Obstetrics Complications Flashcards

(42 cards)

1
Q

Causes of premature birth

A

Infection (chorioamnionitis, genital tract infection e.g. Group B strep)
Maternal pyrexial illness (e.g. pyelonephritis, respiratory tract infection)
Uterine abnormalities
Cervical incompetence
Multiple pregnancies
Fetal abnormalities
Polyhydramnios
Placenta praevia
Abruption placenta
Intra-uterine growth restriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk factors for preterm

A

Previous preterm labour
Unbooked status
Smoking, alcohol
Malnutrition
Multiple pregnancy
Poor socio-economic status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do you diagnose preterm labour

A

Regular painful contractions associated with progressive cervical changes with
or without rupture of membranes
Threatened preterm labour refers to the onset of contractions without cervical
changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How to manage pt who comes in preterm labour

A

If gestational age considered more than 34 weeks: Allow to proceed
If gestational age < 34 weeks or EFW <2kg: Refer to a hospital with neonatal
facilities (preferably in-utero transfer)
Inform neonatal team
Gestational age less than 34 weeks or immature lungs:
1. Admit patient.
2. Observe contractions clinically.
3. CTG
4. Inhibition of progressive contractions: tocolysis if no contra-indications
- Administer Nifedipine(calcium channel blocker) 30mg stat then 20mg after
90 min and if contractions persist, 20mg every 6 hours
- Indomethacin (Indocid) suppository 100mg rectally every 12 hours for 48
hours (only if <32 weeks gestation)
5. Administer Betamethasone 12 mg IM 12 hourly x 2 doses (bene its of steroids
are reduction in intraventricular haemorrhage, necrotizing enterocolitis and
hyaline membrane disease.
6. Regime should be continued for 48 hours, and then reviewed and a
decision made to:
- Discontinue therapy 24 hours after the second Betamethasone dose.
- Discontinue therapy and allow delivery if pathology evident.
7. Treat underlying infection e.g. urinary tract infection

  1. Magnesium Sulphate should be administered for neuroprotection if the
    gestational age is < 34 weeks and should be continued for at least 12 hours in
    patients where delivery is imminent. Magnesium Sulphate protects against
    cerebral palsy. A loading dose of 4g in 200mls normal saline is commenced and
    then a maintenance dose of 1g/hour(50mls/hr). Respiratory rate, re lexes and
    urine output should be monitored hourly in patients on Magnesium sulphate.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Investigations for pt coming in with preterm labour

A

Midstream urine for MC&S
High vaginal swab
CTG
Ultrasound-growth and cervical length

Establish a diagnosis:
Monitor contractions
Vaginal examination 4 hours apart to assess if cervical changes (unless
membranes are ruptured in which case a vaginal exam is contraindicated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Contraindications tocolysis

A

Intrauterine fetal death
IUGR
Chorioamnionitis
Fetal distress
Antepartum haemorrhage
Fatal fetal abnormalities
Pre-eclampsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Side effects of adalat

A

It’s a Ca channel blocker

Nausea and vomiting
Flushing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Contraindications of adalat

A

Hypovolemia
Cardiac conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Side effects of salbutamol

A

It’s a b2 adrenergic receptorMaternal and fetal tachy
Hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Contraindications to salbutamol

A

Sternotic valvular heart lesions
Shock
Diabetes
Thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Side effects of prostaglandins in pregnancy

A

GIT irritation,
renal failure,
suppression of platelet function,
premature closure of fetal ductus arteriosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Contraindications to prostaglandins in pregnancy

A

Fetal gestational >32weeks
Peptic ulcer
Thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What antibiotics do we give for PROM

A

Ampicilin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of premature rupture of membranes (7)

A
  1. Intrauterine infection.
  2. An incompetent cervix.
  3. Iatrogenic rupture of the membranes in order to induce labour.
  4. Interference (this may be associated with intrauterine infection).
  5. As a complication of amniocentesis.
  6. As a complication of external cephalic version.
  7. In association with overdistension of the uterus e.g. polyhydramnios,
    multiple pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Investigations for PrOM (4)

