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Women's Health - Year 4 > Maternal Medicine > Flashcards

Maternal Medicine Flashcards

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1
Q

PRE-ECLAMPSIA / ECLAMPSIA

description

A
  • After 20 weeks gestation
  • Reduced organ perfusion, vasospasm, endothelial activation
  • Characterised by hypertension and proteinuria
  • If untreated, convulsions can occur
  • Severe cases may include hemolysis, elevated liver enzymes and low platelet counts (HELLP syndrome) in 20% of severe pre-eclampsia
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2
Q

PRE-ECLAMPSIA/ ECLAMPSIA

prevalence

A
  • 5-8% of births
  • 18% of maternal deaths
  • Hypertensive disease occurs in 12-22% of pregnancies
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3
Q

PRE-ECLAMPSIA/ ECLAMPSIA

risk factors

A
  • Prior history
  • BMI >32.3
  • African-american
  • Nulliparity
  • Older than 35
  • Younger than 18
  • Multi-fetal pregnancy
  • Fetal hydrops
  • Hydatidiform mole
  • Thrombophilia
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4
Q

PRE-ECLAMPSIA / ECLAMPSIA

signs and symptoms

A
  • Hypertension without proteinuria or oedema = gestational hypertension
  • Hypertension with proteinuria or oedema = preeclampsia
  • Hypertension with proteinuria or oedema and headache, abdominal pain, weight gain, visual disturbances, thrombocytopenia, oliguria, hemoconcentration, pulmonary oedema, proteinuria
  • Hypertension, proteinuria or oedema and seuzires = eclampsia
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5
Q

PRE-ECLAMPSIA / ECLAMPSIA

differentials

A
  • Chronic hypertension
  • Transient hypertension
  • Chronic renal disease
  • Acute or chronic glomerulonephritis
  • Coarctation of the aorta
  • Cushing’s disease
  • Systemic lupus erythematosus
  • Periarteritis nodosa
  • Obesity
  • Epilepsy
  • Encephalitis
  • Cerebral aneurysm or tumour
  • Lupuscerebritis
  • Hysteria
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6
Q

PRE-ECLAMPSIA / ECLAMPSIA

investigations

A
  • Liver and renal function studies
  • Ultrasound to monitor foetal growth
  • Assess fetal lung maturation
  • Blood pressure, urinalysis
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7
Q

PRE-ECLAMPSIA

non pharmacological management

A
  • Frequent prenatal visits, increased fetal surveillance, hospitalisation
  • Only true treatment is delivery
  • Bed rest with severe conditions
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8
Q

PRE-ECLAMPSIA

pharmacological management

A
  • Glucocorticoids – fetal lung maturation
  • Labetalol or nifedipine
  • Magnesium sulfate – IV during labour to stabilise BP /reduce seizure risk
  • IV hydralazine – lower BP during labour
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9
Q

ECLAMPSIA

management

A
  • Keep woman alive during fit, prevent more fits, deliver the baby
  • Magnesium sulphate reduces incidence and severity of fits
  • During fit: turn woman on side, maintain airway, stop fit with iv diazepam and magnesium sulphate
  • After the fit: prevent further fits by magnesium sulphate or diazepam infusion, lower BP with hydralazine, labetalol, magnesium sulphate, deliver aby
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10
Q

PRE-ECLAMPSIA/ ECLAMPSIA

outcome

A
  • Improve after delivery but seizures can occur upto 10 days after delivery (unommon after 48 hours)
  • Eclampsia: 25% of women with eclampsia have a fit before labour, they can be twitching (30secs) tonic phase (30secs), clonic phase (2 mins), coma (10-30mins) which can repeat frequently
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11
Q

PRE-ECLAMPSIA/ ECLAMPSIA

complications (maternal and foetal)

A

Maternal

  • Cardiac decompensation
  • Stroke
  • Pulmonary oedema
  • Respiratory failure
  • Renal ailure
  • Seizures
  • Intracranial haemorrhage
  • Coma
  • Death (0.5-5% mortality)

Fetal
- Growth restriction and death

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12
Q

HYPERTENSIVE DISORDERS OF PREGNANCY

risks for mother

A
  • Cerebrovascular accident.
  • Renal failure
  • Heart failure.
  • Coagulation failure.
  • Liver failure.
  • Adrenal failure.
  • Eclampsia
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13
Q

HYPERTENSIVE DISORDERS OF PREGNANCY

risks for foetus

A
  • Asymmetrical intrauterine growth restriction.
  • Placental abruption.
  • Iatrogenic preterm delivery.
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14
Q

PREGNANCY INDUCED HYPERTENSION

A

hypertension occurring for the first time after 20 weeks’ gestation.

