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Yr4: Obstetrics & Gynaecology > Obstetrics: Antenatal Care- Complications 2 > Flashcards

Obstetrics: Antenatal Care- Complications 2 Flashcards

1
Q

What usually happens to BP during pregnancy?

A
  • Falls in first trimester (particularly diastolic) & continues to fall until 20-24 weeks
  • After 20-24 weeks BP usually increases to pre-pregnancy levels by term
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2
Q

Define the following:

  • Chronic hypertension
  • Pregnancy-induced hypertension/gestational hypertension
A
  • Chronic hypertension: high BP that exists before 20 weeks gestation and is long standing
  • Pregnancy-induced hypertension/gestational hypertension: hypertension occurring after 20 weeks gestation without proteinuria
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3
Q

Define pre-eclampsia

A

Pregnancy induced hypertension/new hypertension in pregnancy with end-organ dysfunction that occurs after 20 weeks gestation when spiral arteries of placenta from abnormally leading to high vascular resistance in these vessels

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4
Q

When during pregnancy does pre-eclampsia occur?

A

After 20 weeks gestation

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5
Q

Describe the pathophysiology of pre-eclampsia

A
  • When blastocyst implants on endometrium the outermost layer, called the syncytiotrophoblast, grows into the endometrium and forms finger like projections called chorionic villi; the chorionic villi contain fetal blood vessels
  • Trophoblast invasion of the endometrium sends signals to spiral arteries in that area of endometrium causing them to reduce their vascular resistance (making them more fragile)
  • Blood flow to spiral arteries increases and eventually they break down leaving pools of blood called lacunae; maternal blood flows into these lacunae and then to fetus via uterine veins. Lacunae form at ~20 weeks gestation
  • If spiral arteries vascular resistance remains high then lacunae formation will be inadequate
  • Leads to poor perfusion placenta → oxidative stress in placenta
  • Placenta releases proinflammatory chemicals into systemic circulation
  • Leads to systemic inflammation (and so vasoconstriction) and impaired endothelial function
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6
Q

Risk factors for pre-eclampsia can be grouped into high-risk and moderate risk. State some risk factors for pre-eclampsia in each category

A

High-risk factors:

  • Pre-existing hypertension
  • Previous hypertension in pregnancy (including gestational hypertension, pre-eclampsia or eclampsia)
  • Existing autoimmune conditions (e.g. systemic lupus erythematosus, antiphospholipid syndrome)
  • Diabetes (T1DM or T2DM)
  • Chronic kidney disease

Moderate-risk factors:

  • Older than 40
  • BMI > 35
  • More than 10 years since previous pregnancy
  • Multiple pregnancy
  • First pregnancy
  • Family history of pre-eclampsia
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7
Q

What is the triad of features in pre-eclampsia?

A
  • Hypertension
  • Proteinuria
  • Oedema
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8
Q

Pre-eclampsia has symptoms because of the complications; state some potential symptoms of pre-eclampsia

A
  • Headache
  • Visual disturbance or blurriness
  • Nausea and vomiting
  • Upper abdominal or epigastric pain (this is due to liver swelling)
  • Oedema
  • Reduced urine output
  • Hyperreflexia
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9
Q

Discuss how pre-eclampsia is diagnosed

A

Diagnosis can be made if:

  • Hypertension defined as systolic BP >140mmHg or diastolic BP >90mmHg PLUS ANY OF:
    • Proteinuria (1+ or more on dipstick)
    • Organ dysfunction (e.g. raised creatine, elevated liver enzymes, thrombocytopenia, haemolytic anaemia)
    • Placental dysfunction (e.g. fetal growth restriction, abnormal doppler studies)

.

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10
Q

If woman has proteinuria 1+ on dipstick you should do further quantitative tests of proteinuria. What tests can be done and what is classed as significant proteinuria?

A
  • Urine protein:creatinine ratio of at least 30 mg/mmol
  • OR urine albumin:creatinine ratio of at least 8 mg/mmol

*****Proteinuria of at least [1+] on dipstick testing should prompt one of these additional tests

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11
Q

Discuss the NICE guidance surrounding placental growth factor (PIGF) testing

A

The NICE guidelines (2019) recommend the use of placental growth factor (PlGF) testing on one occasion during pregnancy in women suspected of having pre-eclampsia. Placental growth factor is a protein released by the placenta that functions to stimulate the development of new blood vessels. In pre-eclampsia, the levels of PlGF are low. NICE recommends using PlGF between 20 and 35 weeks gestation to rule-out pre-eclampsia.