A
  1. Litmus Testing: Liquor is alkaline and turns red litmus blue.
  2. “Ferning” can be observed under a microscope if liquor is placed on a slide
    and left to dry.
  3. Fetal fat cells stain orange with 1% Nile blue sulphate (after 30weeks)
  4. Amnisure: Is used for the detection of PAMG-1 (placental alpha
    macroglobulin 1) in amniotic luid using test strips. Expensive test
    therefore use litmus as initial test and Amnisure only in uncertain cases.
    Highly sensitive and speci ic for amniotic luid.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Management of PROM in pt <34 weeks

A

If GA>34 =/35 weeks) delivery

If <34 weeks conservative tx

Management before 34 weeks 1. Admit the patient and counsel about risks of preterm labour.
2. Avoid vaginal examination unless prolapsed cord suspected because of
abnormal fetal heart rate.
3. Administer antibiotics Azithromycin 500mg daily for 3 days
4. Administer Betamethasone 12mg IMI 12 hourly x 2 doses
5. Midstream urine to exclude urinary tract infection
6. Twice weekly white cell counts
7. Use of sterile pads
8. Growth ultrasound
9. If labour supervenes, consider tocolysis for 48 hours to administer steroids
10. If there are signs of infection such as maternal pyrexia, uterine tenderness
or fetal tachycardia or rising white cell count, induce labour urgently
regardless of the gestational age.
Aim for delivery at 34 weeks if maternal and fetal condition remains stable.
Pressure deformities and pulmonary hypoplasia may follow prolonged severe
oligohydramnios/ anhydramnios, and patients should be counselled regarding
this.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Management of PROM in a pt >34 weeks

A

Expedite delivery after 24 hours of rupture of membranes if not in labour either
with Prostaglandins (e.g. Misoprostol) or Oxytocin. Most patients will go into
labour spontaneously within 24 hours (85-90%). If any signs of infection or
other obstetric indication for delivery, induce labour earlier and do not wait for
24 hours.

patients
should receive IV antibiotics in labour to protect the baby against Group B Strep
- Ampicillin 1g 6 hourly intravenously. Alternatively, Clindamycin 600mg
intravenously 8 hourly for patients who are allergic to penicillin.

If HIV+ deliver within 4hours with IOL if not in labour

18
Q

What do you do in PROM in presence of cervical suture

A

Remove sutures
Management same as the general guideline

19
Q

What are IUGR foetuses at risk of

A
  1. Stillborn
  2. Birth Asphyxia
  3. Meconium Aspiration
  4. Iatrogenic preterm delivery
    5Neonatal complications : hypothermia, hypoglycemia and polycythemia
  5. Impaired neurological development
  6. Metabolic syndrome in adult hood (Barker hypothesis) as a result of genetic
    imprinting due to gene selection that occurs in utero. The affected fetus has an
    increased risk of developing many of the metabolic factors associated with an
    increased risk of vascular disease in later life.
    - Obesity
    - Type 2 diabetes
    - Cardiovascular disease
    - Hypertension
20
Q

Differentiate between Asymmetrical and symmetrical IUGR

A

Asymmetrical
The onset of the precipitating event is usually late in pregnancy (commonly
placental insuf iciency).
The fetus is asymmetrically small. This pattern of growth is as a result of fetal adaptive mechanisms, in order to
compensate for the decreased oxygen and nutrient delivery through the
placenta
1. Fetal centralisation of blood flow: vasoconstriction of splancnic and peripheral arteries and vasodilatation of cerebral circulation
2. Gluconeogenesis from hepatic stores : results in decrease in liver size and small abdo for GA.