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15
Q

HYPERTENSION IN PREGNANCY definition

A
  • Blood pressure of 140/90mmHg on two occasions more than 4 hours apart.
  • A rise of more than 30mmHg in systolic blood pressure over the booking blood pressure.
  • A rise of more than 15 mmHg in diastolic blood pressure over the booking figure.
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16
Q

GESTATIONAL HYPERTENSION

classification

A
  • Mild: a blood pressure up to 140/100mmHg without proteinuria.
  • Moderate: a blood pressure up to 160/110 mmHg without proteinuria. In the absence of pro- teinuria PIH is rarely dangerous to mother or fetus.
  • Severe: a blood pressure of more than 160/ 110 mmHg; and the presence of proteinuria (pre-eclampsia/pre-eclamptic toxaemia (PET)).
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17
Q

PROTEINURIA IN PREGNANCY

definition

A
  • More than 300mg on a 24-hour collection of urine.
  • Oedema associated with hypertension and proteinuria is a sign of worsening pre-eclampsia. Oedema alone is of little significance.
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18
Q

HYPERTENSION IN PREGNANCY

prevelence

A
  • 10-15% of primigravid women some form of hypertension
  • 6% considered to have gestational diabetes
  • 2% develop pre-eclampsia
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19
Q

PRE-ECLAMPSIA

aetiology

A
  • Women who develop pre-eclampsia have a failure of the second wave of trophoblastic invasion.
  • This failure probably leads to a local alteration of the prostacyclin : thromboxane ratio. Both these prostaglandins are produced by trophoblast and exert opposite effects. In gestational diabetes, the balance of the ratio appears to favour thromboxane. This leads to local vasoconstriction and platelet agglutination on already undilated vessels.
  • The combination of the above two factors is associated with failure of the initial fall in peripheral resistance and hence blood pressure in mid- pregnancy is maintained —it normally shows a marked fall. Subsequent narrowing or clotting of the abnormal blood vessels leads to a further increase in peripheral resistance and hence hypertension.
  • The narrowing of the blood vessels also leads to decreased perfusion of the intervillous space and hence the development of an asymmetrical small for gestational age (SGA) fetus.
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20
Q

PRE-ECLAMPSIA -how can prevelance be reduced

A

Antioxidants (vitamin C and E) in pregnancy have been shown to reduce the prevalence of pre-eclampsia in women who are at high risk— previous early onset of gestational diabetes, women with antiphospholipid syndrome.

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21
Q

clinical course of hypertensive disorders of pregnancy

A
  • Gestational diabetes usually presents in primigravidae in late third trimester
  • Usually no treatment or anti-hypertensive therapy
  • Occasionally develops into pre-eclampsia
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22
Q 
HYPERTENSIVE DISORDERS OF PREGNANCY
mild
1. symptoms
2. BP
3. proteinuri
4. reflexes
5.fundi
6. renal
7.bloods
A
  1. none
  2. <140/100
  3. none
  4. normal
  5. normal
  6. normal
  7. normal
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23
Q 
HYPERTENSIVE DISORDERS OF PREGNANCY
moderate
1. symptoms
2. BP
3. proteinuri
4. reflexes
5.fundi
6. renal
7.bloods
8. treatment
A
  1. mild headache, oedema
  2. <160/110
  3. none
  4. normal
  5. nomal
  6. normal
  7. normal FBC, urate raised, LFT normal, clotting normal, foetus normal/SGA
  8. anti-hypertensives, ? delivery
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24
Q 
HYPERTENSIVE DISORDERS OF PREGNANCY
moderate
1. symptoms
2. BP
3. proteinuri
4. reflexes
5.fundi
6. renal
7.bloods
8. treatment
A
  1. frontal headache, oedema, visual disturbance
  2. > 160/110
  3. ++
  4. hyperreflexia
  5. papilloedema
  6. decreased urinary output
  7. HB up or down, decreased platelet, increased urate, LFT, prolonged clotting
  8. anti-hypertensives, anti-epiletics, MgSO4, delivery
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25
Q

TERATOGEN

A
  • An agent which when administered to the pregnancy woman directly or indirectly causes structural or functional abnormalities in the foetus or in the child after birth
  • May not be apparent until later in life
  • Infections, physical agents/chemicals, medicines, alcohol, tobacco, cocaine
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26
Q

CONGENITAL MALFORMATIONS

A
  • 2-3% in normal young fit healthy mothers
  • Factors that increase the risk: Age, poor obstetric history, poor health, drugs, infections such as rubella
  • Causes: genetic, chromosomal aberration, radiation, infection, maternal metabolic disorder, drugs and chemicals (4-6%)
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27
Q

CRITERIA FOR HUMAN TERATOGENS

A
  • Defect associated with drug in a sufficient number of cases
  • Distinctive pattern of defects
  • Correlation with an animal model at equivalent doses
  • Known teratogenic mechanism
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28
Q

