DRANZCOG/Obstetrics Flashcards

1
Q

Risk factors for shoulder dystocia

A

At least 50% of shoulder dystocias have no identifiable risk factors!

Antenatal (5):

  • previous shoulder dystocia
  • macrosomia
  • maternal DM
  • maternal obesity
  • post-term pregnancy

Intrapartum (5)

  • prolonged 1st stage
  • prolonged 2nd stage
  • labour augmentation
  • instrumental delivery
  • post-term pregnancy
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2
Q

Consequences of a shoulder dystocia

A

Neonatal (4)

  • brachial plexus injury (Erb’s palsy)
  • fractures (humeral and clavicular)
  • hypoxia
  • stillbirth

Maternal (6)

  • PPH
  • severe vaginal and perineal trauma (3rd and 4th degree tears)
  • cervical tears
  • uterine rupture
  • bladder rupture
  • psychological distress
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3
Q

When to suspect shoulder dystocia

A
  • prolonged birth of face and chin
  • head emerges and retracts against the perineum (turtle sign)
  • fetus fails to undergo external rotation
  • the anterior shoulder does not emerge with routine axial traction
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4
Q

Reassuring features on intrapartum CTG

A

Baseline FHR 110-160 bpm
Baselines variability of 5-25 bpm

No decels OR early decles OR variable decelerations with NO concerning features for less than 90 minutes

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5
Q

Non-reassuring features on intrapartum CTG

A

Baseline FHR 100-109 OR 161-180
Variability <5 for 30-50 minutes OR >252 for 15-25 minutes

Variable decels WITHOUT concerning characteristics for 90 minutes +
OR
variable decels with any concerning characteristics in <50% of contractions for 30 minutes +
OR
variable decels with any concerning characteristics in OVER 50% of contractions for LESS than 30 minutes
OR
Late decels in >50% of contractions for <30 minutes with no maternal or fetal clinical risk (e.g. signficicant mec, PV bleeding etc. )

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6
Q

ABNORMAL features of an intrapartum CTG

A

Baseline FHR <100 or >180

Variability <5 for more than 50 minutes 
OR 
>25 for more than 25 minutes
OR
Sinusoidal

Variable decels with any concerning characteristics in >50% of contractions for 30 minutes (or less if maternal of fetal clinical risk factors)
OR
Late decels for 30 minutes
OR
Acute bradycardia, or single prolonged deceleration lasting 3 minutes or more

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7
Q

Concerning characteristics of variable decelerations

A
>60 seconds duration
Reduced baseline variability within the deceleration
Failure to return to baseline
Biphasic (W) shape
No shouldering
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8
Q

Interpretation of normal v suspicious etc. intrapartum CTG

A

Normal = all reassuring features

Suspicious = 1 non-reassuring feature + 2 reassuring features

Pathological - 1 ABNORMAL feature OR 2 non-reassuring features

Urgent intervention required: acute bradycardia, or single prolonged deceleration 3+ minutes

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9
Q

Features to assess when describing decelerations on CTG

A
  • timing related to peak of contractions
  • duration of individual decels
  • if FHR returns to baseline
  • how long have decelerations been present
  • do they occur with >50% of contractions
  • presence of a biphasic (W) shape)
  • presence or absence of shouldering
  • normal or reduced variability WITHIN the deceleration
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10
Q

Definition of antepartum haemorrhage

A

Bleeding from the genital tract after the 20th week of pregnancy, and before the onset of labour

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11
Q

Epidemiology of antepartum haemorrhage

A

Occurs in 2-5% of all pregnancies

Up to 20% of preterm babies are born in association with APH

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12
Q

Causes of antepartum haemorrhage

A
  • (non-vaginal e.g. PR bleed)
  • Distal genital tract/gynae causes
  • cervical (ectropion, polyp, cervicitis, cervical dilatation, cervical incompetence)
  • Placental (praevia, abruption, abnormal placentation, abnormal shape, marginal bleed)
  • Uterine (rupture)
  • Foetal (vasa praevia)
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13
Q

Relevant history to obtain in woman presenting with antepartum haemorrhage

A

Gestation
Location of placenta
Bleeding: time of first bleed, pattern, previous APH (this pregnancy or previous)
- Potential causes (postcoital, trauma, exertion)
- CST results
- Pain (site, commencement, frequency, strength, duration)

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14
Q

Maternal assessment in antepartum haemorrhage

A

ABCs
Abdominal palpation (gently) for SFH, lie, presentation, tenderness
USS: placental location if not known
Blood loss (amount, colour, consistency)
Uterine activity and consistency
Bloods (CBE, Group and save +/- crossmatch if heavy bleeding, coagulation profile, Kleihauer if Rh negative)
Speculum examination - swabs (STI, LVS, HVS) and consider CST if not performed in the last 3 months + clear cervical bleeding

(CTG for fetal assessment)

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15
Q

Epidemiology of placental abruption

A

1% of births
- 20-35% of these are concealed, rest are revealed

Perinatal mortality rate of 11.9%

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16
Q

Risk factors for placental abruption

A

Maternal:

  • hypertension
  • thrombophilias
  • increased parity
  • poor nutrition
  • previous abruption (~10% risk of recurrent)
  • cigarette smoking
  • substance abuse (esp. cocaine)

