Complications in Pregnancy Flashcards
Rhesus Isoimmunisation
=Immune Hydrops; Maternal Transplacental Antibody response mounted against Foetal RBC antigens; Ensuing Anaemia leads to Hydrops
Pathophysiology of Rhesus Isoimmunisation
Five Rhesus antigens (C/c, E/e, D); Significant antigens – D, c, E, and atypical Kell
• Foetal cells cross into Maternal circulation in normal pregnancy; Amount increased during sensitising events (E.g. TOP, ERPC, Ectopic, PV bleeding, Blunt trauma, Invasive Uterine
procedures, Intrauterine Death and Delivery)
• Rh D positive foetus vs. Rh D negative mother; Initially, IgM produced
• Re-exposure in subsequent pregnancy causes primed memory B-cells to produce IgG; IgG binds Foetal RBC, which is destroyed in RES leading to Haemolytic Anaemia
o If unable to compensate, severe anaemia leads to HOCF, Foetal Hydrops and Death
o Milder cases – Neonatal Anaemia or Jaundice from increased RBC breakdown
Anti D Prophylaxis
Given to Rh D negative women; Anti-D Immunoglobin binds to Foetal RBC; Prevents maternal
immune system from recognising and becoming sensitised
o RAADP at 28 weeks; Also given within 72h of potentially sensitising event, and after delivery if Neonate is found to be Rh positive
During sensitising events, large Foeto-maternal Haemorrhages might occur; Kleihauer test (HbF in maternal blood) to determine dose of ADP required
o Kleihauer test routine at delivery if Neonate is Rh D positive
Foetal Hydrops
Due to imbalance of Interstitial fluid production and Lymphatic return; Can result from Congestive Heart Failure, Obstructed Lymphatic Flow, or Decreased Plasma Osmotic Pressure
How is foetal hydrops diagnosed?
Diagnosis made by Ultrasound; Might be associated with other structural abnormalities
o Foetal Echocardiography for Cardiac Lesions; Foetal Anaemia measured by Peak
Systolic Velocity MCA flow
o Foetal Blood sampling if Anaemia suspected; In-utero Transfusion in same setting
o Amniotic Fluid, Foetal Blood Karyotyping and Virology
o Maternal Blood testing – Kleihauer (Foeto-maternal Haemorrhage), Antibody
Screening (Immune Hydrops), Virology, Hb Electrophoresis (α-Thalassemia)
Causes of non immune hydrops
Congenital Parvovirus, α-Thalassemia Major,
Massive Foeto-Maternal Haemorrhage, G6PD deficiency, Cardiac Structural and Conductive
Abnormalities, Aneuploidy, Infection (Toxo, Rubella, CMV, VZV), Twin-twin transfusion
What to do in severe polyhydramnios
Amnioreduction may reduce risk of prem; Consider steroids as reduction carries small risk of causing prem
Oligohydramnios
Normal volume depends on Urine production (after 20/40), Foetal Swallowing and Absorption; Measurement by Ultrasound
Causes of Oligohydramnios
SROM, IUGR, Foetal Renal abnormalities, Post-dates, Foetal Urinary obstruction
Complications of Oligohydramnios
Complications can be related to cause (PROM, IUGR) or reduced volume (Lung Hypoplasia if <22/40, Limb Abnormalities if prolonged)
o Should investigate for rupture of membranes; If suspected, FBC, CRP and Swabs taken
o If SROM 34 – 36/40; Induce Labour; CS if other indication
o If before 34/40 – Prophylactic Oral Erythromycin, monitor for signs of infection, Daily
CTG and consider Induction at 34 – 36/40
Causes of polyhydramnios
Maternal DM, Twin-twin Transfusion, Foetal Hydrops, Foetal GI obstruction,
Neurological or Muscular Abnormalities (failure to swallow), Idiopathic (usually mild)
Complications of polyhydramnios
Preterm (due to Uterine stretch), Malpresentation, Maternal discomfort
• Important to exclude maternal diabetes with GTT
What determines growth potential?