*Copied from ZtoF

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12
Q

In the UK pre-eclampsia is classified as mild, moderate or severe; outline this classification

A

Features of severe pre-eclampsia

  • hypertension: typically > 160/110 mmHg and proteinuria as above
  • proteinuria: dipstick ++/+++
  • headache
  • visual disturbance
  • papilloedema
  • RUQ/epigastric pain
  • hyperreflexia
  • platelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome
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13
Q

All pregnant women are routinely monitored for pre-eclampsia at every antenatal appointment; what is involved in this monitoring?

A
  • BP
  • Urine dipstick for proteinuria
  • Asking about symptoms
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14
Q

Discuss who is given pre-eclampsia prophylaxis and what they are given as prophylaxis

A

Prophylaxis with aspirin 75mg-150mg daily from 12 weeks gestation until birth in women with:

  • One high risk factor
  • Two or more moderate risk factors
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15
Q

Discuss the management of gestational hypertension (remember, that is new hypertension in pregnancy without proteinuria)

A
  • Antihypertensive aiming for BP of <135/85mmHg
    • 1st line= labetolol
    • 2nd line= nifedipine
    • 3rd line= methyldopa
  • BP monitoring 1-2 times weekly
  • Monitor for end organ dysfunction
    • Weekly urine dipstick testing
    • Weekly blood tests (FBC, LFTs, U&Es)
  • Additional ultrasound scans to monitor fetal growth (every 2-4 weeks)
  • PIGF testing on one occasion
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16
Q

Management of pre-eclampsia can be categorised into general and medical management; discuss the general management of pre-eclampsia

A

***NOTE: similar to management of gestational hypertension with few key differences

General

  • Scoring systems used to determine whether to admit (fullPIERS or PREP-S)
  • BP monitoring at least every 48hrs
  • Monitor for end organ dysfunction
    • Frequency depends on severity but multiple weekly blood tests e.g. 2-3 (FBC, LFTs, U&Es)
    • **NOTE: dipstick not routine as diagnosis already made
  • Additional ultrasound scans to monitor fetal growth (every 2 weeks)

Medical/pharmacological

  • Antihypertensive aiming for BP of <135/85mmHg
    • 1st line= labetalol
    • 2nd line= nifedipine
    • 3rd line= methyldopa
    • IV hydralazine may be used in critical care in severe pre-eclampsia or eclampsia
  • Magnesium sulphate may also be given prophylactically in severe pre-eclampsia
  • Additional measures surrounding labour:
    • IV magnesium sulphate given during labour & 24hrs afterwards to prevent seizures
    • Fluid restriction may be used in labour in severe pre-eclampsia or eclampsia to avoid fluid overload
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17
Q

Planned early birth may be necessary in pre-eclampsia if the blood pressure cannot be controlled or complications occur; true or false?

A

True

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18
Q

When should pre-eclampsia resolve?

A

Should return to normal over time following delivery of the placenta

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19
Q

What BP monitoring is required following delivery in mother with pre-eclampsia?

A
  • Must monitor mother for at least 24hrs post-partum as still at risk of seizures
  • Monitor BP daily for first 2 days post-partum and then at least once 3-5 days post-partum
  • Need for antihypertensive should then be assessed
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20
Q

What pharmacological treatment do NICE recommend for hypertension during the post-natal period?

A

For medical treatment, NICE recommend after delivery switching to one or a combination of:

  • First line options:
    • Enalapril (first line if wishing to breastfeed)
    • Nifedipine or amlodipine (consider as first-line in black African or Caribbean patients)
  • 3rd line= Labetalol or atenolol
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21
Q

What is eclampsia?

