Obstetrics 2 Flashcards

1
Q

A 28-year-old woman is 34 weeks pregnant. She attends the maternity assessment unit as she felt a gush of fluid down her leg and can now feel something in her vagina. The foetus is in a transverse lie and deep decelerations are seen on the cardiotocograph (CTG). Possible diagnosis?

A

Cord prolapse

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2
Q

Why is cord prolapse an obstetric emergency?

A
  • Cord prolapse → leads to cord compression + umbilical artery vasospasm → preventing venous + arterial blood flow to and from the foetus → leading to birth asphyxia
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3
Q

Risk factors for cord prolapse

A

General:
* Multiparity
* Low birth weight (<2.5kg)
* Preterm labour (< 37 weeks)
* Breech presentation
* Transverse, oblique or unstable lie

Procedure-related:
* Artificial rupture of membranes (ARM) with high presenting part
* Vaginal manipulation of foetus with ruptured membranes
* External cephalic version (ECV)

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4
Q

Clinicals features of cord prolapse

A

Symptoms:
* Cord felt in the vagina

Signs:
* Cord seen in the vagina
* Abnormal foetal heart rate pattern
* There may be no clinical signs or symptoms and a normal foetal heart rate pattern

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5
Q

Ix for cord prolapse

A
  • Vaginal/speculum examination (visualisation of the prolapsed cord)
  • Foetal heart ausculation
  • Cardiotocography (abnormal heart rate) (non-specific to cord prolapse)
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6
Q

Management of cord prolapse

A

Management of cord prolapse = immediate delivery of the foetus

Pre-dlivery:
* Minimal handling of loops of cord lying outside of the vagina
* Elevate presenting foetal part
* Mother in knee-chest or left lateral position
* Tocolysis

Delivery: Caesarean section (if vaginal delivery is not imminent)
* Cat 1 (delivery witin 30 mins)
* Cat 2 (delivery within 75 mins)
* Vaginal (normally operative, forceps or vacuum extraction)

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7
Q

Complications of cord prolapse

A

Maternal:
* Caesarean section
* Operative vaginal delivery

Foetal:
* Low Apgar scores: babies with low Apgar scores at delivery are more likely to require resuscitation
* Birth asphyxia
* Hypoxic brain injury
* Cerebral palsy
* Perinatal death

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8
Q

A 35-year-old woman presents with painless vaginal bleeding. She is currently 32 weeks pregnant, with an uneventful antenatal period so far. She is G3P2 and has had two prior caesarean sections. Possible diagnosis?

A

Placenta accreta

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9
Q

What is placenta accreta?

A
  • Normally, the placenta attaches to the endometrium.
  • Placenta accreta = an obstetric complication where the** placenta abnormally adheres to the myometrium** (the smooth muscle middle layer of the uterine wall)
  • This occurs due to a defect in the endometrial decidua basalis, often as a result of previous uterine surgery e.g. cesarean section or curettage procedure
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10
Q

Info: Placenta accreta is part of the following spectrum of abnormal placental attachment

A

Placenta accreta is part of the following spectrum of abnormal placental attachment:

  • Placenta accreta: the placenta attaches to the myometrium
  • Placenta increta: the placenta invades deeply into the myometrium
  • Placenta percreta: the placenta penetrates the myometrium, reaching the uterine serosa (perimetrium) and potentially adjacent organs

Placenta accreta → ‘creeping’
Placenta increta → ‘invading’
Placenta perceta → ‘perimetrium’

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11
Q

Risk factors for placenta accreta

A
  • Previous placenta accreta
  • Previous caesarean section
  • Previous endometrial curettage procedures
  • Placenta praevia or low-lying placenta
  • Uterine structural abnormality: examples include fibroids or a bicornuate uterus
  • Advanced maternal age: >35
  • Multiparity
  • IVF
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12
Q

How does placenta accreta clinically present?

A

Placenta accreta = typically presents with painless vaginal bleeding - usualy occurring in the third trimester

(May be asymptomatic)

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13
Q

Ix for placenta accreta

A

First line: Transvaginal ultrasound

Investigations to consider:
* FBC: to assess Hb in acute bleeding
* Coagulation screen
* Crossmatch: perform if considering transfusion in a bleeding patient
* MRI: this can be used if ultrasound findings are inconclusive.