EFFECTS OF TERATOGENS

A
  • Chromosomal abnormalities
  • Impairment of implantation of the conceptus-this mechanism is sometimes used in contraception
  • Resorption or abortion of the early embryo
  • Structural malformations
  • Intrauterine growth retardation
  • Foetal death
  • Functional impairment in the neonate eg deathness
  • Behavioural abnormalities
  • Mental retardation
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29
Q

what is teratogenicity

A

The property or capability of producing congenital malformations

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30
Q

effect of tobacco on the foetus

A

Can cause vasoconstriction, hypoxia, CO poisoning leading to problems in foetal development and death

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31
Q

effect of cocaine on foetus

A

Causes vasoconstriction and hypoxia, bad for maternal health

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32
Q

what is behavioural teratology

A

Affect on the behaviour or functional adaptation of the offspring to its environment

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33
Q

what is transplacental carcinogeniticty

A
  • No adverse effects on mother but cancer in offspring

- Eg diethylstilboestrol (DES) causes rare vaginal cancer

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34
Q

what are mutogenicity effects

A
  • Germ cells-sex cells eg reduced fertility with each new generation and eventually infertility
  • Somatic cell-all other body cells eg induction of cancer
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35
Q

mechanisms of teratogens

A
  • May be beneficial or harmless to the mother but harmful or lethal to the embryo or foetus
  • Time of exposure is critically important
  • Susceptibility to some teratogens is genetically determined
  • Teratogenicity is usually dose dependent
  • Teratogenic agents may be synergistic
  • A specific placental barrier does not exist
  • Risk may be altered by individual variation in drug pharmacokinetic metabolism
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36
Q
  1. anacephaly
  2. syndactyly
  3. hypospadias
A
  1. brain and skull don’t develop
  2. fused fingers, webbing of skins or bones fused
  3. opening of urethra not at end of penis
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37
Q

what malformation would be produced with exposure to teratogen at the following days post conception

  1. 24
  2. 12-40
  3. 34
A
  1. anencephaly
  2. limb reduction
  3. transposition of great vessels
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38
Q

what malformation would be produced with exposure to teratogen at the following days post conception

  1. 36
  2. 42
  3. 84
A
  1. cleft lip
  2. ventricular septal defects, syndactyly
  3. hypospasias
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39
Q

FOETAL ALCOHOL SYNDROME

A
  • Behavioural tetralogy
  • Heavy alcohol intake in pregnant women
  • Regular drinking or binge drinking
  • 45ml alcohol/day=FAS in 2.2/1000 live births
  • Often goes unnoticed as facial features are not always that obvious
  • Attention span and lower academic ability often only noted at school
  • Difficult to establish alcohol as the cause as there are many other contributory factors, strong behavioural link
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40
Q

FOETAL ALCOHOL SYNDROME

what advice is given to pregnant women regarding alcohol intake

A
  • Vague
  • No advisory body in England and Wales gives a clear recommendation to abstain from alcohol
  • Safety approach is not to drink at all al during pregnancy, although drinking small amounts of alcohol after three months of pregnancy (not more than one or two units, no more than once or twice a week) does not appear to harmful
  • department of health advice on alcohol: If pregnant or planning to get pregnant avoid alcohol altogether
  • NICE advice on alcohol use in pregnancy: Avoid alcohol in the first three months
  • What both DoH and NICE say about alcohol use in pregnancy: If you opt to have a drink you should stick to no more than one or two units of alcohol once or twice a week to minimise the risk to the baby
  • royal collage of gynaecologists advice regarding drinking in pregnancy: The safest approach is not to drink at all during pregnancy, although drinking small amounts of alcohol after three months of pregnancy (not more than one or two units, not more than once or twice a week) does not appear to be harmful
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41
Q

SEX STEROIDS AND CONTRACEPTIVE AGENTS

A
  • Oral contraceptives and progestins administered in the first trimester have been blamed for a variety of birth defects, but studies have not confirmed any teratogenic risk for these drugs
  • Meta analysis of first trimester sex hormone exposure reveals no association between exposure and foetal genital malformations
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42
Q

ANDROGENIC STEROIDS

A
  • Androgens may masculinise a developing female foetus
  • Progestational agents, most often the synthetic testosterone derivatives, may cause clitoromegaly and labial fusion if administered before 13 weeks of pregnancy
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43
Q

SPERMICIDES

A
  • Reported increased risk for abnormal offspring in mothers who has used spermicides for contraception has not been confirmed
  • Exposed women had 23 infants with abnormalities (5%) compared with 4.5% in the nonexposed controls, which is not a significant difference
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44
Q

FIRST TRIMESTER DRUGS WITH FETOTOXIC EFFECTS

A
  • Androgens: virilisation of female fetus
  • Oestrogens: feminisation of male fetus
  • Warfarin: nasal hypoplasia, skeletal defects
  • Retinoids: craniofacial, cardiovascular and CNS defects
  • Diethylstilboestrol: uterine lesions, transplacental carcinogen
  • Antiepileptics: facial defects, mental retardation, neural tube defects
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45
Q

