectively. If you wait the disappearance of the sound to take the diastolic reading (as in non-pregnant state) you may reach down to zero because of the hyperdynamic circulation during pregnancy.

Diagnosis:

• Use the right arm for measuring because it is more convenient to the physician, but if the reading is 10 mmHg or more higher in the left arm use it in the future readings.
• The blood pressure should be measured in two occasions at least 6 hours apart.


Diagnosis:
• Proteinuria (albuminuria):
• It is urinary protein greater than 0.3gm/L in 24 hours collection or greater than 1gm/L in two random samples obtained at least 6 hours apart.
• It indicates glomerular damage and almost always occurs after hypertension.
• Proteinuria is usually in the range of 1-3 gm daily, of which 50-60% is albumin but in severe cases it may exceed 15gm.

Diagnosis:

Oedema:
It is weight gain of more than 1 kg in any one week or 2.25 kg in any one month.
Clinical oedema is present in about two-thirds of patients with PIH. However, two-thirds of pregnant women with clinical oedema do not develop hypertension.

Diagnosis:

• Symptoms
• These are usually manifestations of severe pre-eclampsia.
• Headache: usually frontal but may be occipital. It is due to cerebral oedema and hypertension.
• Visual disturbances: blurring of vision, flashes of light or blindness.

• Epigastric or right upper quadrant pain: due to enlargement and subcapsular haemorrhage of the liver.
• Nausea and vomiting: due to congestion of gastric mucosa and/ or cerebral oedema.
• Oliguria or anuria: due to kidney pathology.


Investigations:
• Complete urine examination: for proteinuria, pus cells, RBCs, casts, specific gravity, culture and sensitivity.
• Kidney function tests: serum uric acid > 6 mg % is abnormal during pregnancy. It is more specific for pre-eclampsia than creatinine.

• Coagulation status: Platelet count, fibrinogen and FDP as DIC may develop.

• Eye fundus examination.
• Tests for foetal well being: as
• ultrasound,
• daily foetal movement count,
• non-stress test,
• oxytocin challenge test (if needed).

Screening for PIH:

These are tests to predict the development of pre-eclampsia.
A. By tests depend on blood pressure measurement:
Roll-over test:
After resting in the left lateral position turning to a supine position induces a rise in diastolic pressure of 20 mmHg or more is indicative of tendency to develop pre-eclampsia. Subsequent reports have indicated that the test is less satisfactory.

Screening for PIH:

Mid-trimester mean blood pressure:
If the mean arterial blood pressure is more than 90 mmHg, the risk of developing PIH increases by over four folds.


Screening for PIH:
• Hand-grip test:
• Isometric (sustained) contraction of striated muscles is known to cause general sympathetic activation and hence increase systemic arterial pressure in healthy adults. The patient compresses an inflated sphygmomanometer cuff for a 3-minutes period at maximal and then at 50% of maximal voluntary contraction. An increase in diastolic pressure >20 mmHg at 28-32 weeks’ gestation is associated with an increased incidence of PIH.

Screening for PIH:

Forearm venous tone
There is an increase in forearm venous tone (veno-constriction) at least 6 weeks before the diagnosis of PIH. It requires a sophisticated equipment.

B. By investigation:

Urinary assays
• Micro-albuminuria: detected by radioimmunoassay before albuminuria can be detected by the ordinary methods. The drawback is that not all proteinuric pre-eclampsia are preceded by this phase.
• 24 hours urinary calcium excretion: is lower in women with pre-eclampsia than normotensive pregnant women.

• Kallikrein/creatinine ratio: is reduced in patients who develop PIH later on if compared to the increased ratio in normal pregnancy. Kallikrein is a blood pressure reducing agent.
• Prostaglandins metabolites: The end metabolite of prostacyclin is decreased while thromboxane B2 (the metabolite of thromboxane A2) is increased in urine of pre-eclamptic women.