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14
Q
A
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15
Q

Management of placenta accreta

A
  • Delivery at 35 to 36+6 weeks gestation: this reduces the risk of spontaneous labour and delivery, reducing the risk of haemorrhage
  • Hysterectomy: the uterus is removed after delivery of the baby, reducing the risk of severe haemorrhage
  • Uterine preserving surgery: this involves the resection of the placenta and part of the myometrium
  • Expectant management: In selective cases, if future fertility is desired, the placenta may be left in situ to resorb over time. However, this carries significant risk of bleeding and infection and requires careful monitoring
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16
Q

Maternal and foetal complications of placenta accreta

A

Maternal:
* Postpartum haemorrhage: this is because the deeper penetration of the placenta past the endometrium makes separation very difficult during delivery. This can be life-threatening
* Disseminated intravascular coagulation (DIC): bleeding can lead to consumption of clotting factors, with subsequent DIC
* Hysterectomy

Foetal:
* Preterm birth: increased risk of prematurity
* Foetal death

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17
Q

A woman is pregnant with her first child. She is rhesus-D negative. What will happen if the she is not given IM Anti-D injections?

A

The sensitisation process
(If the child is rhesus positive)

  • It is likely at some point in the pregnancy (i.e. childbirth) that the blood from the baby will find a way into the mother’s bloodstream.
  • When this happens, the baby’s red blood cells display the rhesus-D antigen.
  • The mother’s immune system will recognise this rhesus-D antigen as foreign, and produce antibodies to the rhesus-D antigen.
  • The mother has then become sensitised to rhesus-D antigens.

The sensitisation process = usually doesn’t cause problems in the first pregnancy

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18
Q

What will happen if a mother has a second baby (rhesus positive) after the first (with no Anti-D treatment)?

A

Haemolytic disease of the newborn

  • During subsequent pregnancies, the mother’s anti-rhesus-D antibodies can cross the placenta into the fetus.
  • If that fetus is rhesus-D positive, these antibodies attach themselves to the red blood cells of the fetus and causes the immune system of the fetus to attack them, causing the destruction of the red blood cells (haemolysis).
  • The red blood cell destruction caused by antibodies from the mother is called haemolytic disease of the newborn.
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19
Q

What is management for rhesus incompatibility?

A

Prevention of sensitisation = mainstay of management → IM anti-D injections to rhesus-D negative women

Anti-D injections are given routinely on two occasions:
* 28 weeks gestation
* Birth (if the baby’s blood group is found to be rhesus-positive)

Anti-D injections should also be given at any time where sensitisation may occur, such as:
* Antepartum haemorrhage
* Amniocentesis procedures
* Abdominal trauma

(The anti-D medication works by attaching itself to the rhesus-D antigens on the fetal red blood cells in the mothers circulation, causing them to be destroyed. This prevents the mother’s immune system recognising the antigen and creating it’s own antibodies to the antigen. It acts as a prevention for the mother becoming sensitised to the rhesus-D antigen.)

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20
Q

Rhesus incompatibility: What test is performed after 20 weeks gestation to see how much fetal blood has passed into the mother’s blood, to determine whether further doses of anti-D are required?

A

Kleihauer Test

Kleihauer test = checks how much fetal blood has passed into the mother’s blood during a sensitisation event.
* This test is used after any sensitising event past 20 weeks gestation, to assess whether further doses of anti-D is required.

(The Kleihauer test involves adding acid to a sample of the mother’s blood. Fetal haemoglobin is naturally more resistant to acid, so that they are protected against the acidosis that occurs around childbirth. Therefore, fetal haemoglobin persists in response to the added acid, while the mothers haemoglobin is destroyed. The number of cells still containing haemoglobin (the remaining fetal cells) can then be calculated.)

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21
Q

Is Group B streptococcus (GBS) a commensal bacterium?

A

Yes!
(Found in the vagina or rectum of approx. 25% of pregnant women)

22
Q

In most cases of Group B streptococcus colonisation, does it cause any symptoms or sequelae?