DOSE RESPONSE CURVE

A
  • Exposure to teratogens follows a toxicological dose-response curve
  • The small increments in dose can show large increase in effects eg methotrexate (cancer drug) generally be around 7.5mg, above this causes foetal toxicity
  • Not only is the dose important, but also the route of exposure-topical, oral, parenteral
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46
Q

DRUG SYNERGY IN PREGNANCY

A
  • Risk factors may not only additive but potentially synergistic
  • Teratogenicity of a drug may be enhanced by co-administration of a second drug, or even by concomitant exposure to environmental chemicals

Multiple anticonvulsant therapy

  • 1 drug-4% abnormalities
  • 2 drug-6% abnormalities
  • 3 drug -11% abnormalities
  • 4 drug-11% abnormalities
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47
Q

PLACENTAL TRANSFER OF DRUGS

A
  • May occur by passive diffusion, facilitated diffusion or active transport
  • Passive diffusion is increased by high lipid solubility, low protein binding, high maternal blood level of drug
  • Transfer through ‘pores’ of the chorionic membrane, usually by electrolytes and chemicals of very low molecular weight
  • Active transport via enzyme systems or protein carries may also account for the transfer of some drugs
  • Most drugs (mw<1000) cross the placenta freely
  • Large molecular weight drugs (mw>10000) do not cross the placenta eg heparin, insulins, ions, dextran
  • Molecular weight of most drugs ranges between 250-400 so when drugs are prescribed transfer to foetus is inevitable
48
Q

PHARMACOKINETIC CHANGES IN PREGNANCY

A
  • maternal metabolism (can alter through pregnancy),
  • maternal excretion (increased renal blood flow, leads to increase I the elimination rate of renally excreted drugs (eg lithium may require an increased dose,
  • volume of distribution,
  • body water
  • liver metabolism
  • lung function
49
Q

INFLUENCES ON DRUG TRANSFER IN PREGNANCY

A
  • Mothers blood concentration-most important determinant
  • Molecular weight
  • Lipid solubility
  • Ionisation
  • Protein binding
  • Chemical structure
50
Q

WHAT DRUG CAN AFFECT THE FOETUS WITHOUT CROSSING THE PLACENTA

A

Insulin does not cross the placenta yet the glucose produced during episodes of maternal hyperglycaemia may pass across causing the foetus to produce insulin that cannot be cleared

51
Q

how can you assess risks to the foetus with drugs

A
  • Stage of pregnancy
  • Drug/chemical exposure
  • Clinical condition of the mother/patient
  • Previous obstetric history-family history of malformations, history of recurrent abortions
52
Q

principles of prescribing in pregnancy

A
  • Only give drug when necessary-risk vs benefit
  • Lowest effective dose for shortest possible time
  • Consider stage of pregnancy
  • Avoid all drug treatment in first trimester if possible
  • Avoid new drugs
  • Avoid poly-pharmacy
53
Q

treating pain in pregnancy

A
  • Non-pharmacological-implemented before drug therapy is considered
  • Paracetamol-main drug of choice throughout pregnancy
  • Codeine-when paracetamol alone not achieved
  • NSAID-usually ibuprofen for inflammatory pain before 28/40, should not be given after as causes premature closure of ductus arteriosus (backflow of blood in heart)
  • Tramadol
  • Amitriptyline-tricyclic antidepressant
  • Opiates-oramorph or buprenorphine, neonatal withdrawal may be experienced with prolonged or late use-risk of neonatal respiratory depression
54
Q

treating vomiting in pregnancy

A
  • management-small, high carbohydrate, low fat, frequent meals
  • 1st-cyclizine or promethazine
  • 2nd-prochlorperazine /metoclopramide
  • Treatment resistant symptoms-ondansetron
55
Q

treatment constipation in pregnancy

A
  • Increase fibre
  • Increase fluids
  • Increase exercise
  • Bulk forming laxatives
  • Lactulose
  • Glycerine suppositories
  • Bisacodyl
  • Senna
  • Docusate sodium-low doses
56
Q

antibiotic use in pregnancy

A
  • Penicilins and cephalosporins
  • Erythromycin and clindamycin
  • Nitrofurantoin, trimethoprim and co-trimozazole-If strongly indicated only if no folate deficiency
  • Azithromycin, clarithromycin, metronidazole, ciprofloxacin and sodium fusidate/fusidic acid-less information but acceptable to use if necessary
  • Quinolones, tetracyclines (avoid after 15 weeks gestation) and telithromycin-no information and may pose a risk of harm to the developing baby but may occasionally be the best choice in an individual case
57
Q

