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Obstetrics & Gynaecology > Antenatal complications > Flashcards

Antenatal complications Flashcards

1
Q

Uncomplicated nausea and vomiting in prengancy

A

affects 80% of women
Typically week 8-14
10% of pregnancies will have continued n+v beyond 20w until birth

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2
Q

Definition of hyperemesis gravidarum

A

Severe, intractable vomiting in pregnancy that results in inability to maintain hydration orally, metabolic disturbance, and admission to hospital for parenteral hydration

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3
Q

Prevalence of hyperemesis gravidarum

A

Occurs in less than 1% of pregnancies

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4
Q

Pathogenesis of hyperemesis gravidarum

A

Hormonal (hCG and oestrogen)
Mechanical (red LOS tone, gastric peristalsis and gastric emptying)
?Emotional

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5
Q

Complications of hyperemesis gravidarum

A 
Hyponatremia
Hypokalemia
Metabolic hypochloraemic alkalosis
Ketonuria
Raised haematocrit
Increased specific gravity of urine
Wernicke's encephalopathy
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6
Q

Investigations if suspecting hyperemesis gravidarum

A 
Urinalysis and MCS
Stool culture
EUC
BGL (if diabetic)
LFTs
TFTs (?thyrotoxicosis)
Serum amylase (?pancreatitis)
Ultrasound (?ongoing pregnancy, multiple, molar)
Abdominal erect and supine x-rays (?bowel obs)
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7
Q

Management of hyperemesis gravidarum

A

IV hydration if required (0.9% Na + K or Hartmann’s)
Glucose and vitamins (esp. thiamine) if prolonged vomiting
- administer thiamine first to prevent Wernickes
Dietary modification (small frequent low-fat meals, early when hungry)
Alternative (acupuncture, Ginger, multivitamins[B6])
Pharmacologic

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8
Q

Antiemetics for use in Hyperemesis gravidarum

A

Metoclopramide 10mg TDS
Doxylamine 25mg nocte
Promethazine 25mg BD (sedation)
Prochlorperazine 25mg suppository 1-2/day
Ondansetron 4-8mg oral or IV (if IV rehydration, thiamine and electrolyte correction)
Corticosteroids if refractory

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9
Q

Complication of use of corticosteroids in first trimester of pregnancy

A

Increased risk of oral clefting

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10
Q

Definition of oligohydramnios

A

An amniotic fluid volume that is less than expected for gestational age

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11
Q

Causes of oligohydramnios

A 
Placental (3)
- abruption
- twin-twin transfusion
- placental thrombosis/ischaemia
Foetal (6)
- Chromosomal abnormalities
- congenital abnormalities (esp if impairs urine production e.g. renal obstruction)
- Growth restriction (blood flow redirected away from kidneys)
- intrauterine foetal demise
- post-term pregnancy
- ruptured foetal membranes
Maternal (7)
- Medical:
      - chronic HTN
      - collagen vascular disease
      - nephropathy
      - thrombophilia
- Obstetric:
      - Preeclampsia
- medications:
     - ACE-inhibitors
     - NSAIDs
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12
Q

Normal daily foetal urine production

A

800-1200mL/day

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13
Q

Normal volume swallowed by foetus per day

A

500-1000mL/day

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14
Q

Normal measurements of amniotic fluid

A

Deepest volume pocket (DVP) 2-8cm

Amniotic fluid index (sum of 4 quadrant DVP) 5-25

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15
Q

Measurement of oligohydramnios in multiple pregnancy

A

Single deepest pocket (SDP) under 2cm

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16
Q

Components of biophysical profile (5)

A 
Foetal HR
Foetal breathing movements
Foetal activity/gross body movement
Foetal muscle tone
Qualitative AFI
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17
Q

Management of oligohydramnios

A

Identify cause (history, USS)
+/- Increase amniotic fluid
Serial USS to monitor AFI and foetal growth (weekly, 4-weekly respectively)
+Non-stress testing +/- Biophysical profile
Likely to require early delivery