A

No!
However in the presence of certain risk factors - it can cause an infection

23
Q

Name some infections that Group B streptococcus can cause in a neonate

A
  • Sepsis
  • Pneumonia
  • Meningitis

Early onset GBS disease of the newborn

The incidence rate of early onset GBS is 0.05%. There is a 5% mortality rate in babies that develop GBS.

24
Q

What type of bacterium is Group B streptococcus?

A

Streptococci = gram-positive cocci - typically group in chains

Beta haemolyic steptococci are further subdivided into groups A, B, C, D, F, G and H.

25
Q

What is the name of the pathogen in Group B streptococcus?

A

Streptococcus agalactiae

26
Q

What are the risk factors for GBS infection in the neonate?

A
  • GBS infection in a previous baby
  • Prematurity <37 weeks
  • Rupture of membranes >24 hours before delivery
  • Pyrexia during labour
  • Positive test for GBS in the mother
  • Mother diagnosed with a UTI found to be GBS during pregnancy
27
Q

Clinical features of the infections that GBS colonisation causes in the mother.

Maternal vaginal or rectal colonisation does not cause symptoms. However, GBS that leads to infection may manifest in different ways….

A
  • UTI – frequency, urgency, dysuria
  • Chorioamnioitis – fevers, lower abdominal/uterine tenderness, foul discharge, maternal and/or fetal tachycardia (occurs intrapartum).
  • Endometritis – fevers, lower abdominal pain, intermenstrual bleeding, foul discharge (occurs postpartum).
28
Q

Clinical features of GBS infection in neonate

A
  • Pyrexia
  • Cyanosis
  • Difficulty breathing + feeding
  • Floppiness
29
Q

Is GBS screened routinely in pregnancy?

A

Only women at high risk

High risk may include those with symptoms:
* UTI or chorioamnionitis during pregnancy
* Those with STI symptoms pre-pregnancy
* A previous GBS infected baby.

30
Q

What is the management for prevention of Group B streptococcus infection in neonates?

A

High dose IV penicillin (benzylpenicillin) or clindamcyin (if allergic)

31
Q

What are the indications for giving high dose IV penicillin in labour to prevent GBS infection in neonate?

A
  • GBS positive swabs
  • A UTI caused by GBS during this pregnancy
  • Previous baby with GBS infection.
  • Pyrexia during labour
  • Labour onset <37 weeks
  • Rupture of membranes >18 hours

If there is rupture of membranes in a woman of >37 weeks gestation known to be GBS positive, she will be induced immediately (to reduce the amount of time the fetus is exposed).

32
Q

Is high dose IV penicllin indicated in a planned caesarean if the mother is colonised with Group B streptococcus?

A

No!
As it is the rupture of membranes that exposes the baby to GBS.
In addition, GBS carrier status does not affect the methods used for induction of labour.

33
Q

What are the clinical features of primary varicella zoster infection (chickenpox)?

A
  • Fever
  • Malaise
  • Pruritic maculopapular rash (characteristic: vesicular + crusts → then heals)

Incubation period: 10-21 days
The woman = infectious from 48 hours prior to the rash to until the vesicles have crusted.

34
Q

What can primary varicella zoster virus (chickenpox) lead to in mothers?

A
  • Pneumonia
  • Hepatitis
  • Encephalitis

2% mortality in mothers

35
Q

Investigations for primary varicella zoster (chickenpox) in pregnant mothers?

A

Primarily clinical diagnosis (history + examination)

  • Immunofluorescence of basal epithelial cells scrapped from vesicle.
  • PCR for varicella zoster DNA.

To check imunity status:
* Test for IgM + IgG antibodies to varicella zoster
* If present, they indicate the woman has immunity against the virus (usually from previous infection or vaccination).

36
Q

Management of maternal suspected varicella contact

A

If mother describes previous primary varicella zoster infection – assume immunity → No further action is required.

If no previous infection – varicella zoster IgG testing is required to confirm immunity status.
* Less than 20 weeks gestation → prescribe varicella zoster immunoglobulin (VZIG) within 10 days of contact
* More than 20 weeks gestation → VZIG or Aciclovir from 7 to 14 days from exposure

These women should then be managed as potentially infectious from 8 to 28 days.

37
Q

Management of a pregnant mother that has a chickenpox infection

A

Aciclovir (800mg PO 5tds) within 24 hours of rash onset

The mother should be counselled about the symptoms of pneumonia, neurological signs and haematological rash – and instructed to attend hospital immediately should they occur.

