Antepartum Haemorrhage Flashcards

1
Q

What is antepartum haemorrhage?

A

Antepartum haemorrhage (APH) is usually defined as bleeding from the birth canal after the 24th week of pregnancy. It can occur at any time until the second stage of labour is complete; bleeding following the birth of the baby is postpartum haemorrhage.

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2
Q

Causes of antepartum haemorrhage

A

Causes- no definite cause is identified in 50% of cases, however placenta praevia and placental abruption are the major identifiable causes:
• Placenta praevia- insertion of the placenta, partially or fully, in the lower segment of the uterus.
• Placental abruption: premature separation of a normally placed placenta. 70% of cases occur in low-risk pregnancies.
• Local causes- e.g. vulval or cervical infection, trauma or tumours.
• Partner violence.
• Vasa praevia: bleeding from fetal vessels in the fetal membranes, leading to high risk of fetal haemorrhage and death at rupture of the membranes.
• Uterine rupture: rare but very dangerous.
• Inherited bleeding problems.

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3
Q

Presentation of antepartum haemorrhage

A

Antenatal anaemia- may contribute to uterine atony.
Pain or painless bleeding.
Uterine contractions can be provoked.
Malpresentation or failure of the fetal head to engage with placental praevia
Associated signs of foetal distress
Signs of hypovolaemic shock

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4
Q

Management of antepartum haemorrhage

A

-Always admit the patient for assessment and management even if the bleeding is only a very small amount- there may be concealed bleeding.
- Estimate amount of blood loss.
- Bleeding will be arrested by delivery of the foetus.
- Mother’s life should take priority in severe bleeding.
- urgent delivery of baby in foetal distress. Fetal compromise is an important indicator of reduced circulating blood volume.
- No vaginal examination until placenta praevia is excluded by ultrasound
- Blood tests:
FBC and group and save
Clotting studies
Crossmatch four units (major or massive haemorrhage)
LFTs and U&Es
- Gentle palpation of the abdomen to determine gestational age of the foetus, presentation and position.
- Fetal monitoring.
- Rhesus negative women given prophylactic anti-D immunoglobulin
- Maternal corticosteroids should be offered to any woman at risk of preterm birth, who is between 24 and 35+6 weeks of gestation.

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5
Q

Complications of antepartum haemorrhage

A
Premature labour
• DIC
• AKI
• PPH
• Placenta accreta
• Anaemia
• Infection
• Psychological sequelae
• Fetal hypoxia
• FGR
• Prematurity
• Foetal death
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6
Q

What is placenta praevia?

A

Placenta praevia exists when the placenta is inserted wholly or in part into the lower segment of the uterus.

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7
Q

What is placenta accreta?

A

Placenta accreta (morbidly adherent placenta) is a rare but important complication of placenta praevia.

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8
Q

How do you classify placenta praevia?

A

o Major, if the placenta covers the internal os of the cervix.
o Minor or partial, if the leading edge is in the lower segment but not covering the os.

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9
Q

Risk factors of placenta praevia

A
o Previous hx of placenta praevia.
o Previous CS
o Advancing maternal age
o Increasing parity
o Smoking
o Cocaine during pregnancy
o Previous spontaneous or induced abortion.
o Deficient endometrium due to manual removal of placenta or curettage.
o Assisted conception.
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10
Q

How does placenta praevia present?

A

• It may be an incidental finding on routine anomaly ultrasound.
• Painless bleeding starting after the 28th week (although spotting may occur earlier) is usually the main sign:
o Typically, it is sudden and profuse but usually does not last for long and so is only rarely life-threatening.
o Women with placenta praevia are reported to be 14 times more likely to bleed in the antenatal period compared with women without placenta praevia.
• High presenting part or abnormal lie; it may be impossible to push the high presenting part into the pelvic inlet. In 15% of cases the foetus presents in an oblique or transverse lie.
• Usually, there is no indication of fetal distress unless complications occur.

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11
Q

How do you diagnose placenta praevia?

A

Ultrasound cannot exclude a placental abruption which is a clinical diagnosis.
• Clinical suspicion should be high in any woman with vaginal bleeding after 20 weeks of gestation. Irrespective of previous imaging results, a high presenting part, an abnormal lie and painless or bleeding provoked by sexual intercourse are highly suggestive of a low-lying placenta but may not be present.
• The definitive diagnosis relies on determining the site of the leading edge of the placenta on ultrasound imaging.

