complications in pregnancy Flashcards

1
Q

define miscarriage

A

spontaneous loss of pregnancy before 24wks gestation

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2
Q

define abortion

A

voluntary termination of pregnancy

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3
Q

what is the incidence of spontaneous miscarriage

A

15%

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4
Q

categories of spontaneous miscarriage

A
threatened
inevitable 
incomplete
complete
septic 
missed
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5
Q

what is a threatened spontaneous miscarriage

A

bleeding from the gravid uterus before 24wks gestation when there is a viable fetus and no cervical dilatation

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6
Q

what is an inevitable spontaneous miscarriage

A

when the cervix has already begun to dilate

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7
Q

what is an incomplete spontaneous miscarriage

A

partial expulsion of the products of conception

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8
Q

what is a complete spontaneous miscarriage

A

complete expulsion of the products of conception (POC), cervix closed and bleeding has stopped (should ideally have confirmed the POC or should have had a scan previously that confirmed an intrauterine pregnancy)

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9
Q

what is a septic miscarriage

A

following an incomplete miscarriage there is always the risk of an ascending infection which can spread throughout the pelvis

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10
Q

what is a missed spontaneous miscarriage

A

a pregnancy in which the fetus has died but the uterus has made no attempts to expel the products of conception

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11
Q

what is shown in this image

A

threatened miscarriage
vaginal bleeding +/- pain
viable pregnancy
closed cervix on speculum examination

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12
Q

what is shown in this image

A

inevitable miscarriage
viable pregnancy
open cervix with bleeding that could be heavy (+/- clots)

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13
Q

what is shown here

A

missed miscarriage (early fetal demise)
no symptoms, or could have bleeding/brown loss vaginally
gestational sac may be seen on scan
no clear fetus (empty gestational sac) or a fetal pole w/ no fetal heart seen in the gestational sac

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14
Q

what is shown in this image

A

most of pregnancy expelled out, some products of pregnancy remaining in the uterus
open cervix, vaginal bleeding (may be heavy)

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15
Q

aetiology of spontaneous miscarriage

A

abnormal conceptus - chromosomal (~50% of spontaneous miscarriage), genetic, structural
uterine abnormality - congenital, fibroids
cervical weakness - 1y, 2y
maternal - increasing age, diabetes
unknown

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16
Q

aetiology of spontaneous miscarriage

A

abnormal conceptus - chromosomal (~50% of spontaneous miscarriage), genetic, structural
uterine abnormality - congenital, fibroids
cervical weakness - 1y, 2y e.g. trauma following dilatation etc
maternal - increasing age, diabetes, hormonal imbalance
unknown

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17
Q

management of threatened miscarriage

A

conservative

most stop bleeding and are okay

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18
Q

management of inevitable miscarriage

A

if heavy bleeding may need evacuation

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19
Q

management of missed miscarriage

A

conservative
medical - prostaglandins (misoprostol)
surgical - surgical management of miscarriage (SMM)
septic - antibiotics and evacuate uterus

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20
Q

what is an ectopic pregnancy

A

pregnancy implanted outside the uterine cavity

most commonly in the fallopian tube (95-97%, can be ampullary (most common) or isthmus
also can occur: fimbria (very rare), intersitial (cornual, rare 2-5%), ovary (0.5-1%), cervical (0.1%)

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21
Q

incidence of ectopic pregnancy

A

1:90 pregnancies (~1%)

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22
Q

risk factors for ectopic pregnancy

A

pelvic inflammatory disease
previous tubal surgery
previous ectopic
assisted conception

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23
Q

presentation of ectopic pregnancy

A

period of ammenorhoea (w/ +ve urine pregnancy test)
+/- vaginal bleeding
+/- abdo pain
+/- GI/urinary symptoms

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24
Q

investigations to diagnose ectopic pregnancy

A

scan - no intrauterine gestational sac, may see adnexal mass, fluid in pouch of douglas (rectouterine)

serum bHCG levels - may need to serially track levels over 48hr intervals (if a normal early intrauterine pregnancy, HCG levels will increase by at least 60%)