Discuss the management of eclampsia

A
  • Eclampsia= seizures associated with pre-eclampsia
  • Management:
    • A-E
      • Left lateral position/left tilt
      • Oxygen
      • 2 wide bore cannulas: FBC, U&E, LFTs, coagulation
      • Plasma glucose
    • IV magnesium sulphate used to both prevent seizures and as treatment of seizures. Should continue treatment for 24hrs after last seizure or delivery
    • BP control with IV antihypertensives (labetalol or hydralazine) with target MAP of <120mmHg
    • Continuous CTG monitoring
    • Prompt delivery of baby (ideally caesarean but if in established labour may do vaginal). MOTHER MUST BE STABLE BEFORE DELIVERY (not seizing, severe HTN treated, hypoxia corrected)
    • HDU care with careful fluid balance monitoring, monitoring of seizures, monitoring of end organ dysfunction etc…

Will need regular symptom review, regular blood tests (FBC, LFT, creatinine, proteinuria etc…). Other aspects include support (traumatic experience), pre-conception counselling regarding future pregnancies etc..

NOTE: respiratory depression can occur with MgSO4 hence monitor RR & O2 sats (calcium gluconate is 1st line for MgSO4 induced respiratory depression)

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22
Q

What is HELLP syndrome?

A

Severe form of pre-eclampsia in which there is:

  • Haemolysis
  • Elevated Liver enzymes
  • Low Platelets
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23
Q

State some potential complications of pre-eclampsia; split your answer into maternal & fetal complications

A

Maternal complications

  • HELLP syndrome – haemolysis, elevated liver enzymes, low platelets
  • Eclampsia
  • Acute Kidney Injury (AKI)
  • Disseminated Intravascular Coagulation (DIC)
  • Adult Respiratory Distress Syndrome (ARDS)
  • Hypertension (4-fold ↑ risk post-partum)
  • Cerebrovascular haemorrhage (1-2%)
  • Death

Fetal complications

  • Prematurity
  • Intrauterine growth restriction
  • Placental abruption
  • Intrauterine death
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24
Q

Summary of hypertension in pregnancy from PassMed

A
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25
Q

What is gestational diabetes?

A

Any degree of glucose intolerance with onset or first recognition during pregnancy

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26
Q

How common is gestational diabetes?

A
  • 2nd most common medical disorder complicating pregnancy (hypertension is most common)
  • Affects ~5% pregnancies
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27
Q

State some risk factors for gestational diabetes

A
  • Previous gestational diabetes
  • Previous macrosomic baby (≥ 4.5kg/9pount 9lb)
  • BMI > 30
  • Ethnic origin (black Caribbean, Middle Eastern and South Asian)
  • Family history of diabetes (first-degree relative)
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28
Q

Discuss the pathophysiology of gestational diabetes

A
  • In pregnancy, there is progressive insulin resistance (body’s way of preventing maternal cells taking up glucose to increase amount of glucose available to fetus)
  • Hence, more insulin is required to maintain normal blood glucose (increased requirement of ~30%)
  • In gestational diabetes, pancreatic beta cells fail to produce sufficient insulin to meet increased requirements
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29
Q

Who should be screened for gestational diabetes?

When should they be screened?

What is the screening test of choice?

A

Screening test is OGTT (oral glucose tolerance test):

  • Anyone with risk factors should be screened at 24-28 weeks gestation
  • Women with previous gestational diabetes should be screened ASAP after booking clinic AND again at 24-28 weeks if first test is normal
  • Any point during pregnancy if 2+ glycosuria on one occasion, or 1+ on two occasions

***NICE recommend early self monitoring of blood glucose in women who have had gestational diabetes before as alternative to OGTTs

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30
Q

What features may suggest gestational diabetes (think about maternal & fetal findings)

A

Maternal

  • Glucosuria
  • Symptoms of diabetes (but mostly asymptomatic)

Fetal

  • Large for dates
  • Polyhydramnios
31
Q

Discuss:

  • How OGTT is performed
  • What results suggest gestational diabetes
A
  • Pt should fast (at least 8hrs) and fasting plasma glucose measured. Pt then drinks 75g glucose drink. Measure glucose 2hrs later.
  • Normal results:
    • Fasting: ≥5.6mmol/L
    • After 2hrs: ≥7.8mmol/L

Results higher than above indicate gestational diabetes.

