complications in pregnancy Flashcards
define miscarriage
spontaneous loss of pregnancy before 24wks gestation
define abortion
voluntary termination of pregnancy
what is the incidence of spontaneous miscarriage
15%
categories of spontaneous miscarriage
threatened inevitable incomplete complete septic missed
what is a threatened spontaneous miscarriage
bleeding from the gravid uterus before 24wks gestation when there is a viable fetus and no cervical dilatation
what is an inevitable spontaneous miscarriage
when the cervix has already begun to dilate
what is an incomplete spontaneous miscarriage
partial expulsion of the products of conception
what is a complete spontaneous miscarriage
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)
what is a septic miscarriage
following an incomplete miscarriage there is always the risk of an ascending infection which can spread throughout the pelvis
what is a missed spontaneous miscarriage
a pregnancy in which the fetus has died but the uterus has made no attempts to expel the products of conception
what is shown in this image
threatened miscarriage
vaginal bleeding +/- pain
viable pregnancy
closed cervix on speculum examination
what is shown in this image
inevitable miscarriage
viable pregnancy
open cervix with bleeding that could be heavy (+/- clots)
what is shown here
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
what is shown in this image
most of pregnancy expelled out, some products of pregnancy remaining in the uterus
open cervix, vaginal bleeding (may be heavy)
aetiology of spontaneous miscarriage
abnormal conceptus - chromosomal (~50% of spontaneous miscarriage), genetic, structural
uterine abnormality - congenital, fibroids
cervical weakness - 1y, 2y
maternal - increasing age, diabetes
unknown
aetiology of spontaneous miscarriage
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
management of threatened miscarriage
conservative
most stop bleeding and are okay
management of inevitable miscarriage
if heavy bleeding may need evacuation
management of missed miscarriage
conservative
medical - prostaglandins (misoprostol)
surgical - surgical management of miscarriage (SMM)
septic - antibiotics and evacuate uterus
what is an ectopic pregnancy
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%)
incidence of ectopic pregnancy
1:90 pregnancies (~1%)
risk factors for ectopic pregnancy
pelvic inflammatory disease
previous tubal surgery
previous ectopic
assisted conception
presentation of ectopic pregnancy
period of ammenorhoea (w/ +ve urine pregnancy test)
+/- vaginal bleeding
+/- abdo pain
+/- GI/urinary symptoms
investigations to diagnose ectopic pregnancy
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%)
management of ectopic pregnancy
medical - methotrexate
surgical - mostly laparoscopy - salpingectomy, salpingotomy for few indications)
conservative - reserved for pts w/ low bHCG and haemodynamically stable
define antepartum haemorrhage
associated with significant maternal and neonatal mortality and morbidity
haemorrhage from the genital tract after wk24 of pregnancy but before delivery of the baby
causes of antepartum haemorrhage
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
what is placenta praevia
all or part of the placenta implants in the lower uterine segment
what is placental abruption
haemorrhage resulting from premature separation of the placenta before the birth of the baby
associated with retro-placental clot
0.6% of all pregnancies
what is vasa praevia
rupture of fetal vessels within the fetal membrane
usually bleeding is small but can have catastrophic effect on fetus
incidence of placenta praevia
1/200 pregnancies
risk factors for placenta praevia
multiparous women
multiple pregnancies
previous CS
classification of placenta praevia - old classificaton
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
classification of placenta praevia - RCOG classification
low lying - placenta <20mm from internal os
placenta praevia - covering the os
presentation of placenta praevia
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
management of placenta preavia
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
diagnosis of placenta praevia
US scan to locate placental site
diagnosis of posterior placenta praevia is much more difficult
DO NOT DO VAGINAL EXAMINATION
management of PPH
medical - oxytocin, ergometrine, carboprost, tranexemic acid
balloon tamponade
surgical - B lynch suture, ligation of uterine/ iliac vessels, hysterectomy
factors associated with placental abruption
pre-eclampsia/chronic hypertension multiple pregnancy polyhydramnios smoking, increasing age, parity previous abruption cocaine use in pregnancy
classification of placental abruption
revealed - see the blood
concealed - bleeding but internal so not visible
mixed - concealed and revealed
presentation of placental abruption
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
management of APH
varies from expectant treatment to attempting vaginal delivery to immediate CS, depending on:
amount of bleeding
general condition of mother and baby
gestation
complications of placental abruption
maternal shock, collapse - may be disproportionate to amount of bleeding seen fetal distress then death maternal DIC, renal failure PPH couvelaire uterus
what is preterm labour
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
incidence of preterm labour
5-7% in singletons
30-40% multiple pregnancy
predisposing factors to preterm labour
multiple pregnancy polyhydramnios APH pre-eclampsia infection e.g. UTI prelabour premature rupture of membranes
majority idiopathic
morbidity and mortality with preterm labour
major cause of perinatal mortality and morbidity
gestation dependedn
diagnosis of preterm labour
contractions with evidence of cervical change on VE
fetal fibronectin test - +ve = likely to deliver in next 2 wks
consider cause - abruption, infection etc
prognosis of preterm labour
<24-26wks generally regarded as very poor prognosis
decisions made in discussion with parents and neonatologists
all cases considered viable
management of pre-term labour
consider tocolysis to allow steroids/transfer
steroids unless CI
transfer to unit w/ NICU facilities
aim for vaginal delivery
