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Systems: Reproduction AB > Complications of Pregnancy > Flashcards

Complications of Pregnancy Flashcards

1
Q

Abortion or spontaneous miscarriage

A

Termination of loss of pregnancy before 24 weeks gestation

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2
Q

What is the incidence of spontaneous miscarriage?

A

About 15%

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3
Q

What are the types of spontaneous miscarriage?

A
  • Threatened
  • Inevitable
  • Incomplete
  • Complete
  • Septic
  • Missed
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4
Q

What is a threatened miscarriage?

A

Refers to bleeding from the gravid uterus before 24 weeks gestation when there is a viable foetus and no evidence of cervical dilatation

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5
Q

When does abortion in miscarriage become inevitable?

A

When the cervix begins to dilate

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6
Q

What is an incomplete miscarriage?

A

Only partial expulsion of the products of conception

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7
Q

What is a complete miscarriage?

A

When all products of conception are expelled

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8
Q

What is a septic miscarriage?

A

Ascending infection into the uterus which can spread throughout the pelvis

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9
Q

What is a risk factor for septic miscarriage?

A

Incomplete miscarriage

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10
Q

What is a missed miscarriage?

A

A pregnancy in which the foetus has died but the uterus has made no attempt to expel the products of conception

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11
Q

How does a threatened miscarriage present?

A
  • Vaginal bleeding +/-pain
  • Viable pregnancy
  • Closed cervix on speculum examination
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12
Q

How does an inevitable miscarriage present?

A
  • Viable pregnancy

- Open cervix with bleeding that could be heavy (+/-clots)

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13
Q

How does a missed miscarriage present?

A
  • May have no symptoms of could have bleeding/brown loss vaginally
  • Gestation sac is seen on scan
  • No clear foetus (empty gestational sac) or a foetal pole with no foetal heart seen on the scan
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14
Q

How does an incomplete miscarriage present?

A
  • Most of pregnancy expelled out, some products of the pregnancy remain in the uterus
  • Open cervix and vaginal bleeding (may be heavy)
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15
Q

How does a complete miscarriage present?

A
  • Passed all products of conception (POC)
  • Cervix closed and bleeding has stopped (should ideally have confirmed that the POC or should have had a scan that confirmed an intrauterine pregnancy)
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16
Q

How does a septic miscarriage present?

A

With symptoms of infection secondary to miscarriage

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17
Q

What is the aetiology of spontaneous miscarriage?

A
  • Abnormal conceptus (chromosomal, genetic, structural)
  • Uterine abnormality (congenital, fibroids)
  • Cervical incompetence (Primary (congenital), secondary (iatrogenic))
  • Maternal (increasing age, diabetes)
  • Unknown
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18
Q

How are threatened miscarriages managed?

A

Conservatively

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19
Q

How are inevitable miscarriages managed?

A

If bleeding is heavy may need evacuation

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20
Q

How are missed miscarriages managed?

A
  • Conservative
  • Medically with prostaglandins (misoprostol)
  • Surgical management of miscarriage
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21
Q

How are septic miscarriages managed?

A

Antibiotics and evacuate uterus

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22
Q

What is an ectopic pregnancy?

A

Pregnancy which implants outside the uterine cavity

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23
Q

Give examples of sites of miscarriage?

A
  • Ampulla of fallopian tube (most common)
  • Isthmus of fallopian tube
  • Interstium of fallopian tube
  • Ovary (rare)
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24
Q

What is the incidence of ectopic pregnancy?

A

1 in 90 pregnancies

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25
Q

What are the risk factors for ectopic pregnancy?

A
  • Pelvic inflammatory disease
  • Previous tubal surgery
  • previous ectopic surgery
  • Assisted conception
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26
Q

How do ectopic pregnancies present?

A

-Period of ammenorhoea (with +ve urine pregnancy test)
+/- Vaginal bleeding
+/- Pain abdomen
+/- GI or urinary symptoms

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27
Q

How are ectopic pregnancies investigated?

A

Scan – no intrauterine gestational sac, may see adnexal mass, fluid in Pouch of Douglas

Serum BHCG levels – may need to serially track levels over 48 hour intervals- if a normal early intrauterine pregnancy HCG levels will increase by at least 66%ish

Serum Progesterone levels – with viable IU pregnancy high levels > 25ng/ml

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28
Q

How are ectopic pregnancies managed?