Blood tests

• Plasma urate: serial increase is a warning of PIH before appearance of other clinical features.
• Platelet count: a reduction occurs early in pre-eclampsia.
• Anti-thrombin - III activity: begin to decline as much as 13 weeks prior to the development of clinical manifestations of pre-eclampsia.


Angiotensin II sensitivity
Sensitivity to infused angiotensin II: is increased may be due to alteration in vascular smooth muscle A II receptors.
Platelet AII binding: is increased before development of PIH.

Clinical classification :

Mild pre-eclampsia: blood pressure 140/90 mmHg ± oedema.
Severe pre-eclampsia:
blood pressure >140/90 mmHg + proteinuria ± oedema or
diastolic blood pressure >110 mmHg or
cerebral or visual disturbances.

• Imminent eclampsia: It is a state in which the patient is about to develop eclampsia. Usually there are:
• blood pressure much higher than 160 /110 mmHg,
• heavy proteinuria (+++or ++++),
• hyperreflexia,
• severe continuous headache,
• blurring of vision,
• epigastric pain.

• Fulminating pre-eclampsia: a rapidly deteriorating pre-eclampsia to be imminent eclampsia.


Differential Diagnosis:
Other causes of hypertension

Pre-eclampsia

Pre-existing (chronic) Hypertension
Parity
usually primigravida.
usually multigravida.
Past History
of pre-eclampsia may be present.
of hypertension in between pregnancies.
Hypertension
after the 20th week of pregnancy (except in vesicular mole) and disappears within 6 weeks postpartum.
before pregnancy, during the first 20 weeks and persists after 6 weeks postpartum.
Proteinuria
If present, it develops after hypertension.
If present, it develops before hypertension due to underlying renal disease.
Hyperreflexia
may be present.
absent.
Fundus Examination
Normal or retinal vessels spasm, oedema, exudate and papilloedema (oedema of the optic disc).
Sclerotic changes.
Serum Uric Acid
Its increase is not proportionate to serum creatinine
Its increase is propotionate to serum creatinine.


Proteinuria
• Other Causes of proteinuria
• Contamination of urine by vaginal discharge this is excluded by examination of a midstream sample after cleansing the introitus with sterile water or saline or by using a catheter.

• Urinary infection: excluded by microscopic examination and culture of urine.

• Congestive heart failure and severe anaemia due to hypoxia of the kidney.
• Orthostatic proteinuria: Proteinuria is detected at the end of the day while it is absent in the morning. This is due to pressure of the lumbar spines on the left renal vein during standing

Bed side test for proteinuria:

Add few drops of acetic or citric acid to 10 ml of clear urine in a test tube to prevent precipitation of phosphates and boil. If there is proteinuria, a white cloud will appear. Its amount and density indicate roughly the amount of proteins (+,++,+++or ++++).

Oedema

Other causes of oedema
General causes: cardiac, hepatic, renal or nutritional oedema.
Local causes: as inflammatory or deep vein thrombosis (usually unilateral).
Pressure of the gravid uterus: on the pelvic veins may produce ankle oedema.

Complications of Pre-eclampsia

• A. Maternal:
• Convulsions and coma (eclampsia).
• Cerebral haemorrhage.
• Renal failure.
• Heart failure.
• Liver failure.
• Disseminated intravascular coagulation.
• Abruptio placentae.
• Residual chronic hypertension in about 1/3 of cases.
• Recurrent pre-eclampsia in next pregnancies.


Complications
B. Foetal:
Intrauterine growth retardation (IUGR).
Intrauterine foetal death.
Prematurity and its complications.

Treatment

• Prophylactic
• Proper antenatal care:
• To detect the high risk patients who may develop PIH through the screening tests.
• Early detection of cases who are already developed PIH and examine them more frequently.

• Low dose aspirin:

• It inhibits thromboxane production from the platelets and the AII binding sites on platelets.
• A low dose selectively inhibits thromboxane due to higher concentration of such a low dose in the portal circulation than systemic affecting the platelets when pass through the portal circulation. The prostacyclin production form the systemic vessels will not be affected.

