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Obstetrics > Complications in Pregnancy > Flashcards

Complications in Pregnancy Flashcards

1
Q

Rhesus Isoimmunisation

A

=Immune Hydrops; Maternal Transplacental Antibody response mounted against Foetal RBC antigens; Ensuing Anaemia leads to Hydrops

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2
Q

Pathophysiology of Rhesus Isoimmunisation

A

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

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3
Q

Anti D Prophylaxis

A

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

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4
Q

Foetal Hydrops

A

Due to imbalance of Interstitial fluid production and Lymphatic return; Can result from Congestive Heart Failure, Obstructed Lymphatic Flow, or Decreased Plasma Osmotic Pressure

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5
Q

How is foetal hydrops diagnosed?

A

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)

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6
Q

Causes of non immune hydrops

A

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

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7
Q

What to do in severe polyhydramnios

A

Amnioreduction may reduce risk of prem; Consider steroids as reduction carries small risk of causing prem

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8
Q

Oligohydramnios

A

Normal volume depends on Urine production (after 20/40), Foetal Swallowing and Absorption; Measurement by Ultrasound

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9
Q

Causes of Oligohydramnios

A

SROM, IUGR, Foetal Renal abnormalities, Post-dates, Foetal Urinary obstruction

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10
Q

Complications of Oligohydramnios

A

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

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11
Q

Causes of polyhydramnios

A

Maternal DM, Twin-twin Transfusion, Foetal Hydrops, Foetal GI obstruction,
Neurological or Muscular Abnormalities (failure to swallow), Idiopathic (usually mild)

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12
Q

Complications of polyhydramnios

A

Preterm (due to Uterine stretch), Malpresentation, Maternal discomfort
• Important to exclude maternal diabetes with GTT

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13
Q

What determines growth potential?

A

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)

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14
Q

What is IUGR

A

Implies that foetus is pathologically small (=Small for Gestational Age)
o Most commonly set that estimated weight is below tenth percentile

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15
Q

Associations with IUGR

A

IUGR associated with 6 – 10-fold Perinatal Mortality, four-fold increase in Cerebral Palsy; Foetal Distress, Asphyxia, Meconium Aspiration, NEC, Hypoglycaemia and Hypocalcaemia

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16
Q

Symmetric IUGR

A

seen in very early onset IUGR, and with Chromosomal Abnormalities

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17
Q

Asymmetric IUGR

A

(Head-sparing) – Undernourishment and Placental Insufficiency most commonly

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18
Q

Maternal factors causing IUGR

A 
Chronic Maternal Disease (HTN, CVS, CKD), Substance Abuse, Smoking,
Autoimmune Disease (Increasing APLS), Poor Nutrition and Socioeconomic Factors
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19
Q

Placental Insufficiency causing IUGR

A

Abnormal Trophoblast Invasion (Pre-Eclampsia and Accreta), Infarction, Abruption, Praevia, Chorioangiomas, Abnormal Cord/Insertion

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20
Q

Foetal factors causing IUGR

A

Genetics (Aneuploidy), Congenital Abnormalities (Cardiac, Gastroschisis), Congenital Infections (CMV, Rubella, Toxo), Multiple Pregnancies

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21
Q

Management of IUGR

A
  • 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
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22
Q

Effects of poor glycaemic control

A

leads to increased

Foetal and Neonatal Morbidity and Mortality

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23
Q

How many pregnancies does diabetes affect?

A

Established Diabetes affects 1 – 2% of pregnancies;

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24
Q

Which pregnancy hormones are diabetogenic?

A

Many pregnancy hormones (HPL, Cortisol, Glucagon, Oestrogen and Progesterone) are
Diabetogenic; Insulin requirements also increased throughout and peak at term

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25
Q

Effects of hyperglycaemia

A

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

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26
Q

How does pregnancy affect diabetes?

