Complicated pregnancy 6 Flashcards
Hyperemesis gravidarum
Ax
RF [5]
Ax: raised beta-HCG levels RF: - Multiple pregnancies - Trophoblastic disease - Hyperthyroidism - Nulliparity - Obesity
Hyperemesis gravidarum Presentation Onset, duration Diagnostic triad Systemic signs [5]
Extreme form of nausea and vomiting in pregnancy
- usually 8-12w but can persist up to 20w
- Diagnostic triad: 5% pre-pregnancy weight loss, dehydration, electrolyte imbalance
- Dehydration, weight loss, hypokalemia, muscle weakness, tetany
Hyperemesis gravidarum
Investigations [4]
Management [4]
Investigation: • Urinalysis: ketones • U&E and creatinine: hyponatraemia, hypokalaemia • Severity • USS: excl. hydratiform mole - TFTs
Mx:
- Antihistamines promethazine or cyclizine
- Admit for IV fluids if unable to tolerate oral or electrolyte imbalance
- High dose folic acid and pabrinex
- Avoid glucose as it precipitates Wernickes
How do u formally assess severity in hyperemesis gravidarum?
Complications of HG
Maternal [4]
Fetal [2]
Pregnancy Unique Quantification of Emesis (PUQE) score
Complications:
• Maternal: Wernicke’s encephalopathy, Mallory-Weiss tear, central pontine myelinolysis, acute tubular necrosis
• Fetal: SGA, pre-term birth
Why is there an increased risk for thromboembolic disease in HG patients?
The coincidence of pregnancy, dehydration [2] and associated immobility in a woman with hyperemesis increase the risk of venous thromboembolic events
Rationale for doing TFT in HG?
Excessive hCG secretion may cause hyperthyroidism in patients with hyperemesis gravidarum
Jaundice in pregnancy causes [2]
Intrahepatic cholestasis of pregnancy
Acute fatty liver of pregnancy
Intrahepatic cholestasis of pregnancy Ax Symptoms [3] Sign Complications [3]
Ax: impaired release of bile causing bile to build up in the liver
Symptoms:
- Pruritus of palms, abdomen, soles but no rash
- Second half of pregnancy
- Worse at night
Signs: visible jaundice
Cx:
- premature birth, stillbirth, can recur with COCP or future pregnancies
Intrahepatic cholestasis of pregnancy
Ix [2]
Mx [4]
Prognosis
Ix:
- LFTs (mildly elevated AST and ALT with elevated bilirubin)
- clotting
Mx:
- induction of labour (IOL) at 37w (due to increased risk of stillbirth)
- URSODEOXYCHOLIC ACID (symptomatic relief)
- weekly LFTs
- VITAMIN K supplementation (to mum if abnormal clotting and to baby at delivery)
Prognosis: resolves within days of delivery
Acute fatty liver of pregnancy
Presentation [6]
Ix [5]
Sy/Si:
- abdo pain, N&V
- headache
- jaundice
- hypoglycaemia
- pre-eclampsia
- usually after 30w
Ix:
- LFTs (high ALT, bilirubin)
- U&Es (AKI)
- Urate
- Glucose (low)
- Clotting
Acute fatty liver of pregnancy
Mx [3]
Complications [2]
Mx:
- HDU or ITU mx with BP monitoring
- Mx of liver and renal failure, low glc
- Deliver once stabilized
Complications:
- PPH
- Neonatal hypoglycemia
VTE
Investigations [5]
Management
Prevention [3]
- Bloods: FBC, U&E, clotting, LFTs D dimer INACCURATE
- Suspected DVT: duplex USS
- Suspected PE: duplex USS (can presume PE if +ve and chest symptoms)
- if -ve then CXR and V/Q scan if no abnormality on CXR
- do ECG look for right heart strain
Mx:
- treatment dose LMWH for 3m
Pre:
- prophylactic LMWH stat if previous VTE,
- immediately if >4 RFs and from 28w
- if 3 RFs continued until 6w post-natal
Small for gestational age
Define
Non-placental [4]
Placental classified into 2 mechanisms
Born with birth weight < 10th centile
Non-placental
- Structural (gastroschisis)
- Chromosomal
- Inborn errors of metabolism
- TORCH
Placental
- Nutrient transfer
- Implantation and vasculature
What are underlying causes for problems with nutrient transfer causing SGA? [3]
What are underlying causes for problems with IMPLANTATION AND VASCULATURE causing SGA? [3]
- Nutrient transfer
> Low pre-pregnancy weight, undernutrition
> Cocaine, alcohol, smoking
> Severe anemia
- Implantation and vasculature > Pre-eclampsia > Essential HTN > Thrombophilia > Autoimmune > Repeated APH
Define Low birth weight
Association between IUGR and SGA
<2.5kg