***NOTE: It is really easy to remember the cutoff for gestational diabetes as simply 5 – 6 – 7 – 8.

32
Q

Discuss the management of gestational diabetes

A

Managed by doctor in joint diabetes & antenatal clinics with input from dietician. Key aspects of management:

  • Education (what it is, monitoring of glucose, lifestyle advice, complications)
  • Four weekly ultrasound scans, from 28 to 36 weeks gestations, to monitor fetal growth & amniotic fluid volume (so at 28, 32 and 36 weeks)
  • Controlling blood sugar; depends on fasting glucose:
    • <7mmol/L → trial of diet & exercise for 1-2 weeks. If this doesn’t work + metformin, then +insulin if doesn’t work
    • >7mmol/L → insulin +/- metformin
    • >6mmol/L PLUS macrosomia or other complications: insulin +/- metformin
    • **NOTE: glibenclamide (sulphonylurea) can be used if cannot tolerate metformin or decline insulin
  • Aim to deliver at 37-38 weeks (can deliver as late as 40 + 6 weeks)
33
Q

What type of insulin is used to treat gestational diabetes?

A

Short acting

34
Q

What glucose levels should pregnant women with gestational diabetes be aiming for?

A
  • Fasting: 5.3 mmol/l
  • 1 hour post-meal: 7.8 mmol/l
  • 2 hours post-meal: 6.4 mmol/l
  • Avoiding levels of 4 mmol/l or below
35
Q

Gestational diabetes takes months to improve/resolve following birth; true or false?

A

FALSE; improves immediately after birth hence women can stop their diabetic medications immediately after birth BUT require follow up to test fasting glucose after at least 6 weeks

36
Q

State some potential complications of gestational diabetes

A
  • Macrosomia
    • Shoulder dystocia
    • Obstructed/delayed labour
    • Higher rates of instrumental deliveries
  • Polyhydramnios
  • Pre-term delivery
  • Erythropoiesis
  • Cardiomyopathy
  • Transient tachypnoea of newborn (high insulin can cause reduction in phospholipids which can decrease fetal surfactant production)
  • Jaundice
  • Neonatal hypoglycaemia

**KEY ONES TO REMEMBER MACROSOMIA AND NEONATAL HYPOGLYCAEMIA

37
Q

Women with gestational diabetes have increased risk of developing T2DM later in life; true or false?

A

True

38
Q

Babies born to mothers with gestational diabetes require close monitoring for neonatal hypoglycaemia, discuss:

  • What monitoring is involved
  • Blood glucose target
  • Symptoms & signs neonatal hypoglycaemia
  • Management
A
  • Regular blood glucose checks
  • Target is >2mmol/L (many guidelines say <2.6mmol/L is hypoglycaemia but no set figure)
  • Symptoms & signs:
    • Asympatomatic
    • Autonomic: jitteriness, irritable, tachypnoea, pallor
    • Poor feeding
    • Weak cry
    • Drowsy
    • Hypotonia
    • Seizures
  • Management:
    • Asymptomatic: encourage normal feeding & monitor glucose
    • Symptomatic OR very low glucose: admit to neonatal until for IV infusion 10% dextrose
39
Q

Discuss the management of pre-existing diabetes during pregnancy

A
  • Lifestyle (weight loss, healthy diet, regular exercise)
  • Stop oral hypoglycaemic agents, apart from metformin, and commence insulin
  • Retinopathy screening shortly after booking clinic and again at 28 weeks gestation (pregnancy can cause rapid progression of retinopathy)
  • Planned delivery between 37 and 38+6 weeks
  • Sliding scale insulin should be considered for women with T1DM
40
Q

What is obstetric cholestasis/intrahepatic cholestasis of pregnancy?

When does it usually occur?

A
  • Reduced outflow of bile acids from liver during pregnancy (affects ~1% pregnancies). Thought to be due to increased oestrogen and progesterone levels in combination with genetic factors.
  • Later in pregnancy (particularly 3rd trimester)
41
Q

Describe typical presentation of obstetric cholestasis/intrahepatic cholestasis of pregnancy- highlight main symptom

A
  • Pruritis (particularly affecting palms of hands & soles of feet)
  • Fatigue
  • Dark urine
  • Pale, greasy stools
  • Jaundice
42
Q

State some differential diagnoses, other than obstetric cholestasis, for pruritis and deranged LFTs in pregnancy

A
  • Gallstones
  • Acute fatty liver
  • Autoimmune hepatitis
  • Viral hepatitis
43
Q

What investigations are required if you suspect obstetric cholestasis?