survival and handicap rates in the very preterm infant
gestation, total survival rate, survivors with severe disability <24, 6%, 65% 24, 26%, 38% 25, 43%, 31% 26, 48%, 36% 27, 73% 28, 84%
neonatal morbidity resulting from prematurity
respiratory distress syndrome intraventricular haemorrhage cerebral palsy nutrition temperature control jaundice infections visual impairment hearing loss
what is chronic hypertension
hypertension either pre-pregnancy or at booking (≤20wks gestation)
classification of HT
mild 140-49/90-99
moderate 150-159/100-109
severe ≥160/≥110
what is gestational hypertension
PIH - pregnancy indcued hypertension
BP as above but new hypertension (develops after 20wks)
what is pre-eclampsia
new hypertension>20wks in associated w/ significant proteinuria
what is significant proteinuria
automated reagent strip urine protein estimation >1+
spot urinary protein:creatinine ration >30mg/mmol
24hrs urine protein collection >300mg/day
when is chronic hypertension seen more commonly
older mothers
pre-pregnancy care for chronic hypertension
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
examples of ACE inhibitors
why are these CI in pregnancy
ramipril
enalopril
cause birth defects, impaired growth
examples of ARBs
losartan
candesartan
what medications are used for chronic hypertension during pregnancy
labetolol - beta blocker
nifedipine - CCB
methyldopa
define pre-eclampsia
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)
pathophysiology of pre-eclampsia
immunological
genetic predisposition
2y invasion of maternal spiral arterioles by trophoblasts
imparied –> reduced placental perfusion
imbalance between vasodilators/vasoconstrictors in pregnancy (prostocyclin/thromboxane)
complications of pre-eclampsia on baby
chronic placental ischaemia fetal distress prematurity intrauterine growth restriction intrauterine death - increased PN mortality
endothelial dysfunction leads to what in the mother with pre-eclampsia
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
risk factors for developing pre-eclampsia (PET)
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
which systems does pre-eclampsia affect
multisystem multi-organ disorder
renal, liver, vascular, cerebral, pulmonary
maternal pre-eclampsia complications
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
symptoms/signs of severe PET
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)
biochemical abnormalities in severe PET
raised liver enzymes, bilirubin if HELLP present
raised urea and creatinine, raised urate
haematological abnormalities in severe PET
low platelets
low Hb, signs of haemolysis
features of DIC
management of PET
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
management of PET - ‘cure’
only ‘cure’ is delivery of the baby and placenta
management of PET - conservative
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
PET and eclampsia
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
PET - treatment of seizures/impending seizures
magnesium sulphate bolus + IV infusion
control of BP - IV labetolol, hydrallazine (if >160/110)
avoid fluid overload - aim for 80mls/hr fluid intake
prophylaxis for PET in subsequent pregnancy
low dose aspirin from 12wks till delivery
women with PET at a higher risk to develop HT in later life
types of diabetes in pregnancy
pre-existing (type I, less often type II)
gestational diabates
what is gestational diabetes
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
pre-existing diabetes and pregnancy
mother’s insulin requirements increase
fetal hyper-insulinaemia
pre-existing diabetes and pregnancy - increased maternal insulin requirements
human placental lactogen, progesterone, HCG and cortisol from the placenta have anti-insulin action
pre-existing diabetes and pregnancy - fetal hyper-insulinaemia
post-delivery risks
maternal glucose crosses the placenta and induces increased insulin production in the fetus
fetal hyperinsulinaemia –> macrosmia
more risk of neonatal hypoglycaemia and resp distress
effects of diabetes on fetus
increased risks of: fetal congenital abnormalities miscarriage fetal macrosmia, polyhydramnios operative delivery, shoulder dystocia stillbirth, increased perinatal mortality
increased risk of fetal abnormalities with maternal diabates
increased risk of cardiac abnormalities, sacral agenesis
esp if blood sugars high peri-conception
complications of diabetes for mother during pregnancy
increased risk of pre-eclampsia
worsening of maternal nephropathy, retinopaty, hypoglycaemia, reduced awareness of hypoglycaemia
infections
complications of diabetes on neonate
impaired lung maturity
neonatal hypoglycaemia
jaundice
management of maternal T1/2 DM - preconception
better glycaemic control - ideally 4-7mmol/l pre-conception and HbA1c <48mmol/mol
folic acid 5mg - high dose
dietary advice
retinal and renal assessment
management of diabetes during pregnancy - glucose control
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
glucose control during pregnancy - normal limits
fasting <5.3
1hr post prandial <7.8
2hrs post prandial <6.4
before bed <6
management of diabetes during pregnancy - labour and after delivery
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
risk factors for developing GDM/consider screening for GDM
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
screening for GDM
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
management of GDM
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
VTE - Virchow’s triad
stasis
hypercoagulability
vessel wall injury
together lead to increased incidence of VTE
why is there an increased risk of thromboembolism in pregnancy
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
who is at increased risk of VTE
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
VTE prophylaxis in pregnancy
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
signs/symptoms of VTE
pain in calf
increased girth of affected leg
calf muscle tenderness
PE: SOB, pain on breathing, cough, tachycardia, hypoxic, pleural rub
investigations for VTE and treatment
ECG, blood gases, doppler, V/Q (ventilation perfusion) lung scan
CTPA - CT pulmonary angio
appropriate treatment w/ anti-coagulation if VTE confirmed