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12
Q

Management of placenta praevia

A
  • A woman with a minor placenta praevia may be able to deliver vaginally.
  • A placental edge less than 2 cm from the os has been suggested as indicating a need for delivery by caesarean section, especially if it is posterior or thick.
  • If the placenta is anterior, is reaching the os and the woman has previously had a caesarean section, she should be managed as if she has placenta accreta
  • Major placenta praevia will require delivery by CS
  • Women should be advised not to have penetrative intercourse.
  • Where possible, elective caesarean section should be deferred to 38 weeks to minimise neonatal morbidity (36-37 weeks if placenta accreta is suspected).
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13
Q

Complications of placenta praevia

A
  • Potentially fatal hypovolaemic shock resulting from severe antepartum, intrapartum or postpartum bleeding.
  • Venous thromboembolism is associated with prolonged inpatient care.
  • Rare: placenta accreta, percreta
  • Fetal haemorrhage, prematurity, intrauterine asphyxia or birth injury.
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14
Q

What is placental abruption?

A

Abruption is the premature separation of a normally placed placenta before delivery of the foetus, with blood collecting between the placenta and the uterus.

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15
Q

What are the two main forms of placental abruption?

A
o Concealed (20%)- where haemorrhage is confined within the uterine cavity and is the more severe form. The amount of blood lost is easily underestimated.
o Revealed (80%)-  where blood drains through the cervix, usually with incomplete placental detachment and fewer associated problems.
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16
Q

Why does a marginal haemorrhage occur?

A

• Marginal haemorrhage occurs with a painless bleed and clot located along the margin of the placenta with no distortion of its shape. It is usually due to the rupture of a marginal sinus. Women should be admitted for observation and fetal monitoring.

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17
Q

Risk factors for placental abruption

A
  • Previous abruption
  • Multiple pregnancy
  • Trauma- road traffic accident, domestic violence, iatrogenic
  • Threatened miscarriage earlier in current pregnancy.
  • Pre-eclampsia
  • HTN
  • Multiparity
  • Previous C section
  • Non-vertex presentations
  • Smoking
  • Cocaine or amfetamine use during pregnancy
  • Thrombophilia
  • Intrauterine infections
  • Polyhydramnios
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18
Q

How does placental abruption present?

A
  • May present with vaginal bleeding, abdominal pain (usually continuous), uterine contractions, shock or fetal distress.
  • A tense, tender uterus with a ‘woody’ feel on abdominal examination suggests a significant abruption.
  • Fetal hypoxia due to an abruption will lead to heart rate abnormalities seen on cardiotocograph (CTG).
  • Depending on the degree of detachment and the amount of blood loss, the mother may be collapsed and the foetus hypoxic or already dead.
  • Abruption is a clinical diagnosis with no available sensitive or reliable diagnostic tests.
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19
Q

Management of placental abruption

A

Mother’s life should take priority.

Moderate or severe placental abruption is to follow ABCD of resuscitation:
o Assess Airway and Breathing: high-flow oxygen.
o Evaluate Circulation.
o Assess foetus and Decide on Delivery.

20
Q

How do you evaluate circulation?

A

▪ Intravenous access, FBC, coagulation screen, U&E, Kleihauer test, crossmatch four units.

▪ Position in the left lateral position tilted and keep the woman warm.

▪ Until blood is available, infuse up to 2 litres of warmed crystalloid Hartmann’s solution and/or 1-2 litres of colloid as rapidly as required.

▪ With continuing massive haemorrhage and whilst awaiting coagulation studies and haematology advice, up to 4 units of fresh frozen plasma (FFP) and 10 units of cryoprecipitate may be given empirically.

▪ Ideally, measure central venous pressure (CVP) and adjust transfusion accordingly.

21
Q

How do you assess foetus and decide on delivery?

A

▪ If the foetus is alive, perform either caesarean section or artificial rupture of the amniotic membranes. Monitor the foetus and switch to caesarean if fetal distress develops.
▪ Vaginal delivery is the treatment of choice in the presence of a dead foetus, although if the abruption is massive, caesarean may occasionally be indicated to control haemorrhage.
▪ If bleeding has settled and delivery is not imminent, maternal steroids may be indicated in order to promote fetal lung development and reduce the risk of respiratory distress syndrome and intraventricular haemorrhage

22
Q

What is the definition of small for gestational age (SGA)?