Multi organ failure it the placental dysfunction continues
1. Metabolic acidosis
-Olygogydramnios
-loss of fetal breathing movement
Decreased tone
2. Worsened cardiac function
3. Asphyxia due to poor reserves

Symmetrical IUGR:
The precipitating cause of the growth restriction is usually of early pregnancy
onset – typically genetic or infection aetiology
The fetus is symmetrically small
These fetuses are at high risk of postnatal physical and mental retardation

21
Q

Aetiology/physiology of IUGR

A

Nutrient and oxygen delivery to the placenta
- E.g. decreased oxygen carrying capacity due to maternal cyanotic heart
disease, smoking, haemoglobinopathy
Nutrient and oxygen transfer across the placenta
- Maternal vascular disease, e.g. diabetes, hypertension, autoimmune
disease
- Placental damage resulting from smoking, thrombophilia, autoimmune
disease
Fetal uptake of nutrients and oxygen
- E.g. congenital abnormalities
Fetal regulation of growth processes
- E.g. inborn errors of metabolism

22
Q

Causes of IUGR

A

Maternal Causes:
Cardiorespiratory disease
Chronic hypertension
Pregnancy induced hypertensive disorders
Diabetes
Autoimmune disorders
206
Thrombophilias
Haemaglobinopathies
Renal disease
Malignancy
Connective tissue disorders
Anaemia
Fever
Protein energy malnutrition
Smoking
Drug abuse
Alcohol
Fetal Causes:
Congenital infections
- Rubella, CMV, Toxoplasmosis, Syphilis
Structural congenital abnormalities
- Anencephaly, cardiovascular disorders, etc
Chromosomal abnormalities
- Trisomy (13, 18, 21), Turners syndrome, etc
Inborn errors of metabolism

Placental causes:
Twin-to-twin transfusion syndrome
Multiple gestations
Placenta praevia
Recurrent antepartum haemorrhage
Extrauterine pregnancy
Placental
Thrombosis or infarction
Placenta insufficient abnormalities

23
Q

How to diagnose IUGR

A

Risk factors
SF height
US (growth scan)

