Download By tests depend on blood pressure measurement

Forth stage
‫ولدان‬.‫د‬
Obstetrics
Lec-2
6/4/2016
Hypertensive Disorders in Pregnancy II
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 wellbeing: 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:
I.
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.
II.
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.
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III.
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.
IV.
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. 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 preeclamptic 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.
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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
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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.
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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.
 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,
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 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.
Antihypertensive:
Decrease the maternal cerebral and cardiovascular complications but do not
affect the foetal outcome.
1. 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.
2. 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.
3. 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.
4. Adreno-receptor blockers:
 Examples: Labetalol, atenolol, oxprenolol and propranolol.
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 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).
5. 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.
6. Diazoxide (Hyperstat):
 It is a potent vasodilator.
 Dose: 15-30 mg IV and titrated against the blood pressure.
 Side effects: hypotension and hyperglycaemia.
7. 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.
8. 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.
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