A
  • Methotrexate
  • Surgical salpingectomy or salpingotomy
  • Conservative
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29
Q

What is an antepartum haemorrhage?

A

Haemorrhage from the genital tract after the 24th week of pregnancy but before delivery of the baby.

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30
Q

What are some causes of antepartum haemorrhage?

A
  • Placenta praevia
  • Placental abruption
  • APH of unknown origin
  • Local lesions of the genital tract
  • Vasa praevia (very rare)
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31
Q

What is placenta praevia?

A

All or part of the placenta implants in the lower uterine segment

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32
Q

What is the incidence of placenta praevia?

A

1 in 200 pregnancies

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33
Q

Who is placenta praevia more common in?

A
  • Multiparous women
  • Multiple pregnancies
  • Previous C section
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34
Q

What are the classifications of placenta praevia?

A

Grade I Placenta encroaching on the lower segment but not the internal cervical os

Grade II Placenta reaches the internal os

Grade III Placenta eccentrically covers the os

Grade IV Central placenta praevia

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35
Q

How does placenta praevia present?

A
  • Painless PV bleed
  • Malpresentation of the foetus
  • Incidental on US
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36
Q

What are the clinical features of placenta praevia?

A
  • Maternal condition correlates with amount of bleeding PV

- Soft, non tender uterus +/- fetal malpresentation

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37
Q

How is placenta praevia diagnosed?

A

-USS

VAGINAL EXAMINATION MUST NOT BE DONE

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38
Q

How is placenta praevia diagnosed?

A
  • Depends on severity and gestation
  • Mother admitted to hospital and attempts made to allow for maturation of the foetus
  • Delivered by C section
  • Mother may require blood transfusion
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39
Q

What is there a risk of following delivery with placenta praevia?

A

PPH

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40
Q

How is PPH managed?

A

Medical
-Oxytocin, ergometrine, carbaprost, tranexamic acid

Balloon tamponade

Surgical
-Blynch cutre, ligation of the uterine and iliac vessels, hyserterectomy

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41
Q

What is placental abruption?

A

Haemorrhage resulting from premature separation of the placenta before the birth of the baby?

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42
Q

What is the incidence of placental abruption?

A

0.6% of all pregnancies

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43
Q

What factors are associated with placental abruption?

A
  • Pre-eclampsia/ chronic hypertension
  • Multiple pregnancy
  • Polyhydramnios
  • Smoking, increasing age, parity
  • Previous abruption
  • Cocaine use
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44
Q

What are the clinical types of placental abruption?

A
  • Revealed
  • Concealed
  • Mixed
45
Q

How does a placental abruption present?

A
  • Pain
  • Vaginal bleeding (may be minimal)
  • Increased uterine activity
46
Q

What is a revealed placenta abruption?

A

When the major haemorrhage is apparent externally because the blood released from the placenta escapes through the cervical os.

47
Q

What is a concealed placenta abruption?

A
  • When the haemorrhage occurs between the placenta and the uterine wall.
  • The uterine contents increase in volume and the fundal height is larger than would be consistent for gestation.
  • In some situations the blood penetrates the uterine wall and the uterus appears bruised and this is know as a Couvelaire uterus.
48
Q

What does management of APH depend on?

A

Management will vary from expectant treatment to attempting a vaginal delivery to immediate Caesarean section depending on

  • Amount of bleeding
  • General condition of mother and baby
  • Gestation
49
Q

What are the possible complications of placental abruption?

A
  • Maternal shock, collapse (may be disproportionate to the amount of bleeding seen)
  • Foetal death
  • Maternal DIC, renal failure
  • Postpartum haemorrhage ‘couvelaire uterus’
50
Q

What is preterm labour?

A
  • Onset of labour before 37 completed weeks of gestation (259 days)
  • Can be spontaneous or induced
51
Q

What are the classifications of preterm labour?

A
  • 32-36 wks mildly preterm
  • 28-32 wks very preterm
  • 24-28 wks extremely preterm
52
Q

What is the incidence of preterm labour?