Attaining growth potential depends on Maternal, Placental and Foetal factors;
Growth potential is determined by Maternal height (Paternal height to lesser extent), Maternal weight in early pregnancy, Parity, Ethnicity and Foetal Sex)
What is IUGR
Implies that foetus is pathologically small (=Small for Gestational Age)
o Most commonly set that estimated weight is below tenth percentile
Associations with IUGR
IUGR associated with 6 – 10-fold Perinatal Mortality, four-fold increase in Cerebral Palsy; Foetal Distress, Asphyxia, Meconium Aspiration, NEC, Hypoglycaemia and Hypocalcaemia
Symmetric IUGR
seen in very early onset IUGR, and with Chromosomal Abnormalities
Asymmetric IUGR
(Head-sparing) – Undernourishment and Placental Insufficiency most commonly
Maternal factors causing IUGR
Chronic Maternal Disease (HTN, CVS, CKD), Substance Abuse, Smoking, Autoimmune Disease (Increasing APLS), Poor Nutrition and Socioeconomic Factors
Placental Insufficiency causing IUGR
Abnormal Trophoblast Invasion (Pre-Eclampsia and Accreta), Infarction, Abruption, Praevia, Chorioangiomas, Abnormal Cord/Insertion
Foetal factors causing IUGR
Genetics (Aneuploidy), Congenital Abnormalities (Cardiac, Gastroschisis), Congenital Infections (CMV, Rubella, Toxo), Multiple Pregnancies
Management of IUGR
- Early Identification, Foetal Monitoring; Continue Pregnancy as long as safely possible and delivery before excessive compromise
- 1/3 do not reach predicted adult height; Might have neurological deficits
Effects of poor glycaemic control
leads to increased
Foetal and Neonatal Morbidity and Mortality
How many pregnancies does diabetes affect?
Established Diabetes affects 1 – 2% of pregnancies;
Which pregnancy hormones are diabetogenic?
Many pregnancy hormones (HPL, Cortisol, Glucagon, Oestrogen and Progesterone) are
Diabetogenic; Insulin requirements also increased throughout and peak at term
Effects of hyperglycaemia
leads to Foetal Hyperglycaemia and Hyperinsulinism
o Leads to Foetal Macrosomia, Organomegaly, Erythropoiesis and Polyuria which can lead to Polyhydramnios
o At delivery, Neonatal Hypoglycaemia might occur with removal of Maternal glucose supply in the Hyperinsulinaemic Foetus
o Also, Reduced Production of Pulmonary Phospholipids – Increased risk of RDS
How does pregnancy affect diabetes?
Ketoacidosis, Retinopathy (two-fold risk), Nephropathy
(Renal function and proteinuria may worsen in pregnancy), Ischaemia Heart Disease
Antenatal Management
Achieve optimal control: fasting BG between 3.5-5.9mmol
Assess severity: HTN, retinopathy, nephropathy, urinalysis
Education, stop ACEi and other teratogenic drugs
Increased folic acid supplementation
Monitor BG 4 times a day, monthly HbA1c
Glucagon supply
Echo at 20-24 weeks
Diabetes and Labour: Delivery
• Timing and Mode of delivery based on
Estimated Foetal Weight and Obstetric Factors (Previous Pregnancies, Gestation,
Glycaemia Control, Antenatal Complications
• Delivery should be expedited if complications occur; ± Induced Labour
• Vaginal Delivery preferred; Continuous Foetal Monitoring; Elective CS if Macrosomia
o Shoulder Dystocia more common
Diabetes and Labour: Glycaemic Control
Start Sliding scale if >6mmol/L glucose, or mandatory If insulin
dependent at Established labour
o IV fluids given with sliding scale
o If steroids given for Threatened Prem, Monitor for Hyperglycaemia
Diabetes and Labour: Breastfeeding
Encourage Breastfeeding post-delivery; Metformin and Insulin safe to use
o Neonate requires early feeding and glucose monitoring
Diabetes and Labour: Post Partum
Insulin requirements fall dramatically following Placenta delivery; Halve sliding scale, change
back to normal regimen when eating and drinking
o Aim for BG 4 – 9mmol/L in post-partum period
Who is screened for GDM?
