Complications in Pregnancy 2 Flashcards

1
Q

What is mild hypertension?

A
  • Diastolic BP 90-99

* Systolic BP 140-49

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2
Q

What is moderate hypertension?

A
  • Diastolic BP 100-109

* Systolic BP 150-159

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3
Q

What is severe hypertension?

A
  • Diastolic BP ≥110

* Systolic BP ≥ 160

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4
Q

What is classified as chronic hypertension?

A

Hypertension either pre-pregnancy or at booking (≤ 20 weeks gestation)

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5
Q

What is gestational hypertension (pregnancy-induced hypertension)?

A

BP as above but new hypertension (develops after 20 weeks)

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6
Q

What is pre-eclampsia??

A

New hypertension > 20 weeks in association with significant proteinuria

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7
Q

What is classified as significant proteinuria?

A
  • Automated reagent strip urine protein estimation > 1+
  • Spot Urinary Protein: Creatinine Ratio > 30 mg/mmol
  • 24 hours urine protein collection > 300mg/ day
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8
Q

How is chronic hypertension managed in pregnancy?

A

•Ideally patients should have pre-pregnancy care
•Change anti-hypertensive drugs if indicated e.g.:
- ACE inhibitors (eg. Ramipril / Enalopril cause birth defects impaired growth)
- Angiotensin receptor blockers (eg losartan, Candesartan)
- anti diuretics
- lower dietary sodium
•Aim to keep BP < 150/100 (labetolol, nifedipine, methyldopa)
•Monitor for superimposed pre-eclampsia
•Monitor fetal growth
•May have a higher incidence of placental abruption

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9
Q

What is the definition of pre-eclampsia?

A
  • Mild HT on two occasions more than 4 hours apart
  • Moderate to severe
    • proteinuria of more than 300 mgms/ 24 hours
  • Protein urine > and protein:creatinine ratio > 30mgms/mmol
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10
Q

What is the pathophysiology of pre-eclampisa?

A
  • Immunological
  • Genetic predisposition
  • Secondary invasion of maternal spiral arterioles by trophoblasts impaired -> reduced placental perfusion
  • Imbalance between vasodilators/vasoconstrictors in pregnancy (prostocyclin/thromboxane)
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11
Q

What are the risk factors for developing pre-eclampsia toxaemia?

A
  • First pregnancy
  • Extremes of maternal age
  • Pre-eclampsia in a previous pregnancy (esp. severe PET, delivery <34 weeks, IUGR baby, IUD, abruption)
  • Pregnancy interval >10 years
  • BMI > 35
  • Family history of PET
  • Multiple pregnancy
  • Underlying medical disorders
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12
Q

What are the underlying medical disorders which increase risk of PET?

A
  • Chronic hypertension
  • Pre-existing medical conditions
  • Pre-existing diabetes
  • Autoimmune disorders - antiphospholipid antibodies, SLE
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13
Q

Which systems can pre-eclampsia involve?

A
  • Renal
  • Liver
  • Vascular
  • Cerebral
  • Pulmonary
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14
Q

What are the possible complications of pre-eclampsia for the mother?

A
  • Eclampsia - seizures
  • Severe hypertension - cerebral haemorrhage, stroke
  • HELLP (haemolysis, elevated liver enzymes, low platelets)
  • DIC (disseminated intravascular coagulation)
  • Renal failure
  • Pulmonary oedema, cardiac failure
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15
Q

What are the possible complications of pre-eclampsia for the foetus?

A

•Impaired placental perfusion → IUGR, fetal distress, prematurity, increased PN mortality

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16
Q

What are the symptoms of severe PET?

A
  • Headache
  • Blurring of vision
  • Epigastric pain
  • Pain below ribs
  • Vomiting
  • Sudden swelling of hands, face and legs
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17
Q

What are the clinal signs of severe PET?

A
  • Severe Hypertension - > 3+ of urine proteinuria
  • clonus/brisk reflexes
  • Papillodema
  • Epigastric tenderness
  • Reducing urine output
  • Convulsions (Eclampsia)
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18
Q

What are the biochemical abnormalities in PET?

