OBS - Pregnancy Related Disorders Flashcards
Pre-Eclampsia
Pathophysiology
Risk Factors
Clinical Features/Diagnosis
Complications
1.) Pathophysiology - pregnancy-induced HTN with end-organ dysfunction occurring >20w gestation
- due to inadequate formation of lacunae (at 20wks) causing high vascular resistance and low flow in the spiral arteries –> poor placental perfusion
- oxidative stress –> release of systemic inflammatory chemicals and endothelial cell dysfunction –> ↑BP
2.) Risk Factors
- high risk: chronic HTN or previous gestational HTN, autoimmune disease (e.g. SLE), diabetes, CKD
- mod: >40, BMI >35, multiple pregnancies, nulliparity >10yrs between pregnancies, FH of pre-eclampsia
3.) Clinical Features/Diagnosis - HTN + others:
- HTN: sys>140 OR dia>90 on 2 occasions >4hrs apart
- proteinuria: 1+ on dipstick OR >300mg protein in 24hr urine collection, urine P:CR >30mg OR urine A:CR > 8
- organ dysfunction: ↑creatinine, ↑LFTs, haemolytic anaemia (↓Hb), thrombocytopenia (↓plts)
- placental dysfunction: FGR, abnormal Doppler studies
- often asymptomatic until severe where you get sx:
- headaches, visual disturbance, papilledema
- epigastric pain (hepatic distension/infarction), N+V
- hyperreflexia, pitting oedema, ↓urine output
4.) Complications
- maternal: seizures, HELLP syndrome, AKI, DIC, ARDS, chronic HTN, cerebrovascular haemorrhage, death
- HELLP: Haemolysis, Elevated Liver enzymes, Low Platelets
- fetal: prematurity, IUGR, placental abruption, stillbirth
Management of Pre-Eclampsia
Investigations
Preventative Management
General Management of Pre-Eclampsia
Medical Management of Pre-Eclampsia
Antihypertensives
1.) Investigations
- BP, urine dip + 24hr urine collection
- FBC, U+Es +/- PCR/ACR, LFTs
- fetal compromise: growth scans, US/doppler, CTG
- placental growth factor (PlGF): low levels in pre-eclampsia, used between 20-35wks to exclude
2.) Preventative Management
- prophylaxis: aspirin from 12w until birth in those with one high-risk factor OR 2+ mod-risk factors
- routine antenatal monitoring: BP, sx, urine dip
- gestational HTN w/o proteinuria: keep BP <135/85, admission if >160/110, weekly bloods and urine dips, serial growth scans, CTG, PIGF testing on one occasion
3.) General Management of Pre-Eclampsia
- obstetric assessment required if suspected
- admission criteria: use full-PIERS or PREP-S
- monitoring: BP every 48hrs, routing urine dip not necessary, fetal US/doppler performed 2 weekly
- fluid restriction during labour in severe pre-eclampsia
- post-natal: monitoring for >24hrs, daily BP for 2 days, then once every 3-5 days post-partum
- gestational HTN: BP >160/110 will most likely required in-patient admission for observation
4.) Medical Management of Pre-Eclampsia
- definitive Mx: early delivery of the baby
- neuroprotection/eclampsia: IV Mg sulphate during labour and 24hrs after delivery (or last seizure), should monitor reflexes and RR (can cause resp depression, Tx w/ calcium gluconate)
- VTE prophylaxis: often LMWH (enoxaparin)
- antihypertensives
5.) Antihypertensives - given to ↓risk of haemorrhagic stroke and should be continued throughout labour
- 1°labetalol, 2° MR-nifedipine, 3°methyldopa (contra in depression), IV hydralazine in severe/critical care
- epidural anaesthesia can be used to also lower BP
- post-delivery antihypertensive: switch to enalapril (1°) OR nifedipine (safe while breastfeeding) or amlodipine in afro patients, labetalol/atenolol (3°)
Gestational Diabetes (GDM)
Pathophysiology
Oral Glucose Tolerance Test
Fetal Complications of GDM
1.) Pathophysiology - the body can’t produce enough insulin to meet the needs of the pregnancy due to progressive insulin resistance (requirements ↑by 30%)
- can’t respond to the insulin requirements if you have a borderline pancreatic reserve, risk factors include:
- previous GDM or macrosomia (>4.5kg), BMI >30, FH of diabetes (1st gen), ethnicity (Black African/Caribbean, South Asian and Middle Eastern)
2.) Oral Glucose Tolerance Test - screening for GDM at:
- booking: previous pregnancy with GDM