A
  • Around 5- 7% in singletons

- 30 - 40% multiple pregnancy

53
Q

What are some predisposing factors for preterm labour?

A
  • Multiple pregnancy
  • Polyhydramnios
  • APH
  • Pre-eclampsia
  • Infection eg UTI
  • Prelabour premature rupture of membranes
  • Idiopathic
54
Q

How is preterm labour diagnosed?

A
  • Contractions with evidence of cervical change

- Possible cause should be considered

55
Q

How is preterm delivery <24-26 weeks managed?

A
  • Generally regarded as very poor prognosis

- Decisions made in discussion with parents and neonatologists

56
Q

How are preterm deliveries managed in all cases considered viable?

A
  • Consider tocolysis to allow steroids/ transfer
  • Steroids unless contraindicated
  • Transfer to unit with NICU facilities
  • Aim for vaginal delivery
57
Q

What is preterm delivery a major cause of?

A

Perinatal mortality and morbidity

58
Q

What are the survival rates for very preterm infants?

A 
<24 weeks: 6
24 weeks: 26
25 weeks: 43
26 weeks: 48
27 weeks: 73
28 weeks: 84
59
Q

What are the percentage of very preterm delivery survivors with severe disability?

A

<24 weeks: 65
24 weeks: 38
25 weeks: 31
26 weeks: 26

60
Q

What neonatal morbidity may result from prematurity?

A
  • Respiratory distress syndrome
  • Intraventricular haemorrhage
  • Cerebral palsy
  • Nutrition
  • Temperature control
  • Jaundice
  • Infections
  • Visual impairment
  • Hearing loss
61
Q

Give examples of hypertensive disorders in pregnancy.

A
  • Chronic hypertension
  • Gestational hypertension
  • Pre-eclampsia
62
Q

What is chronic hypertension?

A

Hypertension either pre-pregnancy or at booking (≤ 20 weeks gestation)

63
Q

What is considered mild hypertension?

A

Systolic BP
140-149

Diastolic BP
90-99

64
Q

What is considered moderate hypertension?

A

Systolic BP
150-159

Diastolic BP
100-109

65
Q

What is considered severe hypertension?

A

Systolic BP
>160

Diastolic
>110

66
Q

What is gestational hypertension?

A

Pregnancy induced hypertension which develops after 20 weeks

67
Q

What is pre-eclampsia?

A

New hypertension > 20 weeks in association with

significant proteinuria

68
Q

What is considered significant proteinuria?

A
  • Automated reagent strip urine protein estimation > 1+
  • Spot Urinary Protein: Creatinine Ratio > 30 mg/mmol
  • 24 hours urine protein collection > 300mg/ day
69
Q

Who is chronic hypertension commoner in?

A

Older mothers

70
Q

How should chronic hypertension in pregnancy be managed?

A
  • Ideally patient should have pre-pregnancy care
  • Aim to keep BP < 150/100 (labetolol, nifedipine, methyldopa)
  • Monitor for superimposed pre-eclampsia
  • Monitor foetal growth: may have delayed foetal growth
  • May have a higher incidence of placental abruption
71
Q

Give examples of antihypertensives that are safe to use in pregnancy.

A
  • Labetolol
  • Methyldopa
  • Nifedipine
72
Q

How is pre-eclampsia defined?

A
  • Mild HT on two occasions more than 4 hours apart
  • OR Moderate to severe HT

PLUS proteinuria of more than 300 mgms/ 24 hours (protein urine > + protein:creatinine ratio > 30mgms/mmol)

73
Q

What is the pathophysiology of pre-eclampsia?

A

Immunological

Genetic

  • Secondary invasion of maternal spiral arterioles by trophoblasts impaired leading to reduced placental perfusion
  • Imbalance between vasodilators and vasoconstrictors in pregnancy (prostacyclin/thromboxane)
74
Q

What are the risk factors for PET?

A
  • First pregnancy
  • Extremes of age
  • Previous PET
  • Pregnancy interval >10 years
  • BMI >35
  • FMH
  • Multiple pregnancy
  • Underlying medical conditions (HT, renal disease, DM, autoimmune disorders)
75
Q

What are the possible maternal complications of PET?