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18
Q

Indications to increase amniotic fluid volume in oligohydramnios

A

Improve detection of foetal anomalies
Facilitate cephalic version
Prevent foetal sequelae

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19
Q

Methods to increase amniotic fluid volume in oligohydramnios

A

Amnioinfusion
Maternal hydration
Foetal membrane sealants (if leaking PPROM)

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20
Q

Commonest causes for severe polyhydramnios

A

Foetal anomalies (particularly trisomy 21)

Maternal and idiopathic factors are more often associated with milder cases

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21
Q

Incidence of polyhydramnios

A

1-2% of pregnancies

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22
Q

What syndrome is suggested by IUGR plus polyhydramnios

A

Trisomy 18

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23
Q

Causes of polyhydramnios

A 
Foetal (33%)
- Chromosomal anomalies
- CNS: ancephaly, hydrocephalus
- GI: oesophageal atresia/TOF, facial clefts (impaired swallowing)
- Neuromuscular condition inhibiting swallowing
Maternal:
- Type 1 DM (disordered transchorionic flow)
Maternal-foetal
- Chorioangioimas
- Multiple gestation
- Foetal hydrops
Idiopathic (40%)
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24
Q

Causes of foetal hydrops

A

Anaemia (thalassaemia, virus, ABO incompatibility)
Congestive heart failure
Infection (TORCH, syphilis, varicella)
Obstructed lymphatic flow
Red. plasma oncotic pressure (liver disease, nephropathy)
Metabolic storage disease
Thoracic abnormalities (e.g. chylothorax, diaphragmatic hernia)
AV and venous malformations
GI malformations
GU malformations
Twin gestation (twin-twin transfusion syndrome)

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25
Q

Clinical features of polyhydramnios

A

Uterine size large for dates
FLUID THRILL
Mother may experience SOB, uterine irritability and contractions, abdominal discomfort

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26
Q

Ultrasonographic findings of polyhydramnios

A

Single deepest pocket greater than 8cm

AFI greater than 24 cm

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27
Q

Management options of polyhydramnios

A 
Antepartum foetal monitoring
Nonstress test + biophysical profile every 1-2 weeks until 37 weeks (more often if severe)
Amnioreduction if severe and symptomatic
Indomethacin
Generally induce labour early
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28
Q

Indomethacin use in polyhydramnios (dose, side effects, contraindications)

A

25mg orally QID (works in 2-3d)
S/E: nausea, reflux, gastritis, vomiting, platelet dysfunction
Foetal A/E: constriction of ductus arteriosus, necrotising enterocolitis, intraventricular haemorrhage
Contraindicated after 32 weeks (risk of closure of ductus)

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29
Q

Mechanism of action of indomethacin in polyhydramnios

A

Stimulates foetal ADH secretion - antidiuretic response in kidneys + reduced renal blood flow - reduced foetal urine production

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30
Q

Prognosis of polyhydramnios

A

Increased risk of perinatal mortality (2- to 5- fold)

Many IDIOPATHIC cases resolve spontaneously

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31
Q

Complications related to polyhydramnios

A 
Maternal respiratory compromise
Preterm labour, PPROM, preterm delivery
Foetal malposition
Macrosomia
Umbilical cord prolapse
Placental abruption upon rupture of membranes
Postpartum uterine atony - PPH
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32
Q

Definition of IUGR

A

A foetal weight below the 10th percentile for gestational age

  • typically if following normal growth trajectory, normal Doppler of umbilical artery and normal amniotic fluid volume, likely to be constitutional SGA
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33
Q

Categories of IUGR

A

Symmetric: body and head growth reduced

  • begins in EARLY gestation
  • usually INTRINSIC factors (chromosomal, congenital)

Asymmetric (head-sparing): usually just reduced weight(AC) with normal length and head

  • begins in late SECOND or THIRD trimesters
  • Due to reductions in foetal nutrients - limited fat storage but enough to allow continued brain growth
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34
Q

Maternal causes of IUGR (9)

