Medical problems in pregnancy Flashcards
Why can anaemia develop?
- Plasma volume rises more than RBC number
- Iron + folate demand increased because of raised RBC mass
- Fetus uses the iron
- Previous factors like menorrhagia, previous pregnancy, dietary
What are the effects of anaemia on the mother + fetus?
- Mother (most): tiredness, dizzy, SOB, immunosuppression, poor concentration, low mood, higher peripartum blood loss
- Fetus: preterm, reduced birth weight, anaemia in first 3m, slower development
How is anaemia managed?
- Screened at booking and 28w
- Dietary advice
- Oral ferrous sulfate/fumarate on empty stomach w orange juice, continue for 3m PP
- IV iron if not tolerated
Why are pregnant women at a higher risk of VTE, and when is the most risky time?
- Highest risk in T3
- Pregnancy is a hyper coagulable state as there’s more ferritin, factor 7, 8, 9, 10 and 12, and less protein S+antithrombin
- RF like thrombophilia, age>35, obesity, para>3, smoking, varicose veins, multiple pregnancy, pre-eclampsia, caesarean section, prolonged labour, any surgery, dehydration, ovarian hyper stimulation syndrome, sickle cell
How may VTE present?
- DVT: u/l leg pain + swelling, pitting oedema, tender, prominent superficial veins. More likely to be proximal in pregnancy and on left (uterus compresses LIIV)
- PE: dyspnoea (tho many in preg get a ‘thirst for air’ cos of central changes but RR normal), pyrexia, JVP up, pleuritic CP/cough/haemoptysis/pleural rub
How would you investigate and manage VTE?
- Well’s score and D-dimers are NOT used (D-dimers raised anyway, Well’s score not validated)
- Take clotting bloods
- Suspected DVT - duplex US
- Suspected PE - CTPA, ECG, CXR (as VQ scan has higher risk of child getting leukaemia, tho CTPA higher risk of mother breast cancer)
- Management: LMWH until 6-12w postpartum (but stop it 24h before IOL/CS); if diagnosed at term consider IV unfractionated heparin (cos you can stop this 6h before IOL/CS)
- Any CS patients need LMWH for 10d postpartum as prophylaxis
Factor V Leiden
An inherited thrombophilia - activated protein C resistance that increases the risk of venous thrombosis
Unclear if aspirin/LMWH is beneficial but pathway is for LMWH antenatally + 6w PP
Antiphospholipid syndrome
An acquired autoimmune condition, primary or secondary to things like SLE and RA.
- CLOTs: Coagulation defect (arterial or venous or microvascular thrombosis), Livido reticular (reticular skin pattern), Obstetric symptoms (miscarriage, PET, IUGR) and Thrombocytopenia
- Also a/w renal impairment, aortic/mitral regurgitation, catastrophic APS (rare, trauma/surgery/sepsis triggers multi organ infarction)
- Test for antibodies in women with 3+ miscarriages like anti-cardiolipin
- M: all need postpartum LMWH, depending on circumstances may also give low dose aspirin + LMWH throughout the pregnancy
Von Willebrand’s disease
Usually autosomal dominant, reduced vWF which is needed for plt adhesion
- CF range from mild like epistaxis to more severe like menorrhagia, antepartum haemorrhage etc
- vWF is usually raised in preg as is an acute phase reactant so different ref ranges
- Ix: prolonged bleeding time, APTT may be prolonged, factor VIII may be low (as is bound to vWF), defective plt aggregation
- By 28w levels usually up to normal as clotting factors naturally increase
- If at risk of PPH - tranexamic acid for mild bleeding to stabilise clots, desmopressin (raises vWF levels), factor VIII concentrate may be needed
- Type 3 is least common and AR inheritance, most severe
What are the effects of sickle cell disease?
- Preg –> SC: higher chance of crises
* SC –> preg: higher chance of IUGR, IUD, VTE and pre-eclampsia
How would you manage sickle cell disease?
- Folic acid 5mg for 3m pre-conceptually (haemolysis depletes folate)
- Low dose aspirin - reduce thrombosis embolism
- Lower threshold for Abx
- Monitor for transfusion requirement
- Counsel about inheritance
- Avoid dehydration
Effects of thalassaemia?
- Preg –> thal: worsens anaemia so higher transfusion requirement (iron overload complication)
- Thal–>preg: inheritance, higher risk IUGR/preterm
How is HIV of pregnancy managed?
Transmission: transplacental, vaginal birth + breastfeeding; also increases risk of miscarriage, IUGR + preterm. Monitor CD4 + viral load
- Anti-retrovirals: reduce transmission to <1%
- Caesarean section (tho if VL low enough can have vaginal)
- Avoid breastfeeding
- Neonatal post-exposure prophylaxis
- Avoid doing things like amniocentesis + fetal blood sampling
How to manage UTI in pregnancy?