More likely in severe SGA where pathological growth restriction
- majority of SGA babies are actually appropriate for maternal height and ethnicity)
RF for SGA
Major [7]
Major:
- > 40y/o, smoker >11/d
- paternal SGA, previous SGA baby
- cocaine, vigorous daily exercise
- chronic HTN, DM with vascular disease, renal impairment
- anti-phospholipid syndrome
- low PAPP-A
- fetal echogenic bowel
RF for SGA
Minor [7]
Minor:
- > 35y/o
- IVF singleton, nulliparity
- BMI <20 or 25-34.9
- smoker 1-10/d
- low fruit intake before pregnancy
- previous pre-eclampsia
- pregnancy interval <6m
SGA presentation
Investigations that need to be done
SFH >3cm below number of weeks gestation or identified at anomaly scan
- Always check BP and urine for pre-eclampsia
- Serial growth scans from 26-28w (if any major RFs)
- Umbilical artery doppler
- Anomaly scan
- Amniocentesis and karyotype
- Toxoplasmosis and CMV serology
SGA management
Surveillance protocol depends on Doppler scan [4]
Surveillance
o Normal Doppler: serial growth scans NOT indicated unless other cx
o Abnormal Doppler: serial growth scans from 26-28w every 2w and Doppler
Labour & Delivery for SGA:
- If <32w and abnormal Doppler
- If >32w and abnormal Doppler
- If >32w and normal Doppler
o <32w and abnormal Doppler: deliver <32w
o >32w and abnormal Doppler: deliver before 37w
o >32w and normal Doppler: deliver at 37w
LGA definition Risk factor Presentation Ix Mx Cx [4]
Define: Weight at gestation >4.5kg Risk factor: maternal DM, obesity Presentation: picked up on USS Ix: regular growth scans Mx: deliver at 37w Cx: - CS, tears, PPH - Fetal death
Rhesus disease
Ax
Ix
Mx [2]
Ax: mother is Rh-ve and father is Rh +ve
Ix: screen at 8-12w for mothers rhesus status
Mx:
- No abs: give prophylactic anti-D IgG at 28 and 34w to prevent mother making own anti-D
- Antibodies present: monitor pregnancy for signs of fetal anemia
Twin pregnancies
Incidence
Monozygotic
Dizygotic
1 in 105 pregnancies
• Monozygotic: identical; develop from single ovum which has divided to form 2 embryos
• Dizygotic (80%): non-identical; develop from 2 separate ova that are fertilised at the same time
Risk factor for dizygotic twins [4]
RF:
- induced ovulation, IVF
- previous twins, FHx
- increasing maternal age, multigravida
- Afro-Caribbean ethnicity
Dizygotic: dichorionic, diamniotic (DCDA) pathophysiology
Types of monozygotic [3]
DCDA: split days 1-3; usually dizygotic
- Monochorionic diamniotic
- Monochorionic monoamniotic
- Conjoined twins
Pathophysiology of:
- Monochorionic diamniotic (MCDA)
- Monochorionic monoamniotic (MCMA)
- Conjoined twins
- MCDA: split days 4-8, usually monozygotic
- MCMA: split days 8-13, riskiest due to placental insufficiency and cord entanglement
- Conjoined twins: split days 13-15
What are specific associations with monozygotic? [5]
Increased risk of:
- spontaneous miscarriage
- perinatal mortality, IUGR
- malformations
- prematurity
- twin to twin transfusion syndrome
Diagnosis [2]
Confirmed by first ultrasound scan
Lamda sign if dichorionic
Ante-natal care of twin pregnancies [4]
Rest
Monthly USS
Additional Fe, folate
Weekly antenatal care after 30w
Timing of delivery for DCDA, MCDA, MCMA
Labour and delivery of twin pregnancies steps [7]
Timings:
- DCDA at 37-38w
- MCDA at 36-37w
- MCMA at 32-34w
- Requires 2 obstetricians present
- In theatre
- Continuous CTG
- Cord clamping
- 2nd scan to assess presentation of twin 2
- Oxytocin
- Vaginal assisted delivery or C-section
Complications of twin pregnancies
Maternal [5]
Fetal [6]
Maternal
- Pre-eclampsia, GDM
- Polyhydramnios
- APH, PPH
- Placental abruption
- Cord prolapse
Fetal
- Preterm labour
- Congenital malformations
- IUGR
- Placental insufficiency
- Perinatal mortality x5 twins, x8 triplets
- Twin to twin transfusion syndrome
Twin to twin transfusion syndrome pathophysiology [4]
Mx [2]
- Monochorionic twins share chorion
- blood vessels anastomose so donor twin’s blood supply disproportionately goes to recipient twin
- Donor > IUGR and oligohydramnios
- Recipient > larger, polyhydramnios
Mx: serial amniocentesis, laser photocoagulation