A
  • LFTs: deranged
  • Bile acids: raised
44
Q

It is normal for ALP to be raised in pregnancy; why?

A

Placenta produces ALP hence if ALP is raised but other LFTs are normal usually due to placental production of ALP

45
Q

Discuss the management of obstetric cholestasis

A
  • Ursodeoxycholic acid
  • Emollients e.g. calamine lotion to soothe itching
  • Antihistamines (e.g. chloramphenicol) can help sleeping but don’t improve itching!!
  • Vitamin K if clotting is deranged
  • Weekly monitoring of LFTS during pregnancy
  • LFTs at least 10 days after delivery to check for resolution
  • Induction of labour at 37 weeks common practice (planned delivery after 37 weeks may be considered. Early delivery aims to reduce risk of stillbirth)
46
Q

Why is vitamin K given to women with obstetric cholestasis with clotting abnormalities?

A
  • Vit K is fat soluble vitamin
  • Bile acids important in absorption of fat & hence fat soluble vitamins
  • Vit K required for production of certain clotting factors (2, 7, 9, 10) hence deficiency can cause clotting abnormalities
47
Q

Recurrence of obstetric cholestasis in subsequent pregnancies is common; true or false?

A

True (45-90%)

48
Q

What is acute fatty liver of pregnancy?

Is it common?

When does it occur?

A
  • Rapid accumulation of fat in hepatocytes during pregnancy causing acute hepatitis
  • Rare
  • Third trimester
49
Q

Discuss the pathophysiology of acute fatty liver of pregnancy

A
  • Due to impaired processing of fatty acids in placenta
  • Occurs due to genetic condition in fetus that impairs fatty acid metabolism
    • Most commonly this is LCHAD deficiency (long-chain-3-hydroxyacyl-CoA dehydrogenase) which is autosomal recessive
  • LCHAD enzyme important for fatty acid oxidation (breaking down fats to be used as fuel)
  • Fetus & placenta unable to break down fatty acids hence fatty acids enter maternal circulation & accumulate in liver
  • Since it is autosomal recessive, mother must also have defective copy of gene and thought that this may also contribute to accumulation of fatty acids in liver
  • Leads to hepatitis and liver failure
50
Q

Describe typical presentation of acute fatty liver of pregnancy

A

The presentation is with vague symptoms associated with hepatitis :

  • General malaise and fatigue
  • Nausea and vomiting
  • Jaundice
  • Abdominal pain
  • Anorexia (lack of appetite)
  • Ascites
51
Q

What investigations are required if you suspect acute fatty liver of pregnancy?

A
  • LFTs: elevated AST, ALT, bilirubin
  • Coagulation: raised prothrombin & INR
  • FBC: raised WBC, thrombocytopenia

NOTE: In your exams, elevated liver enzymes and low platelets should make you think of HELLP syndrome rather than acute fatty liver of pregnancy. HELLP syndrome is much more common, but keep acute fatty liver of pregnancy in mind as a differential.

52
Q

Discuss the management of acute fatty liver of pregnancy

A
  • Obstetric emergency requiring prompt admission & delivery of baby. Most pts recover after delivery.
  • If acute liver failure occurs, treat as you would any other acute liver failure
53
Q

State some potential complications acute fatty liver of pregnancy

A
  • Liver failure
  • Mortality both mother & fetus
54
Q

When should a woman start to experience fetal movements?

At what gestation would you refer to maternal fetal medicine unit (if hadn’t felt fetal movements)?

A
  • Usually between 18-20 weeks and movements increase until 32 weeks at which point they plateau. Multiparous women may feel movements as early as 16-18 weeks
  • Refer to fetal medicine if not felt fetal movements by 24 weeks
55
Q

There is no established definition for what constitutes RFM however what do RCOG consider to be an indication for further assessment?

A

If >28 weeks gestation, less than 10 movements within 2hrs = indication for further assessment

56
Q

Why do we get concerned about reduced fetal movements/what can it indicate?

