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reproductive system 2 > Complications of Pregnancy > Flashcards

Complications of Pregnancy Flashcards

1
Q

what is miscarriage?

A

spontaneous loss of pregnancy before 24 weeks gestation

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2
Q

what is abortion?

A

voluntary termination

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3
Q

What is the incidence of spontaneous miscarriage?

A

15%

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4
Q

what are the types of spontaneous miscarriage

A

threatened: vaginal bleeding +/- pain, viable pregnancy, closed cervix
inevitable: vaginal bleeding (heavy +/- clots), open cervix
missed: asymptomatic, (brown) vaginal bleeding, empty gestational sac/foetal pole with no foetal heart
incomplete: products of pregnancy remain, vaginal bleeding (heavy), open cervix
complete: passed out all POC, bleeding stopped, cervix closed
septic: cases of incomplete miscarriage

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5
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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6
Q

what is the management of miscarriages?

A

threatened: conservative
inevitable: if heavy bleeding then evacuation of retained products
missed: conservative, medical (prostaglandins), surgical
septic: antibiotics, evacuate uterus

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7
Q

What is an ectopic pregnancy?

A

pregnancy implanted outside the uterine cavity

~1%

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8
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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9
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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10
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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11
Q

How are ectopic pregnancies investigated?

A

scan

  • no intrauterine gestational sac
  • may see adnexal mass
  • fluid in Pouch of Douglas

serum BHCG

  • track levels over 48 hour intervals
  • if normal early intrauterine pregnancy, HCG levels will increase by at least 66%
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12
Q

How are ectopic pregnancies managed?

A
  • medical: methotrexate
  • surgical: laproscopy - salpingectomy or salpingotomy
  • conservative
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13
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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14
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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15
Q

What is placenta praevia?

A

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

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16
Q

What is the incidence of placenta praevia?

A

1 in 200 pregnancies

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17
Q

Who is placenta praevia more common in?

A
  • multiparous women
  • multiple pregnancies
  • previous C section
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18
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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19
Q

How does placenta praevia present?

A
  • painless PV bleed
  • malpresentation of the foetus
  • incidental on US
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20
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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21
Q

How is placenta praevia diagnosed?

A

-USS

VAGINAL EXAMINATION MUST NOT BE DONE

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22
Q

How is placenta praevia managed?

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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23
Q

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

A

PPH

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24
Q

How is PPH managed?

A

medical
- oxytocin, ergometrine, carbaprost, tranexamic acid

balloon tamponade

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

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25
Q

What is placental abruption?

A

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

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26
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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27
Q

What are the clinical types of placental abruption?

A
  • revealed (can see blood)
  • concealed (bleeding inside so can’t see)
  • mixed
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28
Q

How does a placental abruption present?

A
  • pain
  • vaginal bleeding (may be minimal)
  • increased uterine activity
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29
Q

What does management of APH depend on?

A

either:

  • expectant treatment
  • vaginal delivery
  • immediate Caesarean section

depends on:

  • amount of bleeding
  • general condition of mother and baby
  • gestation
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30
Q

What are the possible complications of placental abruption?

A
  • maternal shock, collapse (may be disproportionate to the amount of bleeding seen)
  • foetal distress & death
  • maternal DIC, renal failure
  • postpartum haemorrhage ‘couvelaire uterus’
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31
Q

What is preterm labour?

A

onset of labour before 37 completed weeks of gestation (259 days)

  • 32-36 wks mildly preterm
  • 28-32 wks very preterm
  • 24-28 wks extremely preterm

spontaneous or induced

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32
Q

What is the incidence of preterm labour?

A
  • 5- 7% in singletons

- 30 - 40% multiple pregnancy

33
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
34
Q

How is preterm labour diagnosed?

A
  • contractions with evidence of cervical change
  • test: foetal fibronectin

consider possible cause: abruption, infection

35
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
36
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

37
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
38
Q

Give examples of hypertensive disorders in pregnancy.