Treatment

Curative
Delivery of the foetus and placenta is the only real treatment of pre-eclampsia. As the conditions are not always suitable for this, the treatment aims to prevent or minimise the maternal and foetal complications (see before) till reasonable maturation of the foetus.

General measures:

• Hospitalisation: with complete bed rest more in left lateral position to prevent compression of the inferior vena cava. This lowers the blood pressure, induces diuresis, reduces oedema and increases renal and placental blood flow.
• High protein, low sodium diet.


• Observation:
• Maternal:
• blood pressure twice daily.
• urine volume and proteinuria daily,
• oedema daily,
• body weight twice weekly,
• fundus once weekly,
• blood picture including platelet count, liver and renal functions particularly serum uric acid on admission.

Foetal:

daily foetal movement count,
serial sonography,
non-stress and stress test if needed.

Medical treatment:

• Sedatives: as diazepam 2-5 mg every 8-12 hours.
• Antihypertensives:
• decrease the maternal cerebral and cardiovascular complications but do not affect the foetal outcome.

• Alpha-methyl-dopa (Aldomet):

• It reduces the central sympathetic drive.
• Dose: 250-500 mg every 6-8 hours up to a maximum dose of 4 gm/day. Its effect appears after 48 hours.
• A loading single dose of 2 gm may act within 1-2 hours.
• Side effects: headache, and nightmares.


Hydralazine (Apresoline):
It is a vasodilator, increases renal and uteroplacental blood flow.
Dose: 20 mg slowly IV initially followed by 5mg every 20 min. until diastolic blood pressure is 100-110 mmHg. This regimen is used for severe and acute hypertension. Oral hydralazine can be used in the chronic situation as a second line treatment in a dose of 25-75 mg/ 6 hours.
Side effects: tachycardia, headache, flushing, nausea and vomiting.

Calcium channel blockers (Nifedipine):

It is a vasodilator acting by blocking the Ca influx into smooth muscle cells.
It can be given sublingually (acts within 10 minutes) or orally (acts within 30 minutes) in a dose of 10-20 mg 2-3 times daily.
Side effects: headache and flushing.

Adreno-receptor blockers:

Examples: Labetalol, atenolol, oxprenolol and propranolol.
Side effects: may cause growth retardation, neonatal respiratory depression and hypoglycaemia.
Labetalol is an α and β blocker, causes vasodilatation and given in a dose of 100-200 mg three times daily (tds).

Angiotensin converting enzyme inhibitors:

Example: Captopril.
Inhibit the formation of angiotensin II from the angiotensin I.
Side effects: Foetal renal failure and neonatal hypotension.
It is used in treatment of postpartum hypertension.


Diazoxide (Hyperstat):
It is a potent vasodilator.
Dose: 15-30 mg IV and titrated against the blood pressure.
Side effects: hypotension and hyperglycaemia.

• Diuretics:

• Examples:
• "Loop" diuretics:
Furosemide (Lasix): 20-40 mg IV repeated at intervals of 2-4 hours.
Thiazides: better to be avoided in pregnancy.
• Osmotic diuretics: as mannitol or glucose 25% IV / 8 hours which also decrease brain oedema, supply energy and support the liver.

• Indications: Heart failure and pulmonary oedema.

• Side effects: aggravate the haemoconcentration due to loss of salt and water so it is better to be avoided.

• Other drugs:

• Dexamethasone: is effective in reducing cerebral oedema but its routine use is not recommended.
• Salt-free albumin or plasma protein fraction (PPF): indicated in an oedematous patient with low plasma osmolality and reduced central venous pressure (CVP).

• Antibiotics: for prophylaxis or treatment of infection particularly bronchopneumonia.

• Anticonvulsant therapy: e.g. magnesium sulphate (see below) may be started in case of imminent eclampsia.
• Digitalisation: to guard against or treat heart failure and pulmonary oedema if pulse is persistent >120/min. Digoxin 0.5 mg IV, followed by 0.25-0.5 mg daily.