A
  • SGA refers to an infant born with a birth weight less than the 10th centile.
  • Severe SGA refers to an infant born with a birth weight less than the 3rd centile.
23
Q

How do you classify SGA babies?

A

o Babies whose growth at all gestational ages has been low. They are SGA but otherwise healthy. 50-70% of SGA foetuses are constitutionally small, with fetal growth appropriate for maternal size and ethnicity.
o Growth is normal in the early part of pregnancy but slows in utero by at least two measurements (normally from ultrasound assessments). This is due to IUGR/FGR. The newborn baby has a wasted appearance with little subcutaneous fat and a greater risk of complications.
o Non-placenta mediated growth restriction - eg, structural or chromosomal anomaly, inborn errors of metabolism or fetal infection.

24
Q

Why is SGA different from FGR?

A

o SGA is different to FGR as FGR refers to neonates with clinical features of malnutrition and in-utero growth restriction, irrespective of their birth weight percentile.

25
Q

Minor risk factors for SGA

A
o Maternal age ≥35 years.
o IVF singleton pregnancy.
o Nulliparity.
o BMI <20.
o BMI 25-34.9.
o Smoker - 1-10 cigarettes per day.
o Low fruit intake pre-pregnancy.
o Pregnancy interval <6 months.
o Pregnancy interval ≥60 months.
26
Q

Major risk factors for SGA

A
o Maternal age >40 years.
o Smoker - ≥11 cigarettes per day.
o Paternal or maternal SGA.
o Cocaine use.
o Daily vigorous exercise.
o Previous SGA baby.
o Previous stillbirth.
o Chronic hypertension.
o Diabetes with vascular disease.
o Renal impairment.
o Antiphospholipid syndrome.
o Heavy bleeding similar to menses.
o Pregnancy associated plasm protein-A (PAPP-A) <0.4 multiples of the median (MOM).
27
Q

Diagnosis of SGA

A
  • Serial measurement of symphysis fundal height (SFH) is recommended at each antenatal appointment from 24 weeks of pregnancy as this improves prediction of an SGA neonate.
  • Women with a single SFH which plots below the 10th centile or with serial measurements which demonstrate slow or static growth by crossing centiles should be referred for ultrasound measurement of fetal size.
  • Women in whom measurement of SFH is inaccurate (for example, BMI >35, large fibroids, hydramnios) should be referred for serial assessment of fetal size, using ultrasound.
28
Q

Medications to prevent SGA foetus

A
  • The most effective interventions to prevent the SGA fetus were antiplatelet agents like aspirin before 16 weeks in women at risk of pre-eclampsia, and progesterone therapy for prevention of preterm birth.
  • For the prevention of perinatal mortality in high-risk women, antiplatelets and antenatal corticosteroids were found to be effective interventions
29
Q

Antenatal care for SGA babies

A

o Women who have a major risk factor should be referred for serial ultrasound measurement of fetal size and for assessment of well-being with umbilical artery Doppler from 26-28 weeks of pregnancy.
o Women who have three or more minor risk factors should be referred for uterine artery Doppler at 20-24 weeks of gestation.
o Karyotyping should be offered in severely SGA foetuses with structural anomalies and in those detected before 23 weeks of gestation.
o Women with an SGA foetus between 24+0 and 35+6 weeks of gestation, where delivery is being considered, should receive a single course of antenatal corticosteroids.

30
Q

What should you do if Doppler is abnormal in a SGA foetus?

A

o In the preterm SGA foetus with umbilical artery absent or reversed end-diastolic velocity (AREDV) detected prior to 32 weeks of gestation, delivery is recommended when DV Doppler becomes abnormal or umbilical vein pulsations appear, provided the foetus is considered viable and after completion of steroids. Even when venous Doppler is normal, delivery is recommended by 32 weeks of gestation and should be considered between 30-32 weeks of gestation.
o If MCA Doppler is abnormal, delivery should be recommended no later than 37 weeks of gestation.
o In the SGA foetus detected after 32 weeks of gestation with an abnormal umbilical artery Doppler, delivery no later than 37 weeks of gestation is recommended.
o Delivery by C section is recommended.

31
Q

What is FGR?

A

• This is a condition where a baby’s growth slows or ceases when it is in the uterus.

32
Q

What are the causes of FGR/ IUGR?