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25
Q

management of ectopic pregnancy

A

medical - methotrexate
surgical - mostly laparoscopy - salpingectomy, salpingotomy for few indications)
conservative - reserved for pts w/ low bHCG and haemodynamically stable

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26
Q

define antepartum haemorrhage

A

associated with significant maternal and neonatal mortality and morbidity

haemorrhage from the genital tract after wk24 of pregnancy but before delivery of the baby

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27
Q

causes of antepartum haemorrhage

A

placenta praevia
placental abruption
unknown origin - other causes have been completeley excluded
local lesions of genital tract e.g. cervical erosions and polyps, cancers, infection
vasa praevia - very rare

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28
Q

what is placenta praevia

A

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

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29
Q

what is placental abruption

A

haemorrhage resulting from premature separation of the placenta before the birth of the baby
associated with retro-placental clot
0.6% of all pregnancies

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30
Q

what is vasa praevia

A

rupture of fetal vessels within the fetal membrane

usually bleeding is small but can have catastrophic effect on fetus

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31
Q

incidence of placenta praevia

A

1/200 pregnancies

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32
Q

risk factors for placenta praevia

A

multiparous women
multiple pregnancies
previous CS

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33
Q

classification of placenta praevia - old classificaton

A

I - placenta encroaching on the lower segment but not the internal cervical os
II - placenta reaches the internal os
III - placenta eccentrically covers the os
IV - central placenta praevia

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34
Q

classification of placenta praevia - RCOG classification

A

low lying - placenta <20mm from internal os

placenta praevia - covering the os

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35
Q

presentation of placenta praevia

A

maternal condition correlates with amount of PV bleeding
soft non-tender uterus +/- fetal malpresentation

painless PV bleeding - as placenta separates from wall as lower uterine segment effaces, bleeding is from venous sinuses

incidental finding

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36
Q

management of placenta preavia

A

depends on:
gestation at presentation
severity of blood loss

admission to hospital
vaginal examination is CI
diagnosis confirmed by US

cross match blood, blood transfusion depends on maternal condition

conservative approach depending on maternal and fetal health to prolong pregnancy and then delivery by CS

watch out for PPH

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37
Q

diagnosis of placenta praevia

A

US scan to locate placental site

diagnosis of posterior placenta praevia is much more difficult

DO NOT DO VAGINAL EXAMINATION

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38
Q

management of PPH

A

medical - oxytocin, ergometrine, carboprost, tranexemic acid

balloon tamponade

surgical - B lynch suture, ligation of uterine/ iliac vessels, hysterectomy

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39
Q

factors associated with placental abruption

A
pre-eclampsia/chronic hypertension
multiple pregnancy
polyhydramnios
smoking, increasing age, parity
previous abruption
cocaine use in pregnancy
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40
Q

classification of placental abruption

A

revealed - see the blood
concealed - bleeding but internal so not visible
mixed - concealed and revealed

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41
Q

presentation of placental abruption

A

pain
vaginal bleeding - can be minimal
increased uterine activity

increased volume of uterine contents - fundal height is larger than is expected for that gestation

Couvelaire uterus - blood contents passes through uterine wall, uterus appears bruised

42
Q

management of APH

A

varies from expectant treatment to attempting vaginal delivery to immediate CS, depending on:

amount of bleeding
general condition of mother and baby
gestation

43
Q

complications of placental abruption

A
maternal shock, collapse - may be disproportionate to amount of bleeding seen 
fetal distress then death 
maternal DIC, renal failure 
PPH
couvelaire uterus
44
Q

what is preterm labour

A

onset of labour before 37 completed weeks of gestation

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

can be spontaneous or induced (iatrogenic)