A

Severe starvation
Hypoxaemia
Haematologic/immunologic causing thrombosis
Medical or obstetric conditions associated with vasculopathy (PET, nephropathy, vascular disease)
TORCH, malaria
Substance abuse
Toxin exposure (warfarin, AEDs, folic acid antagonists)
High altitude
Demographic (rage, age, size, previous SGA)

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35
Q

Placental causes of IUGR (9)

A 
Abnormal uteroplacental vasculature
Chronic inflammatory lesions
Abruption
Thrombophilia related pathology
Gross structural anomalies (single umbi art, velamentous insertion, haemangioma)
Infarction
Tumour
Villous placentitis
Confined placental mosaicism
36
Q

Diagnosis of IUGR

A

Ultrasound showing estimated foetal weight OR abdominal circumference below 10th percentile for gestational age

37
Q

In which pregnancies are SFH measurements unsuitable/inaccurate

A

Large fibroids
High maternal BMI
Intentional weight loss while pregnant (e.g. post-bariatric surgery)
Polyhydramnios/oligohydramnios

38
Q

Foetal causes of IUGR (6)

A

Chromosomal anomalies
Genetic syndromes (E.g. Russel-Silver, dwarfism, Bloom)
Major congenital anomalies (congenital heart disease)
Multiple gestation
Metabolic disorders

39
Q

Investigations to consider in IUGR

A 
FTS for T21
Early USS - dating, NT
Uterine artery Doppler (19-23 weeks)
Later USS: EFW, AC, AFV, BPPP, umbilical art Doppler, placental/uterine/foetal abnormalities
Amniocentesis if high risk
TORCH screen
40
Q

Definition of preeclampsia

A

A multisystem disorder characterised by the new onset of hypertension + proteinuria OR end-organ dysfunction after 20 weeks of gestation in a previously normotensive woman

41
Q

HELLP syndrome

A

Haemolysis, Elevated Liver enzymes, Low Platelets

42
Q

Gestational hypertension definition

A

hypertension without proteinuria or other signs of preeclampsia that develops after 20 weeks of gestation and resolves by 12 weeks postpartum

43
Q

Potential complications of preeclampsia/eclampsia

A 
Placental abruption
Acute kidney injury
Cerebral haemorrhage (STROKE)
Hepatic failure or rupture
Pulmonary oedema
Disseminated intravascular coagulation
44
Q

Risk factors predisposing to preeclampsia

A

Past history of PET
Nulliparity
Family history of preeclampsia in first degree relative
Twin pregnancy
Advanced maternal age (over 40)
Pre-existing: DM, HTN, ANTIPHOSPHOLIPID ANTIBODIES, overweight BMI

Women who smoke have a LOWER risk of preeclampsia than non-smokers

45
Q

Clinical presentation of PET

A

After 20w GA (usually after 34)

  • new development of HTN
  • Proteinuria
  • persistent/severe headache (non-responsive to OTC analgesia)
  • Visual abnormalities
  • sudden and rapid weight gain
  • oedema of hands and face
  • upper abdo/epigastric pain
  • nausea, vomiting
  • dyspnoea, retrosternal chest pain
  • altered mental status
46
Q

Pre-eclampsia prior to 20 weeks gestation is usually associated with what type of pregnancy

A

complete or partial molar pregnancy

47
Q

Criteria for diagnosis of PET

A

Systolic BP higher than 140 OR DBP higher than 90
AND
- proteinuria 0.3g in 24h OR ACR 0.3
OR
- signs of end-organ dysfunciton (thrombocytopaenia, raised creatinine, raised transaminases)

48
Q

Mechanism of thrombocytopaenia in PET

A

microangiopathic endothelial injury and activation - platelet and fibrin thrombi - accelerated platelet consumption

49
Q

Incidence of women with PET who develop eclampsia

A

2%

50
Q

Management of PET

A

Severe disease: indicates delivery
When to initiate delivery is based on GA, severity of disease, and maternal and foetal condition
- 37GA+ are delivered
- Serious maternal end-organ dysfunciton or indeterminate tests of foetal health may indicate delivery at any age
- if mother and foetus are stable, close monitoring with conservative approach

