Pregnancy complications 2 Flashcards by Sophie C

Types of disorders (3)

Hypertensive disorders
Thrombosis
Diabetes

How well did you know this?

Not at all

Perfectly

Hypertensive disorders in pregnancy - chronic hypertension

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

How well did you know this?

Not at all

Perfectly

Values for hypertension , mild moderate and severe

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

How well did you know this?

Not at all

Perfectly

Hypertensive disorders in pregnancy - what is gestational hypertension, when does it develop?

Gestational hypertension (PIH – pregnancy induced hypertension)

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

How well did you know this?

Not at all

Perfectly

Pre eclampsia is defined as?

they will have a headache - describe features

protein in urine level is greater than?

New hypertension > 20 weeks in association with
significant proteinuria

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)
Pathophysiology

How well did you know this?

Not at all

Perfectly

Significant Proteinuria - reagent strip

Automated reagent strip urine protein estimation > 1+

How well did you know this?

Not at all

Perfectly

Significant Proteinuria- Spot Urinary Protein

Creatinine Ratio > 30 mg/mmol

How well did you know this?

Not at all

Perfectly

24 hour urine protein collection - significant score

> 300mg/ day

How well did you know this?

Not at all

Perfectly

Essential/ Chronic hypertension

more common in?
patients should have?

older patients ie older mothers

- pre-pregnancy care

How well did you know this?

Not at all

Perfectly

Change of antihypertensive drugs should be changed if indicated - how should you do this ?

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

How well did you know this?

Not at all

Perfectly

Where should you aim to keep blood pressure?

what should you monitor for?

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

How well did you know this?

Not at all

Perfectly

Pathophysiology of PET

- why does this happen (2)

Immunological
- Genetic predisposition
secondary invasion of maternal spiral arterioles by trophoblasts
impaired  reduced placental perfusion
imbalance between vasodilators / vasoconstrictors in pregnancy
(prostocyclin / thromboxane

How well did you know this?

Not at all

Perfectly

Risk factors for developing PET (lots to choose from )

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

How well did you know this?

Not at all

Perfectly

PET is multi organ - systems affected are?

renal, liver, vascular, cerebral, pulmonary

How well did you know this?

Not at all

Perfectly

Complications of PET? MATERNAL (6)

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

How well did you know this?

Not at all

Perfectly

Severe PET - SYMPTOM SIGNS

– 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)

How well did you know this?

Not at all

Perfectly

Biochemical abnormalities in PET? (2)

raised liver enzymes, bilirubin if HELLP present

- raised urea and creatinine, raised urate

Haematological abnormalities (3)

low platelets
low haemoglobin, signs of haemolysis
features of DIC

management for PET

FETAL INESTIGATIONS (2)

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)

Conservative management of PET

anti-hypertensives (labetolol, methyldopa, nifedipine)

- steroids for fetal lung maturity if gestation < 36wks

PET & Eclampsia

5-8% of pregnant women have PET
0.5% women have severe PET & 0.05% have eclamptic seizures
38% of seizures occur antepartum, 18% intrapartum, 44% postpartum

Treatment of seizures/ impending seizures for PET ?

Magnesium sulphate bolus + IV infusion

Control of blood pressure – IV labetolol, hydrallazine (if > 160/110)

Avoid fluid overload – aim for 80mls/hour fluid intake

Diabetes and pregnancy

What is gestational diabetes

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

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

Pre-existing diabetes and pregnancy - what requirements of the mother increase?

what has anti-insulin action?

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 when? what does it cause? what is more likely post delivery?

- 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

Effects of diabetes on mother, fetus & neonate - what are increased risks and give examples?

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

Complications (contd) - for mother and fetes/neonate (4)

- increased risk of pre-eclampsia - Worsening of maternal nephropathy, retinopathy, hypoglycaemia, - reduced awareness of hypoglycaemia Infections neonatal - Impaired lung maturity, neonatal hypoglycemia, jaundice

Management - preconception - diabetes - glycemic controls should be what values?

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

During pregnancy - diabetes - insulin requirements will increase to?

``` 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 ```

to get tighter glucose control you may change? what may you give?

can continueoral anti-diabetic agents (metformin) but may need to change to insulin glucagon injections/ conc. glucose solution to reduce risk of hypoglycaemia - watch for ketonuria

when will repeat retinal assessments be given

28 and 34 weeks

Management continured- diabetes - how will you help prevent macrsomia?

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

Risk factors for GDM / consider screening for GDM

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 type 1 or 2

GDM is associated with?

GDM associated with some increase in maternal complications (eg PET) and fetal complications (macrosomia) but much less than type 1 or 2

Screening for GDM?

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

Management of GDM | - pre and post delivery

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

The risk of thrombo-embolism increased in pregnancy - it is a hypercoaguable state to protect mother against bleeding - what changes occur? (5)

- 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

Increased risks with? (TE and DVT) (11)

- 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

VTE prophylaxis in pregnancy (3)

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

Signs/ symptoms of VTE (

- pain in calf, increased girth of affected leg, calf muscle tenderness - breathlessness, pain on - breathing, cough, tachycardia, hypoxic, pleural rub, etc

Investigate appropriately if any suspicion of VTE? treatment

- ECG, Blood gases, doppler V/Q (ventilation perfusion) lung scan CTPA computed tomography pulmonary angiogram) Appropriate treatment with anticoagulation if VTE confirmed