24
Q

Clinical features of IUGR

A

Small hard head
Small for GA
Oliigohydramnios
Irritable uterus

25
When to refer to hospital for IUGR
4. The symphysis fundal height needs to be measured and plotted at each antenatal clinic visit 5. If there is no growth over 3 consecutive visits, referral and investigation is necessary. 6. If one measurement lies beneath the 10th centile, referral and investigation is necessary. 7. If a measurement is less than that recorded 2 visits previously, referral and investigation is necessary
26
Investigations for IUGR
1. Biometric tests measure SIZE. If performed over time they measure GROWTH. SFH measurements Ultrasound biometry 2. Biophysical tests are designed to predict fetal WELLBEING (which implies the absence of acidaemia) Fetal movement count Auscultation of fetal heart Amniotic luid volume Doppler studies Antenatal cardiotocograph Biophysical pro ile
27
What is the Resistance Index in Doppler US of fetus
Normally placental vascular resistance falls with advancing gestational age because of placental growth, vascularisation and increasing cross-sectional area within the vasculature. This leads to increasing low through the umbilical cord during fetal diastole. Pregnancies in which placental development is impeded fail to show this response and may have diminished or absent low during fetal diastole. This is characterised by measuring the resistance index (RI) in the umbilical artery (Systolic low-end Diastolic low/Systolic low).p
28
Management of IUGR
Refer to hospital for investigations, assessment and definitive management 1. Normal biometry on USS, normal AFI, normal CTG, normal fetal movements (i.e. normal growth and normal wellbeing) Manage at MOU 2. USS showing decreased growth velocity or asymmetry, but normal AFI, umbilical artery doppler, CTG and fetal movements (i.e. poor growth, but normal wellbeing) Identify and address avoidable risk factors (smoking,drugs,diet) Measure BP and urine dipstix at each clinic visit Weekly AFI, doppler, CTG Growth USS every 2-3weeks Fetal kick chart 3. USS showing decreases growth velocity or asymmetry, abnormal AFI, raised umbilical artery doppler (including AEDF), normal CTG (poor growth with decreased well being) Admit to hospital Identify and address avoidable risk factors - Smoking, drugs, diet Daily BP and urine dipstix Betamethazone (BMZ) 12mg daily for 2 days AFI and doppler twice weekly CTG at least daily Fetal kick chart Deliver: - When Fetus reaches 34 weeks - Fetal distress on CTG - Umbilical artery doppler worsens to REDF 4. USS showing decreases growth velocity or asymmetry, decreased AFI, REDF, normal CTG (poor growth, severely compromised fetus) Admit to hospital Identify and address avoidable risk factors - Smoking, drugs, diet Daily BP and urine dipstix Betamethazone 12mg daily for 2 days (to establish fetal lung maturity) Measure BP and urine dipstix at each clinic visit Weekly AFI, doppler, CTG Growth USS every 2-3weeks Fetal kick chart 3. USS showing decreases growth velocity or asymmetry, abnormal AFI, raised umbilical artery doppler (including AEDF), normal CTG (poor growth with decreased well being) Admit to hospital Identify and address avoidable risk factors - Smoking, drugs, diet Daily BP and urine dipstix Betamethazone (BMZ) 12mg daily for 2 days AFI and doppler twice weekly CTG at least daily Fetal kick chart Deliver: - When Fetus reaches 34 weeks - Fetal distress on CTG - Umbilical artery doppler worsens to REDF 4. USS showing decreases growth velocity or asymmetry, decreased AFI, REDF, normal CTG (poor growth, severely compromised fetus) Admit to hospital Identify and address avoidable risk factors - Smoking, drugs, diet Daily BP and urine dipstix Betamethazone 12mg daily for 2 days (to establish fetal lung maturity)
29
4 things to assess fetal wellbeing
CTG AFI Doppler Fetal movement
30
What are monochorionic-diamniotic twins
If the zygote splits in the blastular stage, the foetuses will share one placenta but will have their own amniotic sac
31
Complications of twin pregnancy
1st trimester 1. Abortion 2.hyperremesis gravidum 3. Vanish twin 4. Fetal malformations increase from 2-3 to 6% 5. Incarceration of retroverted uterus 2nd trimester 1. Anaemia 2. UTI 3. IUD of one fetus 3rd trimester 1. Preterm labour 2. GPH 3. Antepartum haemorrhage 4. Polyhydramnios 5. Malpresentation 6. IUGR 7. Gestational DM 8. Cord entanglement in monoamniotic 9. Twin to twin transfusions in monochorionic resulting in growth retardation 10. Twin anaemia polycythemia sequence (TAPS) 11. Maternal mortality double
32
Management of twin pregnancy
1. Diagnosis should be made as early as possible. 2. Treatment of complications as they arise. 3. Monitoring of haemoglobin and prevention of anaemia. 4. Physical activity: uncomplicated twin pregnancies can continue to exercise as in a singleton pregnancy. 5. Measuring cervical length from 16 weeks can be helpful in identifying women at risk for preterm labour, although evidence for this practice is sparse. 6. Ultrasound assessment of growth should be every 4-6 weeks after 20 weeks for dichorionic twins, and 2-4 weekly for monochorionic twins.
33
Management of twin delivery (what should you take into consideration)
