Obstetrics Simplified - Diaa
Hypertensive Disorders in Pregnancy
- Pre-existing (chronic) hypertension:
- Hypertension is present before pregnancy, detected in early
pregnancy (before 20 weeks in absence of vesicular mole) and postpartum.
- essential hypertension,
- secondary to chronic renal disorders e.g. pyelonephritis
and renal artery stenosis,
- coarctation of the aorta, systemic lupus erythematosus and
- Pregnancy-induced hypertension (PIH):
- Transient hypertension:
- Late onset hypertension, without proteinuria or pathologic
- Hypertension with proteinuria and / or oedema after 20 weeks
of pregnancy, but may be earlier in vesicular mole.
- Pre-eclampsia + convulsions.
- 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.
Although eclampsia had been described since 200 years, no definite aetiology
is found for PIH and it is still a disease of theories.
- Primigravidae more than multigravidae.
- Pre-existing hypertension.
- Previous pre-eclampsia.
- Family history of pre-eclampsia.
- Hyperplacentosis i.e. excessive chorionic tissue as in hydatidiform
mole, multiple pregnancy, uncontrolled diabetes mellitus and foetal
- Climatic variations.
- 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.
- 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. Hypoimmune response results
in damage of the placenta and subsequent pre-eclampsia.
- The evidences is that: Pre-eclampsia is less common in previously
stimulated immunity conditions as in:
- Previous pregnancy.
- Previous blood transfusion.
- Consanguineous marriages.
- Increased maternal anti-HLA (human leucocyte antigen)
- 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, their babies and
their sisters who developed PIH.
- 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.
- 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.
- 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
- Neutrophils activation causes damage and dysfunction of the
vascular endothelium leading to platelets aggregation, coagulation
activation, hypertension and proteinuria.
The vascular changes and local hypoxia of the surrounding
tissues lead to haemorrhage, necrosis and other pathological changes.
- Central nervous system: ischaemia, haemorrhages and oedema.
- Liver: subcapsular haemorrhage, periportal necrosis and infarctions.
- 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.
- 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.
- 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.
- 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
- 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 and having lower level of 5-hydroxytryptamine.
The end result of these changes is hypercoagulability and disseminated
intravascular coagulation in severe pre-eclampsia and eclampsia.
Sodium and water retention
There is haemoconcentration with fluid shift from the intravascular to
the extravascular compartment.
N.B. HELLP syndrome is described in PIH which consists of: H = Haemolysis,
EL= Elevated Liver enzymes, LP= Low Platelet count.
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
How to measure the blood pressure in pregnancy?
- The patient should rest for at least 30 min. after arriving to the
- Remove any tight clothing from the right arm.
- 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.
- 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.
- 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.
- Blood pressure measurement phases (Korotkoff):
- Korotkoff I¾ Appearance of the sound¾ systolic reading.
- Korotkoff II¾ Accentuation of the sound.
- Korotkoff III ¾ Sound becomes harsh.
- Korotkoff IV¾ Sound becomes muffled¾ diastolic reading.
- Korotkoff V¾ Disappearance of the sound.
- 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.
- 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.
- 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
- 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.
- 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
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
- Oliguria or anuria: due to kidney pathology.
- 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
- Eye fundus examination.
- Tests for foetal well being: as
- 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.
Tests depend on blood pressure measurement
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.
Mid-trimester mean blood pressure:
If the mean arterial blood pressure (the diastolic pressure +1/3 the
pulse pressure) is more than 90 mmHg, the risk of developing PIH increases
by over four folds.
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.
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.
- 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.
- 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.
- Mild pre-eclampsia: blood pressure ³ 140/90 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 ++++),
- severe continuous headache,
- blurring of vision,
- epigastric pain.
- Fulminating pre-eclampsia: a rapidly deteriorating pre-eclampsia
to be imminent eclampsia.
Other causes of hypertension
may be present.
in between pregnancies.
||after the 20th
week of pregnancy (except in vesicular mole) and disappears within
6 weeks postpartum.
during the first 20 weeks and persists after 6 weeks postpartum.
||If present, it
develops after hypertension.
||If present, it
develops before hypertension due to underlying renal disease.
||may be present.
||Normal or retinal
vessels spasm, oedema, exudate and papilloedema (oedema of the optic
|Serum Uric Acid
is not proportionate to serum creatinine
is propotionate to serum creatinine.
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
- Congestive heart failure and severe anaemia due to hypoxia of the
- 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 ++++).
Other causes of oedema
- General causes: cardiac, hepatic, renal or nutritional oedema.
- Local causes: as inflammatory or deep vein thrombosis (usually
- Pressure of the gravid uterus: on the pelvic veins may produce
- 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.
- Intrauterine growth retardation (IUGR).
- Intrauterine foetal death.
- Prematurity and its complications.
- 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 (60 mg daily) 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.
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.
- 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
- High protein, low sodium diet.
- blood pressure twice daily.
- urine volume and proteinuria daily,
- oedema daily,
- body weight twice weekly,
- fundus oculi once weekly,
- blood picture including platelet count, liver and
renal functions particularly serum uric acid on admission.
- daily foetal movement count,
- serial sonography,
- non-stress and stress test if needed.
- Sedatives: as diazepam 2-5 mg every 8-12 hours.
- 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, athenia and nightmares.
- Hydralazine (Apresoline):
- It is a vasodilator, increases renal and uteroplacental
- 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
- 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
- The higher the starting blood pressure the greater
is the hypotensive effect.
- 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
- 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 every minute and titrated against
the blood pressure.
- Side effects: hypotension and hyperglycaemia.
- "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
- 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.
- Heparin: may be used in treatment of DIC if there is no
- 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
- 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.
- 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,
- 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,
- 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
- 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.
N.B. 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.
It is the development of convulsions in a pre-existing pre-eclampsia.
About 1/1000 pregnancies.
The exact cause is unknown but cerebral ischaemia and oedema were suggested.
- 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.
- 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
- 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.
- Intracranial haemorrhage.
- Brain tumours.
- Strychnine poisoning.
- 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.
- 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.
- The tongue is protected from biting by a plastic mouth gauge.
- Observation for:
- blood pressure,
- respiratory rate,
- tendon reflexes,
- urine (see before),
- number of fits and duration of coma,
- uterine contraction,
- 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.
- Potent and rapidly acting drugs are used when needed.
- Examples are:
- Hydralazine IV.
- Diazoxide IV.
- Anticonvulsant therapy:
- Magnesium sulphate:
- inhibits neuromuscular transmission,
- peripheral vasodilatation,
- 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
- 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
- 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.
- Other drugs
- The policy is that there is no conservative treatment in eclampsia
and the patient should be delivered but convulsions should be controlled
- 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.
PRE-EXISTING (CHRONIC) HYPERTENSION
- Essential hypertension: of unknown aetiology.
- Secondary to chronic renal disorder: e.g.
- 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.
- 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
- Deterioration of the underlying disease.
Effect of Chronic Hypertension on Pregnancy
- superimposed pre-eclampsia/ eclampsia in 15-20% of cases.
- Intrauterine growth retardation.
- Intrauterine foetal death.
General and medical treatment
As pre-eclampsia regarding the following:
- 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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Edited by Aldo Campana,