A
  • Raised liver enzymes, bilirubin if HELLP present

* Raised urea and creatinine, raised urate

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19
Q

What are the haematological abnormalities in PET?

A
  • Low platelets
  • Low haemoglobin, signs of haemolysis
  • Features of DIC (disseminated intravascular coagulation)
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20
Q

How is pre-eclampsia monitored?

A
  • Frequent BP checks
  • Urine protein
  • Check symptomatology – headaches, epigastric pain, visual disturbances
  • Check for hyper-reflexia (clonus)
  • Tenderness over the liver
  • Blood investigations – Full Blood Count (for hemolysis, platelets)
  • Liver Function Tests
  • Renal Function Tests – serum urea, creatinine, urate
  • Coagulation tests if indicated
  • Fetal investigations - scan for growth, cardiotocography (CTG)
21
Q

What is the only cure for PET?

A

Delivery of the baby

22
Q

What is the conservative (aiming for foetal maturity) management of pre-eclampsia?

A
  • Close observation of clinical signs & investigations
  • Anti-hypertensives (labetolol, methyldopa, nifedipine)
  • Steroids for foetal lung maturity if gestation < 36wks
23
Q

What should be considered if maternal or foetal condition deteriorates?

A
  • CS

* Induced labour

24
Q

Does PET monitoring end at birth?

A

Risks of PET may persist into the puerperium therefore monitoring must be continued post delivery

25
Q

When are seizures likely to occur in pre-eclampsia?

A
  • 38% of seizures occur antepartum
  • 18% intrapartum
  • 44% postpartum
26
Q

How are seizures/impending seizures treated in pre-eclampsia?

A
  • Magnesium sulphate bolus + IV infusion
  • Control of blood pressure – IV labetolol, hydrallazine (if > 160/110)
  • Avoid fluid overload – aim for 80mls/hour fluid intake
27
Q

What prophylaxis is used if PET in subsequent pregnancy?

A
  • Low dose aspirin from 12 weeks until delivery

* Women with PET are at higher risk to develop HT in later life

28
Q

What is gestational diabetes?

A
  • Carbohydrate intolerance with onset (or first recognised) in pregnancy
  • Abnormal glucose tolerance that reverts to normal after delivery
  • However, more at risk of developing type II diabetes later in life
29
Q

How does pre-existing diabetes management change in pregnancy?

A

•Insulin requirements of the mother increase
˙•Human placental lactogen, progesterone, human chorionic gonadotrophin and cortisol from the placenta have anti-insulin action

30
Q

How does pre-existing diabetes affect the foetus?

A
  • Maternal glucose crosses the placenta and induces increased insulin production in the foetus
  • The fetal hyperinsulinemia causes macrosomia
31
Q

What are the postnatal risks caused by pre-existing diabetes in pregnancy?

A
  • More risk of neonatal hypoglycaemia

* Increased risk of respiratory distress

32
Q

What are the possible effects of diabetes on the foetus and neonate?

A
  • Foetal congenital abnormalities e.g – cardiac abnormalities, sacral agenesis (especially if blood sugars high peri-conception)
  • Miscarriage
  • Fetal macrosomia, polyhydramnios
  • Operative delivery
  • Shoulder dystocia
  • Stillbirth
  • Increased perinatal mortality
  • Impaired lung maturity
  • Neonatal hypoglycemia
  • Jaundice
33
Q

What are the possible effects of diabetes on the mother?

A
  • Increased risk of pre-eclampsia
  • Worsening of maternal nephropathy, retinopathy, hypoglycaemia
  • Reduced awareness of hypoglycaemia
  • Infections
34
Q

What is the pre-natal management in diabetic mothers hoping to conceive?

A
  • Better glycemic control
  • Ideally, blood sugars should be around 4 – 7 mmol/l pre-conception and HbA1c < 6.5% ( < 48 mmol/mol)
  • Folic acid 5mg
  • Dietary advice
  • Retinal and renal assessment
35
Q

How is diabetes managed in pregnant mothers?