A
  • chronic hypertension
  • gestational hypertension
  • pre-eclampsia
39
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
40
Q

Who is chronic hypertension commoner in?

A

Older mothers

41
Q

How should chronic hypertension in pregnancy be managed?

A
  • pre-pregnancy care
  • keep BP < 150/100
  • monitor for superimposed pre-eclampsia and foetal growth

higher incidence of placental abruption

42
Q

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

A
  • labetolol
  • methyldopa
  • nifedipine
43
Q

describe pre-eclampsia

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

44
Q

describe 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)
45
Q

What are the risk factors for PET?

A
  • first pregnancy
  • extremes of maternal age
  • previous PET
  • pregnancy interval >10 years
  • BMI >35
  • FMH
  • multiple pregnancy
  • underlying medical conditions (HT, renal disease, DM, autoimmune disorders)
46
Q

What are the possible complications of PET?

A

maternal

  • eclampsia (seizures)
  • severe HT (stroke)
  • HELLP (haemolysis, elevated liver enzymes, low platelets)
  • DIC
  • renal failure
  • pulmonary oedema and cardiac failure

foetal
- impaired placental perfusion –> IUGR, foetal distress, prematurity, increased PN mortality

47
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)
48
Q

What biochemical abnormalities can occur in severe PET?

A
  • raised liver enzymes, bilirubin if HELLP present

- raised urea an creatinine, raised urate

49
Q

What haematological abnormalities can occur in severe PET?

A
  • low platelets
  • low haemoglobin, signs of haemolysis
  • features of DIC
50
Q

What is the management for PET?

A
  • frequent BP checks and urine protein
  • check for symptoms: headaches, epigastric pain, visual disturbances
  • check for hyper-reflexia and tenderness over liver
  • bloods: FBC, LFTs, U+Es, coagulation
  • foetal investigations including scans and CTG
51
Q

What is the only cure for PET?

A

Delivery of the baby and placenta

52
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

53
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
54
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
55
Q

What is the prophylaxis for PET in further pregnancies?

A
  • low dose aspirin from 12 weeks to delivery

increased risk to develop hypertension in later life

56
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
57
Q

What effect does pre-existing diabetes have on pregnancy?

A
  • insulin requirements of the mother increase

- foetal hyper-insulinaemia occurs

58
Q

Why do insulin requirements increase in pregnancy?

A
  • human placental lactogen
  • progesterone
  • human chorionic gonadotrophin
  • cortisol
    from placenta have anti-insulin action
59
Q

Why does foetal hyper-insulinaemia occur?

A

maternal glucose crosses the placenta and induces increased insulin production in the foetus.

foetal hyperinsulinemia causes macrosomia

60
Q

What are neonates of diabetic mothers at increased risk of?

A
  • neonatal hypoglycaemia

- respiratory distress

61
Q

What are the increased risks of diabetes in pregnancy?

A
  • foetal congenital abnormalities (cardiac abnormalities, sacral agenesis)
  • miscarriage
  • foetal macrosomia, polyhydramnios
  • operative delivery, shoulder dystocia
  • stillbirth, increased perinatal mortality
62
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
63
Q

What is the management for diabetes and pregnancy preconception?

A
  • folic acid 5mg
  • dietary advice
  • retinal and renal assessment
  • better glycemic control, ideally blood sugars should be
    4 - 7mmo/l and HbA1c <6.5% (<48mmol/mol)
64
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
65
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

66
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
67
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
68
Q

What is GDM associated with?

A

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

69
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

70
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
71
Q

What are the components of Virchow’s triad?

A
  • stasis
  • hypercoaguability
  • vessel wall injury
72
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
73
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
74
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
75
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

76
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
77
Q

How is VTE investigated in pregnancy?

A
  • ECG
  • Blood gases
  • Doppler
  • V/Q lung scan
  • CT pulmonary angiogram
78
Q

How is VTE treated in pregnancy?

A

Appropriate anticoagulation

reproductive system 2 (35 decks)

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