babies should be resuscitated if born after 24wks

45
Q

incidence of preterm labour

A

5-7% in singletons

30-40% multiple pregnancy

46
Q

predisposing factors to preterm labour

A
multiple pregnancy
polyhydramnios
APH
pre-eclampsia
infection e.g. UTI
prelabour premature rupture of membranes 

majority idiopathic

47
Q

morbidity and mortality with preterm labour

A

major cause of perinatal mortality and morbidity

gestation dependedn

48
Q

diagnosis of preterm labour

A

contractions with evidence of cervical change on VE
fetal fibronectin test - +ve = likely to deliver in next 2 wks

consider cause - abruption, infection etc

49
Q

prognosis of preterm labour

A

<24-26wks generally regarded as very poor prognosis
decisions made in discussion with parents and neonatologists

all cases considered viable

50
Q

management of pre-term labour

A

consider tocolysis to allow steroids/transfer
steroids unless CI
transfer to unit w/ NICU facilities
aim for vaginal delivery

51
Q

survival and handicap rates in the very preterm infant

A
gestation, total survival rate, survivors with severe disability
<24, 6%, 65%
24, 26%, 38%
25, 43%, 31%
26, 48%, 36%
27, 73%
28, 84%
52
Q

neonatal morbidity resulting from prematurity

A
respiratory distress syndrome
intraventricular haemorrhage 
cerebral palsy
nutrition
temperature control 
jaundice
infections 
visual impairment
hearing loss
53
Q

what is chronic hypertension

A

hypertension either pre-pregnancy or at booking (≤20wks gestation)

54
Q

classification of HT

A

mild 140-49/90-99
moderate 150-159/100-109
severe ≥160/≥110

55
Q

what is gestational hypertension

A

PIH - pregnancy indcued hypertension

BP as above but new hypertension (develops after 20wks)

56
Q

what is pre-eclampsia

A

new hypertension>20wks in associated w/ significant proteinuria

57
Q

what is significant proteinuria

A

automated reagent strip urine protein estimation >1+
spot urinary protein:creatinine ration >30mg/mmol
24hrs urine protein collection >300mg/day

58
Q

when is chronic hypertension seen more commonly

A

older mothers

59
Q

pre-pregnancy care for chronic hypertension

A

change anti-HT drugs if indicated e.g. ACE inhibitor, angiotensin receptor blockers

lower dietary sodium
anti-diuretics

aim to keep BP <150/100
monitor for superimposed pre-eclampsia
monitor fetal growth
may have a higher incidence of placental abruption

60
Q

examples of ACE inhibitors

why are these CI in pregnancy

A

ramipril
enalopril

cause birth defects, impaired growth

61
Q

examples of ARBs

A

losartan

candesartan

62
Q

what medications are used for chronic hypertension during pregnancy

A

labetolol - beta blocker
nifedipine - CCB
methyldopa

63
Q

define pre-eclampsia

A
mild HT (>140/90) on 2 occasions >4hrs apart
can be moderate to severe HT
associated proteinuria (>300mg/24hrs (protein urine > + protein: creatinine ration >30mg/mmol)
64
Q

pathophysiology of pre-eclampsia

A

immunological
genetic predisposition

2y invasion of maternal spiral arterioles by trophoblasts
imparied –> reduced placental perfusion

imbalance between vasodilators/vasoconstrictors in pregnancy (prostocyclin/thromboxane)

65
Q

complications of pre-eclampsia on baby

A
chronic placental ischaemia 
fetal distress
prematurity 
intrauterine growth 
restriction
intrauterine death - increased PN mortality
66
Q

endothelial dysfunction leads to what in the mother with pre-eclampsia

A

clinical signs in the mother

  • impairment of hepatic endothelium
  • onset of HELLP - haemolysis, elevated liver enzyme and low platelet syndrome
  • impairment of cerebral endothelium - refractory neurological disorders and eclampsia
67
Q

risk factors for developing pre-eclampsia (PET)