A
  • RFM can represent fetal distress
  • Fetus reduces movements to reduce oxygen consumption as a response to chronic hypoxia in utero
  • Concerning as reflects risk of FGR and stillbirth
57
Q

State some risk factors/potential reasons for reduced fetal movements

A
  • Posture (maternal posture can cause changes in fetal movements- typically more prominent when lying down and less when sitting & standing)
  • Distraction (if busy may be less aware)
  • Placental position (if have anterior placenta prior to 28 weeks gestation may have less awareness)
  • Medications/sedatives e.g. alcohol, benzodiazepines, opiates (can temporarily reduce fetal movements)
  • Fetal position (anterior fetal position means movements more noticeable)
  • Body habitus (obese patients less likely to experience prominent movements)
  • Amniotic fluid volume (both oligo- and poly-hydramnios can cause RFM)
  • Fetal size (up to 29% women with RFM with SGA)
58
Q

State what investigations should be done for RFM, think about how it differs for different gestations:

  • ≥28 weeks
  • 24-28 weeks
  • <24 weeks
A

≥ 28 weeks

  • Initially, handheld doppler to confirm fetal heart beat
    • If no fetal heartbeat, immediate ultrasound
  • If fetal heart beat present, CTG for at least 20 mins
  • If, despite normal CTG concerns remain then do urgent (within 24hrs) ultrasound to assess EFW, AC & amniotic fluid volume
  • If RFM are recurrent, further investigations required to consider structural or genetic fetal abnormalities

24-28 weeks

  • Handheld doppler to confirm fetal heartbeat

<24 weeks

  • If fetal movements previously felt → handheld doppler
  • *Remember to refer at 24 weeks if not felt fetal movements*
59
Q

Discuss the prognosis of RFM

A
  • In 70% pregnancies with a single episode of RFM there are no onward complications
  • 40-55% women who have stillbirths have RFM prior to diagnosis
60
Q

State some of the pregnancy-related skin changes/rashes

A
  • Polymorphic eruption of pregnancy
  • Atopic eruption of pregnancy
  • Melasma
  • Pyogenic granuloma
  • Pemphigoid gestationis
61
Q

For polymorphic eruption of pregnancy, discuss:

  • When it occurs
  • Presentation
  • Management
A
  • Usually starts in 3rd trimester
  • Itchy rash that begins on abdomen- particularly associated with striae. Characterised by papules, wheals and plaques
  • Management:
    • Advise tends to get better towards end of pregnancy and after delivery
    • Topical emollients
    • Topical steroids
    • Oral antihistamines
    • Oral steroids (SEVERE cases)
62
Q

For atopic eruption of pregnancy, discuss:

  • What it is
  • When it usually presents
  • Two types
  • Management
A
  • COMMONEST SKIN DISORDER IN PREGNANCY. Eczema that flares up during pregnancy (can occur in women who never had eczema before and those with known eczema)
  • Presents in 1st & 2nd trimester
  • Types:
    • E (eczema) type: typical eczema presentation
    • P (prurigo) type: intensely itchy papules typically on abdomen, back & limbs
  • Management:
    • Advise usually gets better after delivery
    • Topical emollients
    • Topical steroids
    • Phototherapy with UVB (SEVERE)
    • Oral steroids (SEVERE)

**Image shows P-type

63
Q

For melasma, discuss:

  • What is is
  • When else it can occur
  • Management
A
  • Patches of increased pigmentation on face
  • COCP, HRT (and associated with sun exposure, thyroid disease, FH)
  • Management:
    • No active treatment- usually goes away on own after pregnancy
    • Avoid sun exposure & use suncream
    • Makeup (camouflage)
    • Skin lightening creams may be used after pregnancy under specialist care
    • Procedures e.g. chemical peels or laser (not on NHS)
64
Q
  • For pyogenic granuloma, discuss:
  • What it is
  • Typical presentation
  • Management
A
  • Benign, rapidly growing tumour of capillaries
  • Presentation:
    • Discrete lump with red or dark appearance
    • Often on fingers, upper chest, back, neck or head
    • Can be triggered by minor trauma or infection
    • Can bleed or ulcerate if injured
    • More common in pregnancy
  • Management:
    • Exclude other differentials e.g. nodular melanoma
    • Advise usually resolve without treatment after delivery
    • Surgical removal with histology can be done
65
Q