BMI>30
Previous Macrosomia pregnancy
Previous GDM
First-degree FH DM, Ethnicity (South Asia, Afro Caribbean, Middle East)
Diagnosis of GDM
Diagnosis based on OGTT at 26 – 28/40;
Should be repeated at 34/40 if concerns
Management of GDM
Measure BG 4 – 6 times per day; Diet is first line management; Weight should remain steady if diet followed, if poor compliance,
seek Dietitian advice
• Start Insulin if >6mmol/L pre-prandial, 1h post-prandial >7.5mmol/L, Macrosomia on USS
• Care similar to established diabetes; Arrange OGTT 6/52 post-partum to check for DM
o 50% risk of developing T2DM over next 25yrs; Reduced risk by physical activity and avoiding obesity
Causes of thyrotoxicosis
Most commonly due to Graves, most diagnosed prior to pregnancy
o Weight Loss, Tremor, Persistent Tachycardia, Eye Signs; Low TSH, High T3/4
o Graves improves in second and third trimester due to state of relative
immunodeficiency; Deteriorates following delivery
o Maternal and Foetal outcome good if disease control; Untreated Thyrotoxicosis associated with Subfertility, Risk of Miscarriage, IUGR, Prem
When can a thyroid storm occur?
Can occur in poorly controlled Thyroid disease with Infective, Labour or
Operative stressors; Pyrexia, Confusion, Cardiac Failure
Neonatal Thyrotoxicosis
10% of maternal Grave’s (past or current Hx) due to
Transplacental TSHR stimulating Antibodies
Managing women with Grave’s
Check Thyroid Abs in all women with Graves Hx; If present, Monitor FHR, Serial US for growth and Foetal Goitre; Monitor TFTs 4 – 6/52 for new cases
o Treatment with Carbimazole or Propylthiouracil (PTU); Aim for Clinical Euthyroid with
T4 at ULN, using lowest dose to achieve
▪ PTU preferred – Less transplacental and into breast milk
o Surgery – Thyroidectomy can be safely done in Pregnancy; Performed if Dysphagia, Stridor, Suspected Ca Thyroid, Allergies to Antithyroid Drugs
RAI is contraindicated in Pregnancy and Breastfeeding
How often in hypothyroidism in pregnancy
Most diagnosed prior to pregnancy; New diagnosis in pregnancy is rare
Causes of hypothyroidism
Hashimoto (Anti TPO), Atrophic Thyroiditis (TSH blocking), Iatrogenic, Rarely pituitary
Implications of hypothyroidism
Severe disease associated with Miscarriage, Pre-Eclampsia and Low Birthweight
Management of Hypothyroidism
o Foetus requires Maternal T4 for normal brain development before 12/40
o TSH levels should be checked before conception and before each trimester; if first diagnosis in pregnancy, consider starting dose 50mcg/day
Blood Pressure in Pregnancy
In early pregnancy, BP is low until 24/40 due to reduction in PVR; Increases after 24/40 till delivery due to increase in SV; Reduction following delivery
How should BP be monitored in pregnancy
BP should be measured sitting, or supine with Left-tilt, with upper arm at level of heart; Automated BP monitors might under-record BP
Chronic Hypertension
– Increased risk of developing Pre-Eclampsia; Look for secondary
causes if BP is very high
o Secondary Causes – Renal, Cardiac, Endocrine diseases
HTN Treatment
Treatment of BP in pregnancy urgently if
>160/100mmHg for maternal health; Should
not reduce below 120/80mmHg
• Treatment of BP does not alter course of Pre-
Eclampsia, but protects maternal health
Pregnancy Induced Hypertension
=HTN (≥140/90mmHg) after 20/40, in the absence of Proteinuria/Pre-Eclampsia markers
• Increased risk of developing Pre-Eclampsia (15 – 26%); Higher risk if earlier onset; Delivery
should be aimed at time of EDD
• BP usually returns to pre-pregnancy limits within 6/52 of delivery
Post Partum Hypertension
Can either be Physiological, Pre-existing Chronic HTN, or New-onset Pre-Eclampsia; BP peaks on third to fifth day post-partum
Symptoms of post partum hypertension
Epigastric pain, Visual disturbance, New-onset Proteinuria suggestive of Post-Partum Pre-Eclampsia
Post natal management of post partum HTN