- 24-28wks: if risk factors ^^^ are present
- any point: glucosuria (++ or + in 2 occasions)
- OGTT is done in the morning after a fast (water allowed), 75g glucose drink then measure after 2hrs
- GDM: fasting >5.6mM OR at 2 hours >7.8mM
3.) Fetal Complications of GDM
- hyperglycaemia –> hyperinsulinemia (similar to GFs):
- macrosomia, polyhydramnios, organomegaly (heart), erythropoiesis –> polycythaemia, prematurity
- neonatal hypoglycaemia: high insulin levels with no maternal glucose (insulin doesn’t cross the placenta)
- neonatal ARDS: insulin ↓pulmonary phospholipids which are required for surfactant production
Management of Gestational Diabetes
General Management
Medical Management
Managing Pre-Existing Diabetes
Postnatal Care
1.) General Management
- managed in joint diabetes and antenatal clinics, with input from a dietician, need to educate the mother
- need to measure sugar levels several times a day: fasting (<5.3mM), pre-meal, 1hr post meal (<7.8mM), bedtime, avoid anything below 4mM
- additional growth scans at 28, 32, 36 wks to monitor for complications of GDM (e.g. polyhydramnios)
- early delivery: at 37-38wks if on treatment, can be delivered up to 41wks (40+6) if managed by diet
2.) Medical Management - depends on sugar levels
- fasting <7mM: trial diet and exercise for 1-2wks, followed by metformin, then insulin
- fasting >7mM: start insulin +/- metformin
- fasting >6mM + macrosomia: insulin +/- metformin
- glibenclamide (SU) alternative to insulin or metformin
3.) Managing Pre-Existing Diabetes
- should take preconceptual high dose folic acid (5mg)
- aim for the same target insulin levels as with GDM
- T2 DM only managed with metformin and insulin
- diabetic retinopathy screening (ophthalmologist) performed shortly after booking and at 28wks
- planned delivery between 37-39 wks (38+6)
- VRIII can be considered during labour
4.) Postnatal Care
- can stop medications immediately after birth but will need to follow up with OGTT after >6wks
- beware of hypos in those with existing diabetes
- neonatal hypos: need regular BG checks, frequent feeds, aim to keep BG >2mM, may need an NG if not
- other fetal complications: polycythaemia, jaundice, congenital heart disease, cardiomyopathy
Hyperemesis Gravidarum (HG)
Pathophysiology
Clinical Features
Investigations
Management
1.) Pathophysiology - rapid ↑beta-hCG stimulates the CTZ (brainstem), which feeds into the vomiting centre
- N+V of pregnancy (NVP) often starts between wk 4-7, peaking around week 9 and settling by week 20
- HG is prolonged NVP –> dehydration, electrolyte imbalances, and >5% pre-pregnancy weight loss
- risk factors: obesity, nulliparity, multiple pregnancy, molar pregnancy, previous hx of HG, hydatidiform mole,
- smoking is a protective factor (reduced incidence)
2.) Clinical Features - persistent and severe N+V
- diagnostic criteria: dehydration, electrolyte imbalance, 5% pre-pregnancy weight loss
- severity: PUQE score (Pregnancy-Unique Quantification of Emesis)
- <7 = mild NVP, 7-12 = mod, 13-15 = severe NVP
- differentials should be considered if onset >11wks e.g. gastroenteritis, cholecystitis, pancreatitis, UTI/pyelo, etc
3.) Investigations
- bedside: weight, urine dip (ketonuria) +/- MC+S, BM
- bloods: FBC, U+Es, BG, ABG, LFTs, amylase, TFTs
- imaging: USS to confirm viability, gestation and exclude multiple pregnancy and trophoblastic disease
4.) Management
- mild: community-managed, oral antiemetics, oral hydration, dietary advice and reassurance
- mod: ambulatory daycare, IV fluids/antiemetics and thiamine, managed until ketonuria resolves
- severe: inpatient management, thromboprophylaxis
- anti-emetic: 1°antihistamines (cyclizine, promethazine, prochlorperazine), 2° metoclopramide or ondansetron
- ondansetron is linked with an increased risk of cleft-lip/palate when used in the first trimester
- maternal complications: Wernicke’s encephalopathy, Mallory-Weiss tear, central pontine myelinolysis, acute tubular necrosis
- fetal complications: SGA and prematurity
