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Year 3 - Repro and Anaesthetics > Complications in Pregnancy 2 > Flashcards

Complications in Pregnancy 2 Flashcards

1
Q

pregnancy complciaitons in this lecture:

hypertensive disorders

thrombosis

diabetes

A
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2
Q

Hypertensive disorders in pregnancy:

what is chronic hypertension?

A

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

Mild HT – Diastolic BP 90-99, Systolic BP 140-49

Moderate HT - Diastolic BP 100-109, Systolic BP 150-159

Severe HT - Diastolic BP ≥110, Systolic BP ≥ 160

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3
Q

hypertensive disorder sin pregnancy:

what is gestational hypertension

A

(PIH – pregnancy induced hypertension)

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

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4
Q

hypertensive disorder sin pregnancy:

what is pre-eclampsia

A

New hypertension > 20 weeks in association with significant proteinuria

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5
Q

what is classed 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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6
Q

essential/chronic hypertension is common in who

A

older mothers

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7
Q

what is the management of essential/chronic hypertension?

A

Ideally patients should have pre-pregnancy care

Change anti-hypertensive drugs if indicated: eg. - 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 (beta blocker), nifedipine (CCB), methyldopa)

Monitor for superimposed pre-eclampsia

Monitor fetal growth

May have a higher incidence of placental abruption

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8
Q

what is pre-eclampsia (PET)

A
  • Mild HT on two occasions more than 4 hours apart
  • Moderate to severe HT

+ proteinuria of more than 300 mgms/ 24 hours (protein urine > + protein:creatinine ratio > 30mgms/mmol)

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9
Q

what is the pathophysiology of pre-eclampsia?

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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10
Q

what are the risk factrors for developing PET?

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:

  • chronic hypertension
  • pre-existing renal disease
  • pre-existing diabetes
  • autoimmune disorders like – eg. antiphospholipid antibodies, SLE
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11
Q

pre-ecclampdia is a ___________ multi-organ disorder

A

multisystem

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12
Q

what are maternal complications of pre-eclampsia?

A
  • eclampsia - seizures
  • severe hypertension – cerebral haemorrhage, stroke
  • HELLP (hemolysis, elevated liver enzymes, low platelets)
  • DIC (disseminated intravascular coagulation)
  • renal failure
  • pulmonary odema, cardiac failure
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13
Q

what are foetal complciations of pre-eclampsia?

A
  • impaired placental perfusion → IUGR (intrauterine growth restriction), fetal distress, prematurity, increased PN mortality
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14
Q

what are the symptoms/signs of severe PET?

A

– headache, blurring of vision, epigastric pain, pain below ribs, vomiting, sudden swelling of hands face legs

  • Severe Hypertension; > 3+ of urine proteinuria
  • clonus / brisk reflexes ; papillodema, epigastric tenderness
  • reducing urine output
  • convulsions (Eclampsia)
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15
Q

what are biochemical abnormalities in severe PET?

A

raised liver enzymes, bilirubin if HELLP present

raised urea and creatinine, raised urate

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16
Q

what are haematologicla abnoralities in severe PET?

A

low platelets

low haemoglobin, signs of haemolysis

features of DIC

17
Q

what is the managemnt of pre-eclampsia?

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)

18
Q

what is the only cure of PET?

A

delivery of baby and placenta

19
Q

what is the consevrativ emanagement of PET?

A

(aim for fetal maturity)

  • close observation of clinical signs & investigations
  • anti-hypertensives (labetolol, methyldopa, nifedipine)
  • steroids for fetal lung maturity if gestation <36wks

Consider induction of labour / CS if maternal or fetal condition deteriorates, irrespective of gestation

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

20
Q

what is the treatment of seizures?

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

21
Q

what si the prophylaxis for PET in future pregnancies?

A

Low dose Aspirin from 12 weeks till delivery

Women with PET at a higher risk to develop hypertension in later life

22
Q

what are types of diabetes to happen in pregnancy?

A

Pre-existing diabetes (type I & less often type II)

Gestational diabetes

23
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
24
Q

what happens to the insulin requirement of pre-existing diabetes in pregnancies?