Beta Blocker > Methyldopa due to risk of PND; Captopril and Nifedipine may also be used
o Safe to breastfeed with; Should follow up with GP in the community
o Follow up 6 weeks post-natal, when it should be resolved; Investigate if persistent
Pre-eclampsia
Multisystemic; HTN plus Proteinuria and thought to be Placental in origin
o Spectrum of Mild to Severe disease (=Eclampsia); Leading cause of Maternal
morbidity in the UK; Common cause of Prem and Hospital admission
o 5% of Pregnancies; Severe in 1%
Risk factors for Pre eclampsia
Previous Pre-Eclampsia (7-fold; More if Earlier onset, Severe or HELLP),
pre-existing HTN, PIH, low PAPP-A, Raised Uric Acid, Low Platelets, High Hb, Identified on Uterine Artery Doppler at 11-13 weeks or 22-24 weeks
Diagnosis of Pre-eclampsia
BP ≥140/90 plus ≥300mg Proteinuria on 24h collection; If Pre-existing HTN, Rise of SBP
≥30mmHg or Diastolic ≥15mmHg; Other markers including Abnormal Biochemistry and IUGR
Prevention of Pre-eclampsia
Aspirin (75mg PO OD) before 16/40; reduce repeat severe pre-eclampsia by 20%
Presentation of Pre-eclampsia
May present as Headache, Visual Disturbance, Epigastric/RUQ pain, N+V, Facial Oedema, although they might only occur in severe disease
Investigations of Pre-eclampsia
• Confusion, Hyperreflexia, Clonus (>3 beats) are signs of Cerebral irritability; Uterine Tenderness or PV bleeding might occur if Placental Abruption
• Relative high Hb, Thrombocytopaenia; Haemolysis can lead to Anaemia in HELLP; Mildly
prolonged PT and aPTT
• Raised Urate, U/Es, Abnormal LFTs, Raised LDH (due to Haemolysis) and Proteinuria
Management of Pre-eclampsia
Admit all initial presentation of Pre-Eclampsia for assessment and treatment if necessary
o 4-hourly BP, 24h Urine Collection, Daily Urinalysis, Daily CTG, Regular bloods (every 2– 3 days unless worsening), Regular Ultrasound
• If BP ≥150/100, Antihypertensives should be started: Oral Labetalol typically first-line
Complications of Pre-Eclampsia
Severe Complications include Eclampsia, HELLP, Cerebral Haemorrhage, IUGR, Foetal Compromise, Renal Failure and Placental Abruption
Severe Pre-eclampsia
Severe if ≥160/110 plus significant Proteinuria (>1g/24h, 2+ Dip), or Maternal Complications
o Senior help – Obstetrics, Anaesthetics, Midwifery
o Only treatment is delivery, but can be delayed with Intensive monitoring if <34/40
o NB: Pre-Eclampsia often worsens 24h after delivery
Indications for Immediate Delivery
Worsening Thrombocytopaenia or Coagulopathy,
Worsening Liver or Renal Function, Severe Maternal Symptoms (Especially Epigastric pain,
Abnormal LFTs), HELLP syndrome, Eclampsia, Foetal (Abnormal CTG, Reversed UAEDF)
Management of Severe Pre-eclampsia
• Oral Labetalol; If still high after 2 – 3 doses, start on IV Labetalol infusion and titrate until adequate control; Maintenance therapy of Labetalol; Methyldopa if Asthmatic
• FBC, U/Es, LFTs, Clotting; Strict Fluid Monitoring, consider Cath
o CTG until stable; Ultrasound to look for evidence of IUGR
• If <34 weeks, Steroids given, and pregnancy managed expectantly unless worsening
Eclampsia
=Tonic-Clonic Seizure associated with Pre-Eclampsia; Antenatal (38%), Intrapartumv (18%) or Postpartum (44%); Most die from Blood loss, Intracranial Haemorrhage or HELLP
Management of Eclampsia
o ABCDE; Most Eclamptic fits short-lasting, terminate spontaneously
o Mg Sulfate is first line – 4g loading over 5-10mins, 1g/h over 24hrs
▪ Mg Toxicity – Confusion, Loss of Reflexes, Hypotension, Resp depression
▪ If Toxic – 1g Calcium Gluconate over 10 mins
o Diazepam if recurrent; If still fitting, Intubation, Ventilation and Neuroimaging
HELLP
Severe Variant of Pre-Eclampsia; Haemolysis, Elevated Liver Enzymes, Low Platelets
o Haemolysis tends to occur late; May precede permanent Liver or Renal damage
o Epigastric/RUQ pain, N+V, Tea-coloured Urine (Haemolysis)
o Platelet infusions only required if bleeding, if for surgery, or if <40