A

Ketoacidosis, Retinopathy (two-fold risk), Nephropathy

(Renal function and proteinuria may worsen in pregnancy), Ischaemia Heart Disease

27
Q

Antenatal Management

A

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

28
Q

Diabetes and Labour: Delivery

A

• 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

29
Q

Diabetes and Labour: Glycaemic Control

A

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

30
Q

Diabetes and Labour: Breastfeeding

A

Encourage Breastfeeding post-delivery; Metformin and Insulin safe to use
o Neonate requires early feeding and glucose monitoring

31
Q

Diabetes and Labour: Post Partum

A

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

32
Q

Who is screened for GDM?

A

BMI>30
Previous Macrosomia pregnancy
Previous GDM
First-degree FH DM, Ethnicity (South Asia, Afro Caribbean, Middle East)

33
Q

Diagnosis of GDM

A

Diagnosis based on OGTT at 26 – 28/40;

Should be repeated at 34/40 if concerns

34
Q

Management of GDM

A

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

35
Q

Causes of thyrotoxicosis

A

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

36
Q

When can a thyroid storm occur?

A

Can occur in poorly controlled Thyroid disease with Infective, Labour or
Operative stressors; Pyrexia, Confusion, Cardiac Failure

37
Q

Neonatal Thyrotoxicosis

A

10% of maternal Grave’s (past or current Hx) due to

Transplacental TSHR stimulating Antibodies

38
Q

Managing women with Grave’s

A

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

39
Q

How often in hypothyroidism in pregnancy

A

Most diagnosed prior to pregnancy; New diagnosis in pregnancy is rare

40
Q

Causes of hypothyroidism

A

Hashimoto (Anti TPO), Atrophic Thyroiditis (TSH blocking), Iatrogenic, Rarely pituitary

41
Q

Implications of hypothyroidism

A

Severe disease associated with Miscarriage, Pre-Eclampsia and Low Birthweight

42
Q

Management of Hypothyroidism

A

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

43
Q

Blood Pressure in Pregnancy

A

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

44
Q

How should BP be monitored in pregnancy

A

BP should be measured sitting, or supine with Left-tilt, with upper arm at level of heart; Automated BP monitors might under-record BP

45
Q

Chronic Hypertension

A

– Increased risk of developing Pre-Eclampsia; Look for secondary
causes if BP is very high
o Secondary Causes – Renal, Cardiac, Endocrine diseases

46
Q

HTN Treatment

A

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

47
Q

Pregnancy Induced Hypertension

A

=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

48
Q

Post Partum Hypertension

A

Can either be Physiological, Pre-existing Chronic HTN, or New-onset Pre-Eclampsia; BP peaks on third to fifth day post-partum

49
Q

Symptoms of post partum hypertension

A

Epigastric pain, Visual disturbance, New-onset Proteinuria suggestive of Post-Partum Pre-Eclampsia

50
Q

Post natal management of post partum HTN

A

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

51
Q

Pre-eclampsia

A

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%

52
Q

Risk factors for Pre eclampsia

A

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

53
Q

Diagnosis of Pre-eclampsia

A

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

54
Q

Prevention of Pre-eclampsia

A

Aspirin (75mg PO OD) before 16/40; reduce repeat severe pre-eclampsia by 20%

55
Q

Presentation of Pre-eclampsia

A

May present as Headache, Visual Disturbance, Epigastric/RUQ pain, N+V, Facial Oedema, although they might only occur in severe disease

56
Q

Investigations of Pre-eclampsia

A

• 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

57
Q

Management of Pre-eclampsia

A

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

58
Q

Complications of Pre-Eclampsia

A

Severe Complications include Eclampsia, HELLP, Cerebral Haemorrhage, IUGR, Foetal Compromise, Renal Failure and Placental Abruption

59
Q

Severe Pre-eclampsia

A

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

60
Q

Indications for Immediate Delivery

A

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)

61
Q

Management of Severe Pre-eclampsia

A

• 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

62
Q

Eclampsia

A

=Tonic-Clonic Seizure associated with Pre-Eclampsia; Antenatal (38%), Intrapartumv (18%) or Postpartum (44%); Most die from Blood loss, Intracranial Haemorrhage or HELLP

63
Q

Management of Eclampsia

A

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

64
Q

HELLP

A

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

Obstetrics (18 decks)

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