51
Q

Definition of a heterotopic pregnancy

A

An ectopic pregnancy plus an intrauterine pregnancy concomitantly

52
Q

Name for a pregnancy with both ectopic and intrauterine pregnancies

A

Heterotopic pregnancy

53
Q

Incidence of ectopic pregnancy

A

2%
Subsequent risk:
after 1: 10-15% chance of another
after 2: 25-65% chance of another

54
Q

Risk factors for ectopic pregnancy

A 
Previous ectopic
PID
Tubal surgery (e.g. sterilisation or reversal)
IVF
Smoking
Age 35+
Multiple sexual partners

IUCD (50% risk of ectopy if becomes pregnancy as prevents normal plantation in endometrial cavity but not from occuring in tubes)

55
Q

Incidence of heterotopic pregnancy

A

Uncommon in general population (1/4000)

VERY common in IVF cycles - 1%

56
Q

Most common sites for ectopic pregnancy

A

85% in ampulla (S-bend) portion of tube
5% in other areas of tube

Uncommon locations:

  • ovary
  • tubal interstitium (cornual pregnancy)
  • cervical
  • LSCS scar
  • Abdominal
57
Q

Presentation of ectopic pregnancy

A

Amenorrhoea
Pain (RIF or shoulder-tip secondary to intra-abdominal haemorrhage)
+/- PV bleeding (usually light spotting)
+ve pregnancy test

Tachycardia and hypotension if perforated

58
Q

Confirmation of ectopic pregnancy

A

Serial b-hCG rising at slower rate than normal (less than doubling every 2-3 days)
Correlation of single hCG with USS
- ?obvious gestational sac and embryo in extrauterine site
- inability to identify gestational sac and embryo in uterus

59
Q

Management of ectopic pregnancy

A 
GOLD STANDARD: surgery
Laparoscopic slapingectomy (removal of fallopian tube)

Salpingotomy - removal of pregnancy without removal of rest of tube - no increased fertility afterwards compared to salpingectomy
Follow up to ensure pregnancy not persistent

Medical:

  • Prostaglandin or hypertonic saline direct tubal injection
  • MTX by IM injection
  • may be better option if multiple adhesions in abdo (e.g. Crohn’s disease, multiple past laparotomies)

Expectant management if appears to have miscarried?

60
Q

Definition of antepartum haemorrhage

A

Vaginal bleeding associated with intrauterine pregnancy from 24 weeks gestation until the onset of labour

61
Q

Risk factors of antepartum haemorrhage

A 
Domestic violence
Previous C-section
Male gender of foetus
Previous placenta praevia or abruption
Cocaine
Smoking in pregnancy
62
Q

Potential causes for antepartum haemorrhage

A

Vulva/vaginal trauma, inflammation
Cervix: (may be provoked by sex) ectropion, carcinoma, effacement in labour
Placental (praevia, abruption, vasa praevia)
Uterine rupture
Unexplained (most common)

63
Q

Most common causes for antepartum haemorrhage

A 
Placental abruption (30%)
Placenta praevia (20%)
Labour

Uterine rupture, vasa praevia are rare causes

64
Q

Definition of placenta praevia

A

Defined as a placenta encroaching on the lower segment, with the lower segment arbitratily defined on ultrasound as extending 5cm from the internal os

65
Q

Prevalence of placenta praevia

A

0.35-0.5%

66
Q

Complications of placenta praevia

A 
Antepartum haemorrhage
Intrapartum haemorrhage
Postpartum haemorrhage
Need of transfusion
Maternal mortality
Neonatal mortality
Recurrence
Increased risk of other pregnancy complications (malpresentation, placenta accreta, preterm labour and PROM, IUGR, vasa praevia and velementous insertion)
67
Q

Risk factors for placenta praevia

A 
Previous placenta praevia
Older maternal age
Previous C-section
Multiple gestation
Multiparity
Infertility treatment
Previous abortion
Previous intrauterine surgery
Maternal smoking, cocaine
Male foetus
Non-white race
68
Q