A
  • IUGR is the common result of maternal, placental, fetal or genetic factors.
  • Any mismatch between the supply of nutrient by the placenta and the demand of the foetus also leads to IUGR.
33
Q

Maternal causes of FGR

A

o Maternal age (less than 16 years or more than 35 years)
o Low socio-economic status
o Parity (none or more than five births)
o Inter-pregnancy interval less than 6 months or an interval of 120 months or more).
o Previous delivery of an SGA newborn.
o Maternal substance abuse
o Maternal medication
o Maternal pre-pregnancy BMI less than 20, weight less than 45 kg or more than 75 kg.
o Assisted reproductive technologies.
o Pregnancy: moderate to heavy physical work, severe maternal starvation, poor weight gain, high-altitude and maternal hypoxia, poor medical care.
o Maternal medical disorders
o Maternal infection and parasite infestations

34
Q

Substance abuse that can cause FGR

A

Smoking
Alcohol
Marijuana
Cocaine

35
Q

Maternal disorders that can cause FGR

A
Asthma 
Cyanotic congenital heart disease
Hypertensive disorders 
Pre-eclampsia 
Diabetes associated with vasculopathy 
CKD 
SLE 
Antiphospholipid syndrome 
Sickle cell disease 
Acquired thrombophilia
36
Q

Maternal medications that can cause FGR

A
Warfarin
Antiepileptics 
Antineoplastics
Folic acid antagonists 
Steroids
Antimetabolite
37
Q

Maternal infections that can cause FGR

A

TORCH syndrome (= toxoplasmosis, other, rubella, cytomegalovirus, herpes simplex), malaria, tuberculosis, urinary tract infections and bacterial vaginosis).

38
Q

Fetal factors that can cause FGR

A

o Chromosomal abnormalities – e.g., trisomies 13, 18, or 21, autosomal deletions, triploidy, ring chromosomes and uniparental disomy.
o Genetic syndromes – e.g., Russell-Silver syndrome, Rubinstein-Taybi syndrome, Dubowitz’s syndrome, Seckel’s syndrome, Fanconi’s syndrome.
o Major congenital anomalies – e.g., tracheo-oesophageal fistula, congenital heart disease, congenital diaphragmatic hernia, abdominal wall defects (omphalocele or gastroschisis), neural tube defect (eg, anencephaly), anorectal malformation.
o Multiple gestation.
o Congenital infections (TORCH syndrome, malaria, congenital HIV infection, syphilis).
o Metabolic disorders – e.g., congenital lipodystrophy, galactosaemia, generalised gangliosidosis type I, hypophosphatasia, fetal phenylketonuria.

39
Q

Placental factors causing FGR

A

Placental factors – e.g., placental dysfunction (including pre-eclampsia), placental abruption.

40
Q

Classification of FGR

A

• There are predominately three types of IUGR:
o Asymmetrical IUGR (malnourished babies- occurs later in pregnancy)
o Symmetrical IUGR (hypoplastic SGA)- occurs early in pregnancy
o Mixed IUGR- early IUGR complicated by placental dysfucntion

41
Q

Assessment of FGR

A
  • GROW chart

* Umbilical artery doppler scan- reduces perinatal morbidity and mortality in a high-risk population.

42
Q

Short term complications of FGR

A
o Perinatal asphyxia
o Meconium aspiration
o Persistent pulmonary HTN
o Hypothermia
o Hypoglycaemia
o Hyperglycaemia
o Hypocalcaemia
o Polycythaemia
o Jaundice
o Feeding difficulties
o Feed intolerance
43
Q

Long term complications of FGR

A

o Lower scores on cognitive testing
o Cerebral palsy
o Behavioural problems: hyperactive behaviour, ADHD
o Poor perceptual performance
o Susceptible to diabetes, HTN, obesity, metabolic syndrome, CHD.

44
Q

Prevention of FGR

A

o Antiplatelet agents may be effective in preventing SGA in women at high risk of pre-eclampsia, although the effect size is small.
o In women at high risk of pre-eclampsia, antiplatelet agents should be commenced at, or before, 16 weeks of pregnancy.
o There is no consistent evidence that dietary modification, progesterone or calcium prevents SGA.
o Interventions to promote smoking cessation may prevent SGA and should be offered to all pregnant women who smoke.

45
Q

What are the signs of magnesium toxicity?

A

• Signs include loss of tendon reflexes, respiratory depression and cardiac arrest.