Obstetric measures:
• Timing of delivery:
• Severe pre-eclampsia is usually treated conservatively till the end of the 36th week to ensure reasonable maturation of the foetus. Indications of termination before 36th week include:

• Foetal: deteriorating placental function as judged by:

intrauterine growth retardation,
oligohydramnios,
reduced foetal movements,
abnormal foetal heart patterns, or
failing biochemical results.

Maternal: deteriorating maternal condition as judged by:

blood pressure is sustained or exceeds 180/110 mmHg,
urine proteinuria > 5 gm/24 hours,
oliguria,
evidence of DIC, or
imminent or already developed eclampsia.

Method of delivery:

Vaginal delivery may be commenced in vertex presentation by:
amniotomy + oxytocin if the cervix is favourable.
prostaglandin vaginal tablet (PGE2) if the cervix is not favourable.


Method of delivery:
Caesarean section is indicated in:
Foetal distress.
Late deceleration occurs with oxytocin challenge test.
Failure of induction of labour.
Other indications as contracted pelvis, and malpresentations.

Intrapartum care:

Close monitoring of the foetus is indicated.
Proper sedation and analgesia to the mother. Hypotensives may be given if needed.
2nd stage of labour may be shortened by forceps.

Postpartum care:

Methergin is better avoided as it may increase the blood pressure.
Continue observation of the mother for 48 hours.
Sedatives and hypotensive drugs are continued in a decreasing dose for 48 hours.

Mild pre-eclampsia: can be treated as an outpatient with sedatives ± hypotensive drugs with frequent follow up. Pregnancy can be allowed to pass to full term but not after. Delivery is usually vaginal unless there is other indication for caesarean section.

Eclampsia

Definition
It is the development of convulsions in a pre-existing pre-eclampsia.
Incidence
About 1/1000 pregnancies.


Aetiology
The exact cause is unknown but cerebral ischaemia and oedema were suggested.

Clinical Picture

Premonitory stage: the eyes are rolled up with twitches of the face and hands. It lasts for about ½ min.
Tonic stage: generalised tonic contraction of the whole body muscles with opisthotonus and cyanosis. It lasts for about ½ min.

• Clonic stage: convulsions occur where there is alternative contraction and relaxation of the body muscles. The face is congested, tongue may be bitten, blood-stained frothy saliva appears on the mouth, breathing is stertorous, urine and stool may pass involuntarily, temperature rises due to increased muscular activity patient is unconscious. This lasts for about 1 min.
• Coma: it may last for few hours.

Types

Antepartum eclampsia 50%.
Intrapartum eclampsia 25%.
Postpartum eclampsia 25% occurs within 48 hours of delivery. It is usually the most dangerous one.

Severity of Eclampsia

• Eclampsia is considered severe if one or more of the following is present (Eden’s criteria):
• Coma of 6 or more hours.
• Temperature 390C or more.
• Pulse over 120/min.
• Systolic blood pressure over 200 mmHg.
• Respiratory rate over 40/min.
• More than 10 convulsions.


Differential Diagnosis
Epilepsy.
Intracranial haemorrhage.
Hysteria.
Meningitis.
Brain tumours.

Management

General measures
Hospitalisation is mandatory.
Efficient nursing in a single quiet semi-dark room to prevent any auditory or visual stimuli.
After sedation, a self-retained Foley’s catheter is applied. The hourly output of urine is charted. Proteinuria, haematuria and specific gravity are noticed.

Management

• Care for respiratory system by:
• head-down tilt to help drainage of bronchial secretion,
• frequent change of patient position,
• keep upper respiratory tract clear by aspiration of mucous through a plastic airway,
• prophylactic antibiotic and
• oxygen is administered during and after fits.


Management:
• The tongue is protected from biting by a plastic mouth gauge.

• Observation for:

• Maternal:
• pulse,
• temperature,
• blood pressure,
• respiratory rate,
• tendon reflexes,
• urine ,
• number of fits and duration of coma,
• uterine contraction,
• Foetal:
• FHS.