name some teratogenic drugs/condition

A 
ACE inhibitors
alcohol
aminoglycosides
carbamazapine
chloamphenicol
cocaine
diethylstilbesterol
lithium
maternal diabetes mellitus
smoking
tetracyclines
thalidomide
valproate
warfarin
58
Q

teratogenic effects of ACE inhibitors

A

renal dysgenesis

craniofacial abnormalities

59
Q

teratogenic effects of alcohol

A

craniofacial abnormalities

60
Q

teratogenic effects of

aminoglycosides

A

ototoxicity

61
Q

teratogenic effects of carbamazepine

A

neural tube defects

craniofacial abnormalities

62
Q

teratogenic effects of cocoaine

A

intrauterine growth retardation

preterm labour

63
Q

teratogenic effects of diehtylstilbesterol

A

vaginal clear cell adenocarcinoma

64
Q

teratogenic effects of lithium

A

ebstein’s anomaly (atrialized right ventricle)

65
Q

teratogenic effects of maternal diabetes mellitus?

A 
macrosomia
neural tube defects 
polyhydramnios
preterm labour
caudal regression syndrome
66
Q

teratogenic effects of smoking

A

preterm labour

intrauterine growth retardation

67
Q

teratogenic effects of tetracyclines

A

discoloured teeth

68
Q

teratogenic effects of thalidomide

A

limb reduction defects

69
Q

teratogenic effects of valproate

A

neural tube defects

craniofacial abnormalities

70
Q

teratogenic effects of warfarin

A

craniofacial abnormalities

71
Q

EPILEPSY IN PREGNANCY

seizure frequency

A

Seizure frequency: increase in 37%, decrease in 13% and remain unchanged in 50%

72
Q

EPILEPSY IN PREGNANCY

what are the risks to the fetus

A
  • Increase risk of fetal demise with status epilepticus

- 2-5% increased risk of major congenital anomalies mainly due to medications, multiple drugs has higher risk

73
Q

EPILEPSY IN PREGNANCY

medication

A
  • Change in anticonvulsant medications should be changed before pregnancy, once pregnancy diagnosed don’t change medications as teratogenic risk exposure has already occurred
  • folic acid 5mg
74
Q

EPILEPSY IN PREGNANCY

anticonvulsant fetal risks

A

teratogenicity, neonatal withdrawal, vitamin K deficiency causing haemorrhagic disease of newborn, developmental delay, behavioural problems

75
Q

EPILEPSY IN PREGNANCY

pre pregnancy counselling

A

counselling involving neurologist, optimise treatment, least number of drugs at lowest dose, consider stopping drugs if 2 yrs seizure free, folic acid 5mg 12 weeks pre conception

76
Q

EPILEPSY IN PREGNANCY

antenatal care

A

don’t change medication, prenatal screening including alpha fetoprotein and detalied anomaly scan, consider fetal echo at 22-24 weeks, consider vit K 10mg/day last 4 weeks

77
Q

EPILEPSY IN PREGNANCY

intrapartum

A

aim for vaginal delivery, increased risk of seizures, seizure control with benzodiazepines, ensure meds taken at right time

78
Q

EPILEPSY IN PREGNANCY

postnatal care

A

neonatal vit K, breast feeding not contraindicated

79
Q

CEREBROVASCULAR ACCIDENT IN PREGNANCY

A
  • Rare but increased risk in post partum period(9 fold for infarcts and 28 fold for haemorrhagic stroke
  • Subarachnoid haemorrhage: arteriovenous malformations due to oestrogen causing dilatation
80
Q

CARDIAC DISEASE IN PREGNANCY

antenatal management

A

MDT, preconception counselling to modify meds, optimise CVD status, discuss risks. Ability to tolerate pregnancy depends on NYHA class, presence of pulmonary hypertension or left heart obstruction or cyanosis. Decide if termination recommended, correct factors that may lead to decompensation such as anaemia, infection, hypertension and arrythmias. Monitor for signs of heart failure, monitor fetal growth

81
Q

CARDIAC DISEASE IN PREGNANCY

intrapartum and postpartum management

A

aim for vaginal delivery, in labour maternal cardiac monitoring may be required, avoid aortocaval compression, decide on endocarditis prophylaxis, active management of 3rd stage to reduce blood loss, epidural may reduce heart rate and BP changes associated with pain, strict fluid balance, contraception discussion

82
Q

CARDIAC DISEASE IN PREGNANCY

high risk

A

pulmonary hypertension, aortic dissection, complicated aortic coarctation, marfans syndrome, MI

83
Q

CARDIAC DISEASE IN PREGNANCY

moderate risk

A

mitral stenosis NYHA class 3 or 4, severe aortic stenosis, mechanical heart valves

84
Q

CARDIAC DISEASE IN PREGNANCY

minimal risk

A

ASD, VSD, PDA, corrected tetralogy of fallot, tissue valve prosthesis, pulmonary and tricuspid valve disease, mild mitral stenosis, arrythmias

