Obstetrics Complications Flashcards
(42 cards)
Causes of premature birth
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
Risk factors for preterm
Previous preterm labour
Unbooked status
Smoking, alcohol
Malnutrition
Multiple pregnancy
Poor socio-economic status
How do you diagnose preterm labour
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 to manage pt who comes in preterm labour
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
- 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.
Investigations for pt coming in with preterm labour
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)
Contraindications tocolysis
Intrauterine fetal death
IUGR
Chorioamnionitis
Fetal distress
Antepartum haemorrhage
Fatal fetal abnormalities
Pre-eclampsia
Side effects of adalat
It’s a Ca channel blocker
Nausea and vomiting
Flushing
Contraindications of adalat
Hypovolemia
Cardiac conditions
Side effects of salbutamol
It’s a b2 adrenergic receptorMaternal and fetal tachy
Hyperglycemia
Contraindications to salbutamol
Sternotic valvular heart lesions
Shock
Diabetes
Thyrotoxicosis
Side effects of prostaglandins in pregnancy
GIT irritation,
renal failure,
suppression of platelet function,
premature closure of fetal ductus arteriosus
Contraindications to prostaglandins in pregnancy
Fetal gestational >32weeks
Peptic ulcer
Thrombocytopenia
What antibiotics do we give for PROM
Ampicilin
Causes of premature rupture of membranes (7)
- Intrauterine infection.
- An incompetent cervix.
- Iatrogenic rupture of the membranes in order to induce labour.
- Interference (this may be associated with intrauterine infection).
- As a complication of amniocentesis.
- As a complication of external cephalic version.
- In association with overdistension of the uterus e.g. polyhydramnios,
multiple pregnancy
Investigations for PrOM (4)
- Litmus Testing: Liquor is alkaline and turns red litmus blue.
- “Ferning” can be observed under a microscope if liquor is placed on a slide
and left to dry. - Fetal fat cells stain orange with 1% Nile blue sulphate (after 30weeks)
- 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.
Management of PROM in pt <34 weeks
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.
Management of PROM in a pt >34 weeks
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
What do you do in PROM in presence of cervical suture
Remove sutures
Management same as the general guideline
What are IUGR foetuses at risk of
- Stillborn
- Birth Asphyxia
- Meconium Aspiration
- Iatrogenic preterm delivery
5Neonatal complications : hypothermia, hypoglycemia and polycythemia - Impaired neurological development
- 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
Differentiate between Asymmetrical and symmetrical IUGR
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
Aetiology/physiology of IUGR
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
Causes of IUGR
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
How to diagnose IUGR
Risk factors
SF height
US (growth scan)
Clinical features of IUGR
Small hard head
Small for GA
Oliigohydramnios
Irritable uterus