Preterm labour is common. Preterm infants withstand hypoxia and trauma poorly. Intra-uterine growth restriction is more common and may affect one or both foetuses. Congenital abnormalities are more common. Placenta praevia is more common. Abruptio placentae is more common. Malposition and malpresentation occur frequently. Polyhydramnios, early rupture of membranes and cord prolapse is often associated. Associated pregnancy related disease such as pre-eclampsia and anaemia are more common. Induction of labour is not contra-indicated, neither is augmentation with oxytocin. The position of the second twin does not usually influence the choice of mode of delivery.
34
Indications for CS before delivery in a twin pregnancy
1. Any presentation other than cephalic in leading twin 2. Monoamniotic twins 3. Cephalic presentation of leading twin and non cephalic of second twin wheresize of head >20%of leading twin. Risk of head entrapment 4. Majority indications same for singletons
35
Timing of delivery of twins
Dichorionic diamniotic twins: planned delivery between 37+0 weeks and 37+6 weeks reduces the risk of stillbirth Monochorionic diamniotic twins: planned delivery between 36+0 and 36+6 weeks Monochorionic monoamniotic twins: planned delivery between 32+0 and 34+0 weeks because of the high risk of stillbirth despite close monitoring
36
Which immunoglobulin can cross placenta
IgG
37
Effect of the following drugs in pregnancy 1. Progestogens 2. Sodium valproate 3. Phenytoin sodium 4. Barbituates 5. Warfarin 6. Tetracyclines 7.Sulphanamides 8.Alcohol
In early pregnancy: Progestogens Masculinization of female fetus Sodium valproate Neural tube defects Phenytoin Sodium Cleft lip, diaphragmatic hernia Barbiturates Cleft lip and palate Warfarin Nasal hypoplasia, microcephaly In later pregnancy: Tetracyclines Teeth discolouration, Interference with bone growth Sulphonamides Hyperbilirubinaemia Alcohol Fetal alcohol syndrome
38
Management of Rhesus Negative Patient without Atypical Antibodies:
The father’s blood group and probable Rh genotype are established. If he is Rh negative, fetal haemolytic problems are not anticipated, and further routine tests are unnecessary. If the father is Rh positive or blood group unknown, the mother’s blood is examined every 4 weeks, from 20 weeks until delivery, for atypical antibodies because of possible sensitisation occurring during the pregnancy. If no antibodies develop, the patient is delivered at term. After delivery, anti-Rh immunoglobulins (100 ug by intramuscular injection) is administered if the fetus is Rh positive or if its blood group is unknown. It is also given after abortion or ectopic pregnancy in Rh negative patients. Rh Immunoglobulin (Rhogam) Not indicated id the patient already has antibodies. If no antibodies are present, anti-D immunoglobuin G is given IM within 72 hours postpartum. The patient is temporarily passively immunised to prevent permanent active immunisation. 100 ug of Rh immune globulin can neutralise 10 ml of D positive blood
39
Management of the Rh Negative Patient with Atypical Antibodies:
Check father’s blood group and genotype. Determine the gestational age of the fetus and the placental localisation by ultrasound. Estimate mother’s antibody titre every 2 weeks. If the titre is > 1:8, an ultrasound examination of the fetal middle cerebral artery is performed. It has been shown that, in anaemic fetuses (due to haemolysis), the peak systolic velocity in the middle cerebral artery is increased. Affected fetuses can thus be identified with a high degree of accuracy. This test is repeated 1-2 weekly and, if it rises to > 1.5 MOM, significant anaemia in the fetus is assumed. If the fetus is 34 weeks pregnant or more, delivery may be considered. If the fetus is premature, an intrauterine blood transfusion is planned. A cordocentesis is performed and blood taken for an immediate measure of the haemoglobin. If the anaemia is confirmed, pre-crossmatched blood is transfused into the fetal umbilical cord. The amount needed to raise the haemoglobin is calculated by a formula. The transfusion is repeated every 2-3 weeks depending on the peak systolic velocity in the middle cerebral artery. Delivery is close to term. In the absence of a facility to do fetal blood transfusions, the fetus may be delivered prematurely after steroid administration.
40
Congenital abnormalities associated with Polyhydramnios
oesophageal atresia, duodenal atresia, anencephaly
41
Screening tests for chromosomal abnormalities in pregnancy
1. Nuchal translucency scan: (11-14 weeks). Other ultrasound features can be added to this to increase the sensitivity, e.g. nasal bone measurement, tricuspid incompetence, ductus venosus measurement. This combination can have up to 95% sensitivity for the detection of Down syndrome. 2. Triple test: (16 weeks) Measures -HCG, alpha-fetoprotein and oestriol. 70% sensitive with 5% false positive rate 3. Fetal anomaly scan: (20 weeks) Looking for ‘soft’ markers of chromosomal abnormalities. This is also a screening test for structural abnormalities. 4. NIPT (non-invasive prenatal testing). This is a new test which is done on maternal blood and is thus non-invasive. It has a 995 sensitivity for detection of Down syndrome. It is, however, expensive
42
Diagnostic tests for fetal anomalies
Amniocentesis Chorionic villous sampling Cordocentesis