Complications in Pregnancy 2 Flashcards

1
Q

mild hypertensive disorder cut off

A

Diastolic BP 90-99, Systolic BP 140-49

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2
Q

moderate hypertensive disorder cut off

A

Diastolic BP 100-109, Systolic BP 150-159

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3
Q

severe hypertensive disorder cut off

A

Diastolic BP ≥110, Systolic BP ≥ 160

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4
Q

chronic hypertension definition

A

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

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5
Q

gestational hypertension

A

new hypertension in pregnancy usually develops after 20 weeks

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6
Q

pre-eclampsia hypertension

A

New hypertension > 20 weeks in association with significant proteinuria

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7
Q

significant proteinuria cut off

A

Spot Urinary Protein: Creatinine Ratio > 30 mg/mmol

24 hours urine protein collection > 300mg/ day

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8
Q

management plan for 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, nifedipine, methyldopa)

Monitor for superimposed pre-eclampsia
Monitor fetal growth
May have a higher incidence of placental abruption

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9
Q

definition of preeclampsia

A

-Hypertension on two occasions more than 4 hours apart
+ proteinuria of more than 300 mgs/ 24 hours (protein urine > + protein:creatinine ratio > 30mgms/mmol)

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10
Q

pathophysiology of pre-eclampsia

A

affects 2-8% pregnancies, underlying pathophysiology is poorly understood

Complex + multifactorial (Immunological / Genetic predisposition) – abnormal placentation + maternal microvascular disease

  • impaired secondary invasion of maternal spiral arterioles by trophoblasts → reduced placental perfusion – placental ischaemia
  • low level chronic inflammation – endothelial damage
  • imbalance between angiogenic (PlGF)and antiangiogenic (sFlt-1)factors in pregnancy -FMS like tyrosine kinase inhibits neovascularisation and in pregnancy with preeclampsia PlGF is lower
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11
Q

what are risk factors 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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12
Q

is preeclampsia a multi system disorder

A

yes

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13
Q

maternal complications 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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14
Q

fetal complications pre-eclampsia

A
  • impaired placental perfusion → IUGR, fetal distress, prematurity, increased PN mortality
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15
Q

symptoms and signs of severe pre eclampsia

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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16
Q

biochemical abnormalities of pre-eclampsia

A

raised liver enzymes, bilirubin if HELLP present

raised urea and creatinine, raised urate

17
Q

haematological abnormalities of pre-eclampsia

A

low platelets
low haemoglobin, signs of haemolysis
features of DIC

18
Q

management of preeclampsia in pregnant women

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)

19
Q

what is the only cure for pre-eclampsia

A

Only ‘cure’ for PET is delivery of the baby and placenta

20
Q

conservative management pre-eclampsia

A

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

21
Q

treatment of seizures / impending 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

22
Q

Prophylaxis for PET in subsequent pregnancy

A

Low dose Aspirin from 12 weeks till delivery

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

23
Q

preexisting diabetes effect of pregnancy

A

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

Fetal hyper-insulinemia occurs
Maternal glucose crosses the placenta and induces increased insulin
production in the fetus. The fetal hyperinsulinemia causes macrosomia

Post delivery – more risk of neonatal hypoglycaemia
                         increased risk of respiratory distress
24
Q

effects of diabetes on mother, foetus and neonate

A

increased risk of

Fetal 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

increased risk of pre-eclampsia
Worsening of maternal nephropathy, retinopathy, hypoglycaemia,
reduced awareness of hypoglycaemia
Infections

neonatal -  Impaired lung maturity, neonatal hypoglycemia, jaundice
25
Q

management 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

26
Q

management 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
27
Q

management diabetes later into pregnancy and labour

A

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

28
Q

Risk factors for GDM / when to 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

29
Q

screening offered 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

30
Q

how is gestational diabetes managed

A

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

31
Q

why is the risk of thrombo-embolism greater 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 
        - decrease in fibrinolysis

Increased stasis – progesterone, effects of enlarging uterus

May be vascular damage at delivery/ caesearean section

32
Q

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

33
Q

what are 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

34
Q

what investigations should be done for VTE

A

ECG, Blood gases, doppler
V/Q (ventilation perfusion) lung scan

CTPA
computed tomography pulmonary angiogram)

Appropriate treatment with anticoagulation
if VTE confirmed