Medical measures

Sedation:
Morphine 10-20 mg IM or,
Diazepam one ampule (10mg) IV over 4 min. then maintain by IV infusion 40 mg in 500 ml glucose 5% over 12-24 hours. Diazepam is used as an anticonvulsant as well.


Antihypertensives:
Potent and rapidly acting drugs are used when needed.
Examples are:
Hydralazine IV.
Diazoxide IV.

Anticonvulsant therapy:

Magnesium sulphate:
Action:
inhibits neuromuscular transmission,
sedation,
peripheral vasodilatation,
diuresis.

• Dose: A loading dose 4 gm of 20% solution is given IV over not less than 3 minutes, followed by 1gm/hour. A total dose of 24 gm/24 hours should not be exceeded and therapy continues during the 24 hours postpartum. The aim is to keep the plasma level at 6-8 mEq/L. At this level tendon reflexes are still present. They disappear at >10 mEq/L and toxic effect including respiratory failure appears at 15 mEq/L.

• Before each maintenance dose the following criteria should be checked:

knee jerk should be present,
respiratory rate not less than 16/min. and
urine output not less than 30 ml/ hour.


Magnesium sulphate can be given by IM injection of 50% solution. Loading dose is 6-10 gm divided on both buttocks then 4-5 gm/ 6 hours. This regimen is not preferred due to ill control of the blood level of MgSo4 in addition to pain and inflammation of the injection site.
The antidote: is 10 ml of 10% calcium gluconate given slowly IV.

Phenytoin:

An anti-epileptic drug which can be used to prevent recurrence of fits not for its termination as it acts after about 20 min.
Dose: 18 gm/kg body weight slowly IV.

Sodium thiopentone (Intraval):

It is a short acting general anaesthetic.
Used in emergency as frequent convulsions.
Dose: 25 mg increments IV until convulsions are controlled.

Muscle relaxants:

usually used prior to procedures that might trigger off a convulsion as endotracheal intubation.
Diuretics

Obstetric measures:

• The policy is that there is no conservative treatment in eclampsia and the patient should be delivered but convulsions should be controlled first.

• Spontaneous labour usually commences within 6 hours. If not induce labour by oxytocin as long as there is no other indication for caesarean section and vaginal delivery is anticipated within 8-12 hours. Otherwise, caesarean section is indicated but never give general anaesthesia before control of convulsions or if the patient is in coma.
• Intra-and postpartum care: as in pre-eclampsia.


Preexisting (chronic) hypertention:
Causes
• Essential hypertension: of unknown aetiology.
• Secondary to chronic renal disorder: e.g.
• Glomerulonephritis.
• Hydronephrosis.
• Pyelonephritis.
• Renal artery stenosis.

• Secondary to cardiovascular disease: e.g.

• Coarctation of the aorta.
• Polyartheritis nodosa.
• Systemic lupus erythematosus.
• Secondary to endocrine disorders: e.g.
• Primary aldosteronism.
• Phaeochromocytoma.
• Adrenocortical tumours.
• Diabetes mellitus.

Effect of Pregnancy on Chronic Hypertension

Blood pressure falls by the second trimester in most of cases, but rises during the third trimester to a level some what above that in early pregnancy.
Deterioration of the underlying disease.


Effect of Chronic Hypertension on Pregnancy
Maternal:
superimposed pre-eclampsia/ eclampsia in 15-20% of cases.
Foetal:
Intrauterine growth retardation.
Intrauterine foetal death.

Treatment:

General and medical treatment
As pre-eclampsia regarding the following:
Rest,
Sedatives,
Antihypertensives,
Diuretics,
Observation.

Obstetric measures:

• Therapeutic abortion: in severe cases not responding to treatment.
• Preterm delivery if there is:
• marked deterioration of the underlying disease.
• indication for termination as in pre-eclampsia if it is superimposed.
• intrauterine growth retardation.


• Delivery at 37 completed weeks as intrauterine foetal death may result from deteriorating placental functions.

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