85
Q

ARTIFICIAL HEART VALVES

risks in pregnancy

A
  • Near normal cardiac function and therefore tolerate pregnancy well
  • Main risk is anticoagulation, warfarin is better for mother yet heparin is better for fetus
86
Q

ARTIFICIAL HEART VALVES

use of LMWH and warfarin

A
  • LMWH: less maternal bleeding, no risk to fetus, increased risk of embolic events, increased risk of valve thrombosis, osteoporosis
  • Warfarin: increased risk of miscarriage, warfarin embryopathy, maternal and neonatal bleeding, long half life
87
Q

ARTIFICIAL HEART VALVES

management

A
  • Antenatally; continue warfarin, INR of 3, conceive on warfarin change to LMWH from 6-12 weeks, then warfarin from 12-37 weeks
  • Warfarin: high risk of bleeding in labour so change to LMWH at 37 weeks stop during labour and start after delivery, start warfarin 7-10 days post partum
  • Reversal in event of life threatening bleeding. Warfarin = fresh frozen plasma, vit K, prothrombin complex concentrates. LMWH = protamine sulphate
  • Warfarin and heparin safe to breast feeding mothers
  • Low dose aspirin should be given with LMWH
88
Q

MITRAL STENOSIS

risks in pregnancy

A

Increased risk of pulmonary oedema in pregnancy, greatest in labour: increase in heart rate in pregnancy, decrease in ventricular filling time, and increased pulmonary blood volume leading to pulmonary oedema
risk of thromboembolism 1.5% in pregnancy, treat with LMWH

89
Q

MITRAL STENOSIS

management

A
  • first line treatment for pulmonary oedema in pregnancy should be diuretics. β-blockers also used to slow heart rate and improve left atrial emptying (add digoxin if in atrial fibrillation (AF)
  • most likely lesion to require treatment for pulmonary oedema, heart failure or surgery in pregnancy
  • if severe consider surgery prior to surgery
90
Q

PULMONARY HYPERTENSION AND EISENMENGERS SYNDROME

eisenmengers syndrome

A

In Eisenmenger’s syndrome there is pulmonary hypertension with reversal of the initial left-to-right shunt and consequent cyanosis. There is a fixed high pulmonary vascular resistance and inability to increase pulmonary blood flow. This leads to slowly worsening hypoxaemia.

91
Q

PULMONARY HYPERTENSION AND EISENMENGERS SYNDROME

mortality

A
  • High maternal mortality, usually first few days post partum
  • Women should be advised to avoid getting pregnant and termination offered if pregnancy occurs.
92
Q

PULMONARY HYPERTENSION AND EISENMENGERS SYNDROME

where should the pregnancy be managed

A

Pregnancy should be managed in a pulmonary hypertension centre with multidisciplinary care from cardiologists, obstetricians, and anaesthetists.

93
Q

PULMONARY HYPERTENSION AND EISENMENGERS SYNDROME

antenatal care

A
  • anticoagulation, oxygen, bed rest, and serial assessment of fetal growth.
  • Avoid manoevures that suddenly increase vagal tone (with resultant bradycardia) and venous return, e.g. ergometrine.
  • Avoid PGF2α which is associated with pulmonary vasoconstriction and pulmonary hypertensive crisis.
94
Q

PULMONARY HYPERTENSION AND EISENMENGERS SYNDROME

intrapartum

A
  • Delivery should be in a high dependency unit with tight control of blood pressure, fluid balance, and oxygen saturations.
  • Mode of delivery and epidural use are controversial.
95
Q

MI in pregnnacy

A
  • Increasing due to increased age at pregnancy and lifestyle factors
  • High mortality
96
Q

PERIPARTUM CARDIOMYOPATHY

A
  • Rare
  • Occurs between 32 weeks and 6 months after delivery
  • Mortality 25-50% and high recurrence in future pregnnacies
97
Q

MARFANS SYNDROME

A
  • Risk of aortic dissection and rupture

- Aim for vaginal delivery with short second stage

98
Q

COARCTATION OF AORTA

A
  • Usually corrected before pregnancy
  • Main risk is aortic dissection
  • Avoid balloon angioplasty in pregnancy
  • Deliver via c-section if associated with aortic dilatation
99
Q

FALLOTS TETRALOGY

A
  • Main risks are paradoxical emboli causing stroke and cyanosis leading increased risk of miscarriage
  • Minimise risk with anticoagulation
100
Q

IRON DEFICIENCY ANAEMIA

  1. diagnosis
  2. treatment
A
  1. most common cause of anaemia in pregnancy (90% of cases). Diagnosis: decreased MCV, MCHC, and ferritin. Often asymptomatic and detected on screening.
  2. Treat by oral iron supplementation: vitamin C (orange juice) increased absorption, tea decreased absorption.
    Parenteral iron should be considered in those who do not tolerate the oral preparations (corrects the anaemia more rapidly).
    The expected improvement in haemoglobin is 71g/dL/wk.
    In situations such as multiple pregnancy or known depletion of iron stores, consider prophylactic supplementation even if no anaemia.
101
Q