A

increases

due to human placental lactogen, progesterone, human chorionic gonadotrophin, and cortisol from the placenta have anti-insulin action

25
Q

Fetal hyper-insulinemia occurs - how does this hhapen and what is its effects?

A

Maternal glucose crosses the placenta and induces increased insulin production in the fetus. The fetal hyperinsulinemia causes macrosomia (large baby)

Post delivery – more risk of neonatal hypoglycaemia, increased risk of respiratory distress

26
Q

what are the Effects of diabetes on mother, fetus & neonate?

A

Fetal congenital abnormalities e.g – cardiac abnormalities, sacral agenesis (especially if blood sugars high peri-conception)

  • Miscarriage
  • Fetal macrosomia, polyhydramnios (increased fluid around baby)
  • Operative delivery, shoulder dystocia
  • Stillbirth, increased perinatal mortality
27
Q

pregnancy complicated with diabetes may also suffer what complications?

A

increased risk of pre-eclampsia

Worsening of maternal nephropathy, retinopathy, hypoglycaemia, reduced awareness of hypoglycaemia

Infections

neonatal - Impaired lung maturity, neonatal hypoglycemia, jaundice

28
Q

what is the managemnt of diabetes pre-conception?

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
29
Q

what is the management of diabetes during pregnancy?

A
  • optimise glucose control – insulin requirements will increase

< 5.3 mmol/l - Fasting

< 7.8 mmol/l - 1 hour postprandial

< 6.4 mmol/l - 2 hours postprandial

< 6 mmol/l – before bedtime

  • Could continue oral anti-diabetic agents
    (metformin) but may need to change to insulin for tighter glucose control
  • should be aware of the risk of hypoglycemia - provide glucagon injections/ conc. glucose solution
  • watch for ketonuria/ infections
  • repeat retinal assessments 28 and 34 weeks
  • watch fetal growth

Management (contd)

  • observe for PET
  • labour usually induced 38-40 weeks, earlier if fetal or maternal concerns
  • consider elective caesarean section if significant fetal macrosomia
  • maintain blood sugar in labour with insulin – dextrose insulin infusion
  • continuous CTG fetal monitoring in labour
  • Early feeding of baby to reduce neonatal hypoglycemia
  • Can go back to pre-pregnancy regimen of insulin post delivery
30
Q

gestational diabetes mellitus:

What aere the Risk factors for GDM / consider screening for 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

GDM associated with some increase in maternal complications (eg PET) and fetal complications (macrosomia) but much less than with type I or II diabetes

31
Q

what is the screening for GDM?

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

32
Q

what is the management of GDM?

A

essentially making sure blood levels are normal

control blood sugars – diet, metformin/ insulin if sugars remain high

Post delivery – check OGTT 6 to 8 weeks PN

Yearly check on HbA1C/ blood sugars as at a higher risk of developing overt diabetes

33
Q

venous thrombo-embolism:

pregnancy is an example of what that may lead to this?

A
34
Q

Risk of thrombo-embolism increased in pregnancy:

why is this?

A

Risk of thrombo-embolism increased in pregnancy

  • 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
  • Increased stasis – progesterone, effects of enlarging uterus
  • May be vascular damage at delivery/ caesearean section
35
Q

there is increased risk of thrombo-embolism in women who….

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

36
Q

what is the prophylaxis for VTE 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

37
Q

what are the signs/symptoms of VTE?

A

VTE - pain in calf, increased girth of affected leg, calf muscle tenderness

Pulmonary embolism - breathlessness, pain on breathing, cough, tachycardia, hypoxic, pleural rub, etc

38
Q

Investigate appropriately if any suspicion of VTE

how is this done?

A

ECG, Blood gases, doppler

V/Q (ventilation perfusion) lung scan

CTPA (computed tomography pulmonary angiogram)

39
Q

Appropriate treatment with ___________ if VTE confirmed

A

anticoagulation

Year 3 - Repro and Anaesthetics (50 decks)

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