Treat all with Abx as risk of pyelonephritis is higher in preg (relative immunosuppression) which has a higher risk of bacteraemia
UTIs mostly caused by E coli
Management of viral hepatitis
- don’t normally affect pregnancy
- in hep B give baby hep B Ig and early full vaccination course
- in hep C follow up to see if baby contracted as no treatment
- cannot be transmitted by breastfeeding
- little evidence to suggest CS reduces VT
Cytomegalovirus
- most infected mothers asymptomatic or mild flu-like illness
- not all mothers are infected and not all with infected mothers get infected
- highest damage to fetus risk is in T1, can diagnose in fetus with amnio. no treatment so offer TOP is positive or offer serial US to assess for damage
- congenital CMV: 20-30% mortality - IUGR, liver/spleen enlargement, TTP, microencephaly, chorioretinitis, jaundice
- by 2y old 10% will have SNHL/vision impairment/developmental delay
Parvovirus B19
Aka ‘slapped cheek’/erythema infectiosum/fifth disease, respiratory + vertical transmission, infectious 3-5d before rash
- Adults: mild fever, may have symmetrical arthralgia
- Child: URTI, red maculopapular rash, may spread but spares soles+palms, don’t need exclusion from school as not infectious when rash comes, rash may recur with triggers weeks-months after recover
- May precipitate aplastic crisis in SCD
- Fetus: in first 20w may cause spontaneous MC/IUD, fetal hydrops
- M: antipyretics, analgesia, serial US to check for hydrops
Group B streptococcus
In 25% of women GBS is a vaginal/rectal commensal, and 0.05% will cause neonatal sepsis/meningitis/pneumonia, or chorioamnionitis or endometritis in the mother
RF: previous pregnancy with GBS, prem, ROM >24h, pyrexia in labour, GBS-UTI during pregnancy
Screening is done if high risk, as not all who screen + are still + at delivery and vv for negative!
M: IV benzylpenicillin during labour (none needed in ELCS, as it’s the ROM that exposes the baby)
Rubella
Airborne virus, not screened anymore cos of MMR
- Mother: asymptomatic or coryza + fine maculopapular rash
- IgM=acute infection, IgG post-infection/vaccine. No treatment
- If <12w consider TOP as 90% chance of CRS
- 12-20w decide TOP or US surveillance
- > 20w no additional risk of CRS
- Congenital rubella syndrome: SNHL, heart defects (PS, PDA, VSD), retinopathy/cataracts, thrombocytopenia, LD, microencephaly, Blueberry muffin appearance due to extra-medullary haemopoiesis (widespread purpura), long term issues
Varicella zoster infection
- VZV IgG confirms immunity, if not give IgG vaccine if mother exposed to chickenpox/shingles before the rash comes
- Serial US monitoring
- Congenital varicella syndrome: a risk <20w. Skin scars, optic atrophy, limb hypoplasia, microencephaly, corticospinal atrophy, seizures, Horner’s syndrome
What are the causes of hypertension in pregnancy?
- Essential HTN - HTN before 20w, exaggerated physiological response, consider secondary causes
- Gestational HTN - HTN after 20w, new onset, without significant proteinuria or oedema. Due to abnormal trophoblast invasion, reduced vasodilation
- Pre-eclampsia superimposed on chronic HTN
- Pre-eclampsia: due to abnormal placental function - poor perfusion - remodelling of spiral arteries - high resistance low flow circulation - HTN, hypoxia, oxidative stress - inflammatory response
Define hypertension in pregnancy
>140/90 on 2 occasions >4h apart or single diastolic reading >110 or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic
How does pre-eclampsia present and what ix would you request?
CF:
- Sym: headache, visual blurring/diplopia/flashing, epigastric/RUQ pain (hepatic capsule distension), non-pitting oedema, vomiting
- Signs: hyper-reflexia, oedema, epigastric tenderness
Ix: 24h urinary protein, measure organ dysfunction (low plt + Hb, raised urea + creatinine + urate, reduced pH, raised ALT/AST)
Risk factors for pre-eclampsia?
- Moderate: nulliparity, >40y, BMI>35 @ booking, FH, preg interval >10y, multiple pregnancy
- High: chronic HTN, previous pre-eclapmsia/HTN in pregnancy, CKD, T1/2DM, autoimmune like SLE/APS
How is pre-eclampsia managed?
- Monitoring BP, urinalysis, growth scans, CTG
- Delivery is the only cure, if fetal compromise need to delivery (give steroids if <35w for lung maturation)
- Anti-hypertensives to reduce maternal haemorrhage stroke risk - labetalol (CI in asthma, caution in T1DM as stops palps which are a hypo warning, s/e include fatigue headache N+V), 2nd line nifedipine MR (so don’t drop BP too quick, s/e peripheral oedema dizzy flush headache), 3rd line methyldopa (alpha agonist, central action)
- At 37w: plan delivery within 24-48h, if severe HTN consider IV magnesium sulphate for seizure prophylaxis (reduces BP to stop seizure but just used in critical care settings)
- VTE prophylaxis: LMWH
Resolves once placenta delivered, monitor for 24h PP as risk of eclampsia
What are the complications of pre-eclampsia?
- Maternal: haemorrhagic stroke, eclampsia/cerebral oedema, ARDS/pulmonary oedema, renal tubular necrosis, hepatic rupture, HELLP, DIC/MAH, placental infarct/abruption
- Fetal: low bw, IUGR, abruption, IUD, premature delivery, cerebral palsy (prematurity + pre-eclampsia)
- HELLP: an extension of DIC. Haemolysis, Elevated liver enzymes (cos of endothelial dysfunction + hypoxia), Low platelets (often severe) – need TOP if have this
Aetiology of GDM
- Higher insulin resistance as placenta makes anti-insulin hormones (HPL, glucagon + cortisol); if pancreas doesn’t also increase insulin get GDM
- Insulin can’t cross the placenta so fetus remains hyperglycaemic
- RF: BMI>30, prev macrocosmic baby >4.5kg, prev GDM, FH of DM in a 1st degree relative, ethnic origin with high DM prevalence
How is GDM diagnosed?
- OGTT at 28w if they have RF
- Previous GDM - early self-monitoring of BGL or offer OGTT at booking + laer
- Diagnosed when 2h OGTT is 7.8 or more, or fasting plasma glucose is 5.6 or more
- Don’t use HbA1c - as pregnancy lowers levels so they need different reference ranges but not established yet