Grading of placenta praevia

A

I: encroaches on lower segment - MINOR
II: reaches margin of internal os - MINOR
III: partially covers internal os - MAJOR
IV: Completely covers internal os - MAJOR

69
Q

Presentation of placenta praevia (not diagnosed on antenatal scans)

A

Painless vaginal bleeding after 20 weeks gestation (60% after 30 weeks)
+/- uterine contractions

70
Q

Management of placenta praevia discovered at morphology scan

A

Follow up transvaginal USS at 32 weeks,

If placental edge still less than 2cm from internal os, follow-up at 36 weeks

71
Q

Reducing risk of bleeding in woman with known placenta praevia

A

Avoid vaginal intercourse after 20 weeks gestation
Reduce overall physical activity in third trimester
Seek immediate attentino if contractions or bleeding occur

72
Q

Management of asymptomatic woman with confirmed placenta praevia in late pregnancy

A

Elective delivery at 38-39 weeks

73
Q

Management of acutely bleeding placenta praevia

A

Achieve/maintain haemodynamic stability in mother
Determine if C-section indicated
- non-reassuring FHR
- life-threatening refractory haemorrhage
- significant vaginal bleeding after 24 weeks

74
Q

Indications for c-section delivery in woman with low-lying placenta

A

Placenta less than 20mm from internal os

75
Q

Definition of placental abruption

A

Bleeding at the decidual-placental interface that causes partial or total placental detachment prior to the delivery of the foetus after 20 weeks gestation

76
Q

Incidence of placental abruption

A

less than 1% of pregnancies

77
Q

Common gestation at which placental abruption occurs

A

40-60% before 37 weeks

15% before 32 weeks

78
Q

Risk factors for placental abruption

A 
Severe maternal trauma
Uterine abnormalities
Cocaine and cigarettes
Polyhydramnios (occurs at SROM)
HTN, PET or eclampsia
PROM
Chorioamnionitis
Previous PET IUGR or abruption
Advanced maternal age
Multiparity
Male sex
79
Q

Presentation of acute placental abruption

A

Acute onset vaginal bleeding + abdominal/back pain + contractions

Contractions typically high frequency, low amplitude

Couvelaire uterus (firm, rigid and tender uterus during and between contractions)

80
Q

Presentation of concealed placental abruption

A

Preterm labour with no or scant bleeding

10-20% of women with abruption

81
Q

Investigations in placental abruption

A

USS - only sensitive in 25-50%
CBE, biochem, renal function
Blood type and crossmatch
Coagulation studies
Fibrinogen (best correlation with severity of bleeding - initial levels less than 200mg/dL predict severe PPH)
D-dimer, fibrin degradation products (evidence of acute DIC)
Kleihauer-Betke test (foetal bleeding)

82
Q

Complications of placental abruption

A

PPH
Excessive blood loss and DIC (end organ failure, hypovolaemic shock, peripartum hysterectomy, need for blood transfusion)
Emergency C-section
Recurrence
Perinatal morbidity and mortality (hypoxaemia, asphyxia, low birth weight, preterm)
IUGR (with chronic abruption)

83
Q

Management of abruption

A

ABCs, stabilise mother
Indications for delivery:
- severe abruption at any gestational age OR
- non-severe abruption at less than 36 weeks
Vaginal if mother stable and FHR reassuring
Emergency C-section if:
- mother unstable or FHR non-reassuring and vaginal delivery not imminent
- vaginal delivery contraindicated (e.g. malpresentation)
- failure to progress with vaginal delivery
Non-severe less than 36 weeks: close monitoring or deliver if risk of developing sudden severe abruption
Delivery of further pregnancies before 37 weeks

84
Q

Antihypertensives used in pre-eclampsia

A

Labetalol
Methyldopa
Nifedipine (FAST-ACTING - often not available in rural sites)

85
Q

Role of antihypertensives in pre-eclampsia

A

Reduces maternal end organ failure and stroke
No reduction in risk of eclampsia progression
No change in outcomes for foetus

Obstetrics & Gynaecology (22 decks)

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