A
  • Optimise glucose control - insulin requirements will increase
  • Can continue oral diabetic treatment (metformin) but may need to change to insulin for tighter control
  • Should be aware of the risk of hypoglycaemia - provide glucagon injections/concentrated glucose solution
  • Watch for ketonuria/infections
  • Repeat retinal assessments - 28 and 34 weeks
  • Watch foetal growth
36
Q

How is diabetes managed perinatally in pregnant mothers?

A
  • Observe for PET
  • Labour usually induced 38-40 weeks - maybe earlier if cause for concern
  • Consider ECS - macrosomia
  • Maintain blood sugar level wit insulin in labour - dextrose insulin infusion
  • Continuous CTG foetal monitoring in labour
  • Early feeding - to prevent neonatal hypoglycaemia
  • Can revert to pre-pregnancy management regime postnatally
37
Q

What are the risk factors associated with gestational diabetes mellitus (GDM)?

A
  • Increased BMI >30
  • Previous macrosomic baby > 4.5kg
  • Previous GDM
  • Family history of diabetes
  • Women from high risk groups for developing diabetes – eg. •Asian origin
  • Polyhydramnios or big baby in current pregnancy
  • Recurrent glycosuria in current pregnancy
38
Q

Of TI & TIIDM and GDM, which is more dangerous?

A

TI & TIIDM

39
Q

How is GDM screened for?

A

•If risk factor present, offer HbA1C estimation at booking

  • if > 6% (43 mmol/mol), 75gms OGTT to be done
  • if OGTT normal, repeat OGTT at 24 -28 weeks

•Can also offer OGTT at around 16 weeks and repeat at 28 weeks if significant risk factors (eg. Previous GDM) present

40
Q

How is GDM managed?

A
  • Control blood sugar with diet
  • Use metformin/insulin if blood sugars remain high
  • Post-deliver - check OGTT 6-8 weeks PN
  • Yearly check on HbA1C/ blood sugars as at a higher risk of developing overt diabetes
41
Q

What comprises Virchow’s Triad?

A
  • Stasis
  • Vessel wall injury
  • Hypercoagulbility
42
Q

What causes hypercoagubility in pregnancy?

A

•Pregnancy a hypercoagulable state (to protect mother against bleeding post delivery)

  • Increase in fibrinogen, factor VIII, VW factor, platelets
  • Decrease in natural anticoagulants – antithrombin III
  • Increase in fibrinolysis
43
Q

What causes increased stasis in pregnancy?

A
  • Progesterone

* Effects of enlarging uterus

44
Q

What may be a cause of vascular damage in pregnancy?

A
  • Delivery

* CS

45
Q

What are the risk factor for venous thromboembolism in pregnancy?

A
  • Older mothers, increasing parity
  • Increased BMI
  • Smokers
  • IV drug users
  • PET
  • Dehydration – hyperemesis
  • Decreased mobility
  • Infections
  • Operative delivery
  • Prolonged labour
  • Haemorrhage, blood loss > 2 l
  • Previous VTE (not explained by other predisposing eg. fractures, injury)
  • Those with thrombophilia (protein C, protein S, Anti thrombin III deficiencies, etc)
  • Strong family history of VTE
  • Sickle cell disease
46
Q

What VTE prophylaxis in pregnancy?

A
  • TED stockings
  • Advice increased mobility, hydration
  • Prophylactic anti-coagulation with 3 or more risk factors (may be indicated even with one risk factor if significant risk), may need to continue 6 weeks postpartum
47
Q

What are the signs and symptoms of VTE?

A
  • Pain in calf
  • Increased girth of affected leg
  • Calf muscle tenderness
  • Breathlessness
  • Pain on breathing
  • Cough
  • Tachycardia
  • Hypoxic
  • Pleural rub, etc
48
Q

What are the investigations for a suspected VTE?

A
  • ECG
  • Blood gases
  • Doppler
  • V/Q scan
  • CTPA
49
Q

How is a VTE managed?

A

Appropriate anticoagulation