A
1st pregnancy 
extremes of maternal age 
pre-eclampsia in a previous pregnancy (esp severe PET, delivery <34wks, IUGR baby, IUD, abruption)
pregnancy interval >10yrs
BMI >35
FHx PET
multiple pregnancy 
underlying medical disorders - chronic HT, pre-existing renal disease/diabetes, AI disorders
68
Q

which systems does pre-eclampsia affect

A

multisystem multi-organ disorder

renal, liver, vascular, cerebral, pulmonary

69
Q

maternal pre-eclampsia complications

A

eclampsia - seizures due to HT
severe HT - cerebral haemorrhage, stroke
HELLP (haemolysis, elevated liver enzymes, low platelets)
DIC (disseminated intravascular coagulation)
renal failure
pulmonary oedema
cardiac failure

70
Q

symptoms/signs of severe PET

A

headache, blurring of vision, epigastric pain, pain below ribs, vomiting, sudden swelling of hands/face/legs
severe HT; >3+ of urine proteinuria
clobus/brisk reflexes, papilloedema, epigastric tenderness
reduced urine ouput
convulsions (eclampsia)

71
Q

biochemical abnormalities in severe PET

A

raised liver enzymes, bilirubin if HELLP present

raised urea and creatinine, raised urate

72
Q

haematological abnormalities in severe PET

A

low platelets
low Hb, signs of haemolysis
features of DIC

73
Q

management of PET

A

frequent BP checks, urine protein
check symptomatology - headaches, epigastric pain, visual disturbances
check for hyper-reflexia (clonus), tenderness over the liver
bloods - FBC (haemolysis, platelets), LFTs, RFTs (serum urea, creatinine, urate), coagulation tests if indicated
fetal investigations - growth, CTG

74
Q

management of PET - ‘cure’

A

only ‘cure’ is delivery of the baby and placenta

75
Q

management of PET - conservative

A

aim for fetal maturity
close observation of clinical signs and investigations
anti-HT - labetolol, methyldopa, nifedipine
steroids for fetal lung maturity if gestation <36wks

consider induction of labour/CS if maternal/fetal condition deteriorates, irrespective of gestation

risks of PET may persist into the puerperium therefore monitoring must be considered post delivery

76
Q

PET and eclampsia

A

5-8% of pregnant women have PET
0.5% of women have severe PET and 0.05% have eclamptic seizures
38% of seizures occur antepartum, 18% intrapartum, 44% postpartum

77
Q

PET - treatment of seizures/impending seizures

A

magnesium sulphate bolus + IV infusion
control of BP - IV labetolol, hydrallazine (if >160/110)
avoid fluid overload - aim for 80mls/hr fluid intake

78
Q

prophylaxis for PET in subsequent pregnancy

A

low dose aspirin from 12wks till delivery

women with PET at a higher risk to develop HT in later life

79
Q

types of diabetes in pregnancy

A

pre-existing (type I, less often type II)

gestational diabates

80
Q

what is gestational diabetes

A

carbohydrate intolerance with onset (or first recognised) in pregnancy
abnormal glucose tolerance that reverts to normal after delivery
more at risk of developing type II diabetes later in life

81
Q

pre-existing diabetes and pregnancy

A

mother’s insulin requirements increase

fetal hyper-insulinaemia

82
Q

pre-existing diabetes and pregnancy - increased maternal insulin requirements

A

human placental lactogen, progesterone, HCG and cortisol from the placenta have anti-insulin action

83
Q

pre-existing diabetes and pregnancy - fetal hyper-insulinaemia

post-delivery risks

A

maternal glucose crosses the placenta and induces increased insulin production in the fetus
fetal hyperinsulinaemia –> macrosmia

more risk of neonatal hypoglycaemia and resp distress

84
Q

effects of diabetes on fetus

A
increased risks of: 
fetal congenital abnormalities
miscarriage 
fetal macrosmia, polyhydramnios
operative delivery, shoulder dystocia
stillbirth, increased perinatal mortality
85
Q

increased risk of fetal abnormalities with maternal diabates

A

increased risk of cardiac abnormalities, sacral agenesis

esp if blood sugars high peri-conception

86
Q

complications of diabetes for mother during pregnancy

A

increased risk of pre-eclampsia
worsening of maternal nephropathy, retinopaty, hypoglycaemia, reduced awareness of hypoglycaemia
infections