A
  • Eclampsia (seizures)
  • Severe HT (stroke)
  • HELLP (haemolysis, elevated liver enzymes, low platelets)
  • DIC
  • Renal failure
  • Pulmonary oedema and cardiac failure
76
Q

What are the possible foetal complications of PET?

A

Impaired placental perfusion leading to

  • IUGR
  • Foetal distress
  • Prematurity
  • Increased PN mortality
77
Q

What are the signs and symptoms of severe PET?

A
  • Headache, blurring of vision, epigastric pain, pain below ribs, vomiting, sudden swelling of hands face legs
  • Severe Hypertension; > 3+ of urine proteinuria
  • Clonus/brisk reflexes; papillodema, epigastric tenderness
  • Reducing urine output
  • Convulsions (Eclampsia)
78
Q

What biochemical abnormalities can occur in severe PET?

A
  • Raised liver enzymes, bilirubin if HELLP present

- Raised urea an creatinine, raised urate

79
Q

What haematological abnormalities can occur in severe PET?

A
  • Low platelets
  • Low haemoglobin, signs of haemolysis
  • Features of DIC
80
Q

What is the management for PET?

A
  • Frequent BP checks and urine protein
  • Check for symptoms
  • Check for hyper-reflexia and tenderness over liver
  • Bloods: FBC, LFTs, U+Es, coagulation
  • Foetal investigations including scans and CTG
81
Q

What is the only cure for PET?

A

Delivery of the baby and placenta

82
Q

What is the conservative approach for PET?

A
  • Close observation of clinical signs & investigations
  • Anti-hypertensives (labetolol, methyldopa, nifedipine)
  • Steroids for fetal lung maturity if gestation < 36wks
  • Consider induction of labour / CS if maternal or fetal condition deteriorates, irrespective of gestation
  • Risks of PET may persist into the puerperium therefore monitoring must be continued post delivery
83
Q

What is the epidemiology of PET and eclampsia?

A
  • 5-8% of pregnant women have PET
  • 0.5% women have severe PET & 0.05% have eclamptic seizures
  • 38% of seizures occur antepartum, 18% intrapartum, 44% postpartum
84
Q

How are eclamptic seizures and impending seizures treated?

A
  • Magnesium sulphate bolus + IV infusion
  • Control of blood pressure – IV labetolol, hydrallazine (if > 160/110)
  • Avoid fluid overload – aim for 80mls/hour fluid intake
85
Q

What is the prophylaxis for PET in further pregnancies?

A
  • Low dose aspirin from 12 weeks to delivery

- Awareness of increased risk of chronic hypertension

86
Q

What is gestational diabetes?

A
  • Carbohydrate intolerance with onset (or first recognised) in pregnancy
  • Abnormal glucose tolerance that reverts to normal after delivery
  • However, more at risk of developing type II diabetes later in life
87
Q

What effect does pre-existing diabetes have on pregnancy?

A
  • Insulin requirements of the mother increase

- Foetal hyper-insulinaemia occurs

88
Q

Why do insulin requirements increase in pregnancy?

A

Human placental lactogen, progesterone, human chorionic gonadotrophin, and cortisol from the placenta have anti-insulin action

89
Q

Why does foetal hyper-insulinaemia occur?

A

Maternal glucose crosses the placenta and induces increased insulin production in the fetus. The fetal hyperinsulinemia causes macrosomia

90
Q

What are neonates of diabetic mothers at increased risk of?

A
  • Neonatal hypoglycaemia

- Respiratory distress

91
Q

What are the increased risks of diabetes in pregnancy?

A
  • Foetal congenital abnormalities e.g – cardiac abnormalities, sacral agenesis (especially if blood sugars high peri-conception
  • Miscarriage
  • Fetal macrosomia, polyhydramnios
  • Operative delivery, shoulder dystocia
  • Stillbirth, increased perinatal mortality
92
Q

What are the possible complications of diabetes in pregnancy?

A
  • Increased risk of pre-eclampsia
  • Worsening of maternal nephropathy, retinopathy, hypoglycaemia, reduced awareness of hypoglycaemia
  • Infections
  • Neonatal: impaired lung maturity, neonatal hypoglycaemia, jaundice
93
Q

What is the management for diabetes and pregnancy preconception?