In addition, she should be referred to a fetal medicine specialist, with serial ultrasound examinations beginning at 5 weeks post infection to identify any fetal abnormalities.

38
Q

Is varicella vaccination recommended during pregnancy?

A

No
If a woman is found to be seronegative for varicella zoster IgG, pre-pregnancy or postpartum vaccination should be considered. Vaccination is not recommended during pregnancy as a matter of caution,

39
Q

If maternal chickenpox occurs within the last 24 hours of pregnancy, what is there a significant risk of?

A

Varicella infection of the newborn (50%)

This can be asymptomatic

Possible routes of infection: n
* Transplacental
* Vaginal
* Direct contact after birth

Varicella of the newborn is treated with varicella-zoster immunoglobulin (VZIG) ± aciclovir.

40
Q

What is fetal varicella syndrome?

A

Fetal varicella syndrome = caused by subsequent reactivation of the virus in utero as herpes zoster.
This reactivation = only occurs when the fetus is infected by maternal varicella before 20 weeks gestation.

41
Q

What are the clinical features of fetal varicella syndrome?

A
  • Skin scarring in a dermatomal distribution
  • Eye defects (microphthalmia, choriorenitis, cataracts, optic atrophy)
  • **Hypoplasia of limbs **
  • Neurological abnormalities (microenphaly, cortical and spinal cord atrophy, seizures, Horner’s syndrome)
42
Q

Are pregnant at more risk of developing cystitis and pyelonephritis?

A

Yes

43
Q

What are some major complications of UTI in pregnancy?

A
  • Preterm delivery
  • Low birth weight
  • Pre-eclampsia
44
Q

What is asymptomatic bacteriuria?

A

Asymptomatic bacteruria = refers to bacteria present in the urine, without symptoms of infection.

Pregnant women with asymptomatic bacteriuria are at higher risk of developing lower urinary tract infections and pyelonephritis, → subsequently at risk of preterm birth.

45
Q

Info: Asymptomatic bacteriuria

A

Pregnant women are tested for asymptomatic bacteriuria at booking and routinely throughout pregnancy. This involves sending a urine sample to the lab for microscopy, culture and sensitivities (MC&S).

Testing for bacteria in the urine of asymptomatic patients is not recommended as it may lead to unnecessary antibiotics. Pregnant women are an exception to this rule, due to the adverse outcomes associated with infection.

46
Q

Clinical presentation for lower urinary tract infection

A
  • Dysuria (pain, stinging or burning when passing urine)
  • Suprapubic pain or discomfort
  • Increased frequency of urination
  • Urgency
  • Incontinence
  • Haematuria
47
Q

Clinical features of pyelonephritis

A
  • Fever (more prominent than in lower urinary tract infections)
  • Loin, suprapubic or back pain (this may be bilateral or unilateral)
  • Looking and feeling generally unwell
  • Vomiting
  • Loss of appetite
  • Haematuria
  • Renal angle tenderness on examination
48
Q

Causative organisms for UTIs

A
  • E. coli (most common) - gram-negative, anaerobic, rod-shaped bacteria that is part of the normal lower intestinal microbiome. It is found in faeces, and can easily spread to the bladder.
  • Klebsiella pneumoniae (gram-negative anaerobic rod)
  • Enterococcus
  • Pseudomonas aeruginosa
  • Staphylococcus saprophyticus
  • Candida albicans (fungal)
49
Q

Management of UTI in pregnancy

A

7 day course = required
* Nitrofurantoin (avoid in the third trimester)
* Amoxicillin (only after sensitivities are known)
* Cefalexin

50
Q

Why should nitrofurantoin be avoided in the third trimester?

A

Risk of neonatal haemolysis (destruction of the neonatal red blood cells)

51
Q

Why should trimethoprim be avoided in the first trimester?

A

Trimethoprim = folate antagonist

  • Folate is important in early pregnancy for the normal development of the fetus.
  • Trimethoprim in early pregnancy can cause congenital malformations, particularly neural tube defects (i.e. spina bifida). It is not known to be harmful later in pregnancy, but is generally avoided unless necessary.