SEVERE IRON DEFICIENCY ANAEMIA

A
  • If severe iron-deficiency anaemia (Hb <7g/dL) is diagnosed near term, blood transfusion may be considered.
  • Vomiting in pregnancy can affect absorption of iro
  • Increased demands of iron in pregnancy particularly if multiple pregnancies, grand multiparity, pregnancies close together
  • Increased diet intake, oral iron with vitamin C , if no improvement IV or IM.
  • If severe admit to hospital, if after 36 weeks transfuse prior to labour
102
Q

FOLATE DEFICIENCY

risk factors

A
  • common in pregnancy (5% of cases of anaemia).
  • Risk factors: poor nutritional status, haematological problems with a rapid turnover of blood cells, e.g. haemolytic anaemia and haemoglobinopathies, drug interaction with folate metabolism, e.g. antiepileptics.
103
Q

FOLATE DEFICIENCY

diagnosis

A

increased MCV, decreased serum, and decreased red cell folate.

104
Q

FOLATE DEFICIENCY

folate use in pregnancy

A
  • Folic acid given preconception and in early pregnancy to reduce risk of
  • neural tube defects (400 micrograms/day for general population).
  • Women with high risk of neural tube defects should take 5mg folic acid daily. The high-risk group includes those women: on anticonvulsants, with a previous child affected with a neural tube defect, with demonstrated deficiency, with diabetes, with a BMI >35, with sickle cell disease.
105
Q

VITAMIN B12 DEFICIENCY

A
  • Occurs in pernicious anaemia, terminal ileum disease, and strict vegans.
  • It is uncommon to make a new diagnosis in pregnancy.
  • Women with a previous diagnosis should continue treatment throughout pregnancy.
106
Q

SICKLE CELL DISEASE

A
  • Crises are more common during pregnancy.
  • increased risk of pre-eclampsia, increased risk of delivery by CS secondary to fetal distress.
  • Counselling and screening
  • Consider thromboprophylaxis
  • Regular assessment of fetal growth
  • Treat crisis with analgesia, oxygen, rehydration, antibiotics
  • Folic acid 5mg/day
  • Risks: miscarriage, IUGR, prematurity, stillbirth
107
Q

HYPERTENSION IN PREGNANCY

risks in mother

A

cerebrovascular accident, renal failure, heart failure, coagulation failure, liver failure, adrenal failure, eclampsia

108
Q

HYPERTENSION IN PREGNANCY

risk in fetus

A

asymmetrical intrauterine growth restriction, placental abruption, iatrogenic preterm delivery

109
Q

HYPERTENSION IN PREGNANCY

pregnancy induced hypertension

A
  • occurring after 20 weeks, BP over 140/90 on 2 occasions, rise over 30 systolic over booking blood pressure, rise over 15 diastolic over booking BP
  • It can be mild (upto 140/100, no proteinuria), moderate (upto160/110 without proteinuria), severe (BP more than 160/110 with proteinuria)
  • Mild: discharged and assessed as outpatients, monitor BP twice a week and fetal growth fortnightly by ultrasound
  • Moderate: monitor in day assessment uniti or hospital. BP-oral methyldopa, nifedipine or labetalol. Assess renal function, fetal ultrasound
110
Q

PREGNANCY INDUCED HYPERTENSION

aetiology

A
  • failure of second wave of trophoblastic invasion causing local alteration of prostacyclin: thromboxane ratio causing local vasoconstriction and platelet agglutination on undiluted vessels. This is associated with failure of initial fall in peripheral resistance so BP in mid pregnancy is maintained, further narrowing or clotting leads to further increase in peripheral resistance and hypertension and also causes decreased perfusion of intervillous space so asymmetrical small for gestational age
  • Can develop to pre-eclampsia
111
Q

HEART DISEASE

cardiac complications in pregnancy

A
  • Mitral stenosis: pulmonary oedema, right sided congestive failure
  • Aortic stenosis: left sided congestive failure, rare to start de novo in pregnancy
  • Eisenmenger’s syndrome: risk of cardiac failure
  • Coarctation of aorta: risk of rupture in late pregnancy
  • Artificial valves: thrombosis
112
Q

HEART DISEASE

management

A
  • Diagnose early, assess severity early
  • ECG, CXR, echo, catheter studies, 24hr ECG
  • Book hospital delivery, extra rest at home, anticoagulation, labour plan with cardiologist, anaesthetist and obstetrician
  • In labour: good analgesia, head up, antibiotics, short second stage, syntometrine only if high risk postpartum haeorrhae, manage pulmonary oedema if it occurs
  • In puerperium: rest, physiotherapy to legs
  • Mortality: 9% maternal deaths due to heart disease
  • Morbidity: increased risk of deterioration of heart condition
  • Fetal prognosis: little increased risk if mother kept healthy
113
Q