A
  • Folic acid 5mg
  • Dietary advice
  • Retinal and renal assessment

Better glycaemic control, ideally blood sugars should be
4-7mmo/l
HbA1c <6.5% (<48mmol/mol)

94
Q

What is the management for diabetes during pregnancy?

A
  • Optimise glucose control
  • Continue oral agents but may need to change to insulin
  • Be aware of hypoglycaemia risk
  • Watch for ketonuria/infections
  • Repeat retinal assessments at 28 and 34 weeks
  • Watch foetal growth
95
Q

What blood sugars are optimal during pregnancy?

A

<5.3mmol/l Fasting
<7.8mmol/l 1 hour postprandial
<6.4mmol/l 2 hours postprandial
<6mmol/l Before bedtime

96
Q

What is the management of diabetes regarding birth?

A
  • Observe for PET
  • Labour induced 38-40 weeks or earlier
  • Consider C section if macrosomnia
  • Maintain blood sugar with insulin and dextrose insulin solution
  • CTG monitoring
  • Early feeding of new-born to prevent hypoglycaemia
  • Pre-pregnancy insulin regime post delivery
97
Q

What are the risk factors for gestation diabetes mellitus?

A
  • BMI >30
  • Previous macrosomic baby > 4.5kg
  • Previous GDM
  • FMH of diabetes
  • Women from high risk groups for developing diabetes – eg. Asian origin
  • Polyhydramnios or big baby in current pregnancy
  • Recurrent glycosuria in current pregnancy
98
Q

What is GDM associated with?

A

GDM associated with some increase in maternal complications (eg PET) and fetal complications (macrosomia) but much less than with type I or II diabetes

99
Q

When is GDM screened for?

A

If risk factor present, offer HbA1C estimation at booking:

  • If > 6% (43 mmol/mol), 75gms OGTT to be done.
  • If OGTT normal, repeat OGTT at 24 -28 weeks

Can also offer OGTT at around 16 weeks and repeat at 28 weeks if significant risk factors (eg. Previous GDM) present

100
Q

How is GDM managed?

A
  • Control blood sugars through metformin and diet (insulin may be required)
  • Post delivery: check OFTT 6-8 weeks PN
  • Yearly check on Hb1AC/blood sugars as at higher risk of developing overt diabetes
101
Q

What are the components of Virchow’s triad?

A
  • Stasis
  • Hypercoaguability
  • Vessel wall injury
102
Q

Why is the risk of VTE increased in pregnancy?

A
  • Pregnancy is a Hypercoaguable state (protect mother against bleeding post delivery)
  • Increased stasis due to progesterone and effects of enlarged uterus
  • May be vascular damage at delivery/ C section
103
Q

What is the physiology of the Hypercoaguable state of pregnancy?

A
  • Increase in fibrinogen, factor VIII, VW factor, platelets
  • Decrease in natural anticoagulants – antithrombin III
  • Increase in fibrinolysis
104
Q

What are the risk factors for VTE in pregnancy?

A
  • Older mothers with increased parity
  • High BMI, smokers
  • IVDU
  • PET
  • Dehydration
  • Decreased mobility
  • Infection
  • Operative delivery, long labour
  • Haemorrhage or blood loss >2L
  • Previous VTE, FMH, thrombophilia
  • Sickle cell disease
105
Q

What is the prophylaxis fro VTE in pregnancy?

A
  • TED stockings
  • Advice increased mobility, hydration

Prophylactic anti-coagulation with 3 or more risk factors (may be indicated even with one risk factor if significant risk), may need to continue 6 weeks postpartum

106
Q

What are the signs and symptoms of VTE?

A
  • Pain in calf
  • Increase girth of affected leg
  • Calf muscle tenderness
  • Breathlessness
  • Pain on breathing
  • Cough
  • Tachycardia
  • Hypoxic
  • Pleural rub
107
Q

How is VTE investigated in pregnancy?

A
  • ECG
  • Blood gases
  • Doppler
  • V/Q lung scan
  • CT pulmonary angiogram
108
Q

How is VTE treated in pregnancy?

A

Appropriate anticoagulation

Systems: Reproduction AB (35 decks)

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