87
Q

complications of diabetes on neonate

A

impaired lung maturity
neonatal hypoglycaemia
jaundice

88
Q

management of maternal T1/2 DM - preconception

A

better glycaemic control - ideally 4-7mmol/l pre-conception and HbA1c <48mmol/mol
folic acid 5mg - high dose
dietary advice
retinal and renal assessment

89
Q

management of diabetes during pregnancy - glucose control

A

optimise glucose control
could continue oral anti-diabetic agents but may need to change to insulin for tighter glucose control
should be aware of risk of hypos - provide glucagon injections/conc glucose solution
repeat retinal assessments 28 + 34wks
watch for ketonuria/infections
watch fetal growth
observe for PET

90
Q

glucose control during pregnancy - normal limits

A

fasting <5.3
1hr post prandial <7.8
2hrs post prandial <6.4
before bed <6

91
Q

management of diabetes during pregnancy - labour and after delivery

A

labour induced 38-40wks, early if fetal/maternal concerns
consider elective CS if significant fetal macrosmia
maintain blood sugar in labour w/ dextrose insulin infusion
continuous CTG fetal monitoring in labour
early feeding of baby - reduce neonatal hypoglycaemia
can go back to pre-pregnancy insulin regimen post delivery

92
Q

risk factors for developing GDM/consider screening for GDM

A

BMI >30
previous macrosmic baby >4.5kg
previous GDM
FHx DM
women from high risk groups for developing diabetes - e.g. Asian ethnicity
polyhydramnios/large baby in current pregnancy
recurrent glycosuria in current pregnancy

93
Q

screening for GDM

A

if risk factor present:
offer HbA1c estimation at booking
if >43/6% - 75gms OGTT to be done
if OGTT normal, repeat OGTT at 24-48wks

can also offer OGTT at around 16wks and repeat at 28wks if sig. risk factors present

94
Q

management of GDM

A

control blood sugars - diet, metformin/insulin if sugars remain high
post-delivery - check OGTT 6-8wks PN
yrly check on HbA1c/blood sugars - higher risk of developing overt DM

95
Q

VTE - Virchow’s triad

A

stasis
hypercoagulability
vessel wall injury

together lead to increased incidence of VTE

96
Q

why is there an increased risk of thromboembolism in pregnancy

A

hypercoagulable state (protects mother against PPH) - increase in fibrinogen, factor VII, VW factor and platelets; decrease in natural anticoagulants (antithrombin III) and fibrinolysis

increased stasis - progesterone, enlarging uterus

risk of vascular damage at delivery/CS

97
Q

who is at increased risk of VTE

A
older mothers
increasing parity
increased BMI 
smokers
IVDU
PET
dehydration - hyperemesis
decreased mobility
infections 
operative delivery, prolonged labour
haemorrhage, >2L blood loss
previous VTE (not explained by other predisposing factors e.g. fractures, injury), thrombophilia (protein C/S, antithrombin III deficiency), strong FHx of VTE
sickle cell
98
Q

VTE prophylaxis in pregnancy

A

TED stockings
increased mobility and hydration
prophylactic anti-coagulation w/ ≥3 risk factors (may be indicated w/ 1 significant risk factor), may need to continue 6wks PP

99
Q

signs/symptoms of VTE

A

pain in calf
increased girth of affected leg
calf muscle tenderness

PE: SOB, pain on breathing, cough, tachycardia, hypoxic, pleural rub

100
Q

investigations for VTE and treatment

A

ECG, blood gases, doppler, V/Q (ventilation perfusion) lung scan
CTPA - CT pulmonary angio

appropriate treatment w/ anti-coagulation if VTE confirmed