ASTHMA

A
  • Emotional factors are involved, so asthma may worsen if pregnancy is resented
  • Be careful of new therapies as may be teratogenic so used well established drugs such as bronchial antispasmodics, antibiotics, steroids
  • Asthmatics don’t tend to deteriorate in pregnancy but may in puerperium
  • In labour: deliver so mothers respiratory effort is minimal, may require antispasmodics, if on steroids hydrocortisone needed to cover labour, babies can be small for date if asthma control was poor
114
Q

DIABETES

glucose homeostasis in pregnancy

A
  • Normally fasting glucose 4-5mmol/l
  • To maintain glucose levels there is doubling secretion of insulin in second and third trimester of pregnancy
  • Pregnancy represents a relatively insulin resistant state due to placental secretion of oestrogen, progestogen and human placental lactogen and change in peripheral insulin receptors
  • Glucoe crosses placenta by facilitated diffusion resulting in fetal glucose of 1mmol/l less than mother, this system is saturated at maternal levels of 11-12mmol/l so the fetus is never subject to levels greater than 11mmol/l
115
Q

DIABETES

established diabetes mellitus

A
  • 1-2% of pregnant population
  • Insulin requirements increase and rapidly fall after delivery, it aggravates proliferative diabetic retinopathy, those with diabetic nephropathy are more likely to develop pre-eclampsia and poor renal function during pregnancy
  • Associated with increased risk of first trimester miscarriage, second trimester miscarriages. Congenital abnormalities increased such as multiple malformations and cauda regression
  • Pregnancy induced hypertension, preterm delivery, polyhydramnios, macrosomic infants, sudden intrauterine death in last 4 weeks, perinatal mortality x2-3
  • Effects on infancts: macrosomia, shoulder dystocia, asphyxia in delivery, respiratory distress syndrome, hypoglycaemia, hypercalcaemia, hypothermia, hyperbilirubinaemia
116
Q

DIABETES

management

A
  • Good control prior to conception and first weeks decreases abnormalities and miscarriage
  • Pre-pregnancy care: all diabetics should take contraception until ready for pregnancy, pre-pregnancy counselling, twice daily insulin minimum for pregnancy, long acting insulin at night and short acting at meals, self monitor blood sugar
  • Pregnancy: joint clinic with diabetic physician and obstetrician. Aim to maintain normoglycaemia may cause hypoglycaemic attacks but not harmful to fetus (fetal death rate with hyperglycaemic coma is 25%), seen fortnightly, at home management, each antenatal visit should check diabetic record, BP, symptoms of infection, fetal growth. Insulin requirements increased during pregnancy
  • Ultrasound: 7 weeks (confirm fetal life), 16-20 weeks (structural abnormalities), 22-24 weeks (cardiac abnormalities), insulin depndent diabetes not indication to perform karyotyping, monthly fetal growth and amniotic fluid volume monitored
  • Delivery: allow spontaneous labour but induce soon after EDD, IV insulin and iv glucose, check blood glucose every hour (4-10mmol/l), epidural encouraged, accelerate labour with syntocinon if reading more than 2 hours to right of partogram, senior obstetrician should be present, C-section rate higher due to failed induction, fetal distressm macrosomia, abnormal lie
  • Care of baby: paediatrician should be present; resusciton, dry and warm, help prick for glucose at 30mins, 1 hour, 4 hours, 8 hours, 12 hours and 24 hours, feed early with glucose, examine for congenital abnormalities, serum bilirubin on 2nd day
117
Q

GESTATIONAL DIABETES

A
  • Onset of diabetes for first time during pregnancy
  • Not associated with congenital abnormalities
  • Main effects are; development of polyhydramnios, increase in preterm labour, production of macrosomia
  • Screen with glucose tolerance test in high risk women, oral glucose load and blood sugar estimation 2 hours later, random blood sugar at 28 weeks 2 hours after meal
  • Treatment: home monitoring, fasting and 1 hour blood sugar after each meal on 2 days a week, no treatment If fasting blood sugar level is <5.5mmol/l and postprandial figures are <9mmol/l. if higher levels woman should start carbohydrate restriced diet, blood sugars tested twice a week and test for ketones, if diet restriction not successful twice daily insulin regime needed. If ketosis relax diet and start insulin, ultrasouns for fetal growth and amniotic fluid volume. If no evidence of excessive fetal growth spontaneous labour can be awaited upto 42 weeks. Macrosomia induced at term. Control blood sugar in labor, when placenta delivered insulin requirements disappear. 40% chance of becoming diabetic in long term, doubling if woman is obese, usually recurs in future pregnancies

Women's Health - Year 4 (15 decks)

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