For pemphigoid gestationis, discuss:

  • What is is
  • Whether it is common
  • When it usually occurs
  • Presentation
  • Management
  • Risk to baby
A
  • Autoimmune condition in which autoantibodies damage connection between epidermis and dermis causing epidermis and dermis to separate resulting in bullae. Antibodies are produced in response to placental tissue.
  • Rare
  • 2nd or 3rd trimester
  • Presentation:
    • Itchy red papular or blistering rash around umbilicus
    • Then spreads to other parts of body
    • Bullae form over several weeks
  • Management:
    • Usually resolves without treatment after delivery (blisters heal without scarring)
    • Treatment may include:
      • Topical emollients
      • Topical steroids
      • Oral steroids (severe)
      • Immunosuppressants (severe)
      • Abx if infection
  • Risk to baby:
    • Fetal growth restriction
    • Preterm delivery
    • Blistering rash after delivery (if antibodies pass to baby)
66
Q

Remind yourself of the 8 reversible causes of cardiac arrest (4H’s & 4T’s)

A

4 Ts:

  • Thrombosis (i.e. PE or MI)
  • Tension pneumothorax
  • Toxins
  • Tamponade (cardiac)

4 Hs:

  • Hypoxia
  • Hypovolaemia
  • Hypothermia
  • Hyperkalaemia, hypoglycaemia, and other metabolic abnormalities
67
Q

Alongside 8 reversible causes of cardiac arrest, there are additional potential causes of cardiac arrest in pregnancy; state these

A
  • Eclampsia
  • Intracranial haemorrhage
68
Q

What are the 3 major causes of cardiac arrest in pregnancy?

A
  • Obstetric haemorrhage (hypovolaemia)
  • Pulmonary embolism (hypoxia)
  • Sepsis leading to metabolic acidosis and septic shock (hypoxia, hypovolaemia etc…)
69
Q

State some potential causes of obstetric haemorrhage (a major cause of severe hypovolaemia and cardiac arrest)

A
  • Ectopic pregnancy (early pregnancy)
  • Placental abruption (including concealed haemorrhage)
  • Placenta praevia
  • Placenta accreta
  • Uterine rupture
70
Q

Discuss:

  • What aortocaval compression is
  • Why it is a problem
  • Management
A
  • After 20 weeks uterus is significant size. When woman lies on her back mass of uterus can compress IVC and aorta; compression of IVC most significant
  • Compression IVC → reduced venous return → reduced cardiac output → hypotension and in some cases may lead to significantly decreased cardiac output and cardiac arrest
  • Management:
    • Place woman in left lateral position (since vena cava is slightly to R lying on left side positions uterus away from IVC and can relieve compression)
71
Q

State some factors that make resuscitation more complicated in pregnancy

A
  • Aortocaval compression
  • Increased oxygen requirements
  • Splinting of the diaphragm by the pregnant abdomen
  • Difficulty with intubation
  • Increased risk of aspiration
  • Ongoing obstetric haemorrhage
72
Q

Resuscitation in pregnancy follows same principles as standard adult life support but has 5 key differences/additions; state these

A
  • 15 degree tile to left side for CPR (to relieve compression on IVC & aorta)
  • Early supplementary oxygen
  • Early intubation to protect airway
  • Aggressive fluid resuscitation (caution in pre-eclampsia)
  • Delivery of baby after 4 minutes of CPR (aiming to deliver within 5 mins of starting CPR)

*NOTE: caesarean section will performed at site of arrest

73
Q

What is the primary reason for immediate delivery in cardiac arrest in pregnant woman?

A

Improve survival of mother as delivery:

  • Improves venous return to the heart
  • Improves cardiac output
  • Reduces oxygen consumption
  • Can help with ventilation and chest compressions

Delivery can also improve survival of the baby however this is SECONDARY to survival of the mother

74
Q

Why do we get concerned about reduced fetal movements/what can it indicate?

A

Yr4: Obstetrics & Gynaecology (24 decks)

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