Uterine factors:

  • Prolonged ROM (especially if PPROM)
  • chorioamnionitis
  • severe IUGR
  • polyhydramnios (sudden decrease in uterine volume post SROM)
  • Multiple pregnancy (sudden decrease in uterine volume following delivery of twin 1)
  • abdominal trauma
  • ECV
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17
Q

Presentation in placental abruption

A

Vaginal bleeding associated with PAIN, usually very distressed (out of proportion to amount of bleeding)

Usually dark, non-clotting b lood
Abdominal pain Or uterine contractions/tenderness/irritability
Can be associated with faint/collapse or haemorrhagic shock

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18
Q

Complications/associations of placental abruption (9)

A
  • preterm labour
  • foetal compromise
  • uterine irritability (>5:10 contractions)
  • coagulopathy
  • disseminated intravascular coagulopathy
  • postpartum haemorrhage
  • renal failure
  • Acute tubular necrosis (from hypovolaemia and DIC)
  • perinatal mortality
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19
Q

What is the most common OBSTETRIC cause of coagulopathy

A

Placental abruption

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20
Q

Management in placental abruption

A
  • IV access
  • IDC and fluid balance
  • Close maternal obs + CTG
  • Resuscitation as indicated
  • Urgent Group and cross-match, CBE, Coagulation studies, D-dimer, fibrinogen levels, EUC, LFT
  • Anti-D prophylaxis for Rh neg (+ Kleihauer)
  • delivery (LSCS if acute fetal compromise or other indication - be prepared for precipitous labour)
  • prepare for increased risk of PPH
  • examine placenta and send for histopathology
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21
Q

Perineal injury classifications

A

1st deg: injury to skin only

Second degree: injury to perineal muscles but NOT the anal sphincter

3rd degree: injury involving anal sphincter complex

3a: <50% external anal sphincter thickness torn
3b: >50% external anal sphincter rotn
3c: Internal anal sphincter town

4th degree: injury involving anal sphincter complex AND anal epithelium

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22
Q

Appropriate analgesia to use for perineal repair

A

1% lignocaine +/- adrenaline (or equiv)

Without adrenaline is preferred for labial tears to reduce risk of tissue ischaemia

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23
Q

Preferred suturing technique for vaginal wall and muscle layer

A

Continuous, non-locked

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24
Q

Approximate epidemiology of perineal injury

A

25% of NVD: intact perineum
12% episiotomy
40% tear requiring repair

Other minor tears that don’t require repair

Women with epidural higher risk of instrumental delivery and associated perineal morbidities

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25
Antenatal methods to protect against perineal morbidity
- Perineal massage 1-2x/week from 35/40 - Pelvic floor muscle training for women (Continence Foundation of Australia) Insufficient evidence to recommend raspberry leaf tea
26
Intrapartum care to protect from perineal morbidity
No specific position or pushing technique recommended Warm compresses and perineal massage: lowers risk of 3rd and 4th degree tears During crowning: - minimise active pushing following crowning to ensure slower descent of head. - If rapid, consider counter pressure on foetal head if appropriate - maximise flexion to help reduce presenting diameter
27
When to use episiotomy
Imminent perineal tear OR High risk of severe laceration: 1. Soft tissue dystocia 2. Foetal compromise indicating expedited delivery 3. Instrumental delivery (not always required for vacuum) 4. History of female genital mutilation 5. Past history of pelvic floor repair or third-degree tear
28
Anatomy involved in episiotomy
Vaginal mucosa Perineal skin Bulbocavernosus muscle Transverse perineal muscle
29
Technique to perform episiotomy
``` Appropriate analgesia (e.g. 1% lignocaine) Incision 3-5cm length from the fourchette ad 60-80 degree angle from midline (will become 45 degrees following delivery, loss of distension) ```
30
Immediate postpartum perineal care
Repair if indicated Rectal NSAID unless PPH if torn If tear within close proximity of urethra, consider indwelling catheter
31
Postpartum perineal care recommendations
Cold packs (10-20 minute intervals) first 1-3 days PRN PO paracetamol and NSAID Urinary alkalinisers Avoid opioids Fibre rich, balance diet, adequate hydration ``` Support perineal wound when coughing or defecating Correct toileting position Avoid constipation Wash and pat dry post toileting Shower at least daily Check wound daily with hand mirror ``` Pelvic floor muscle training for women Avoid sitting/propped positions (dependent perineal oedema) Avoid increased intra-abdominal pressure for 6-12 weeks (e.g. straining, lifting etc.)
32
Postpartum perineal care methods that lack evidence currently
Sitz baths Perineal ultrasound for perineal pain or dyspareunia Topical anaesthetics Ray lamps Donut cushions (may lead to more dependent oedema) Herbal remedies e.g. arnica
33
Anatomy of the Bartholin glands
Paired glands located in labia minor at 4 and 8 o'clock positions Approx 5mm in diameter Secrete mucus into 2.5cm ducts which emerge either side of vagina, inferior to the hymen
34
Pathophysiology of Bartholin gland cyst
Nonspecific inflammation or trauma -> obstruction of opening of duct -> distension of gland or duct
35
Pathophysiology of bartholin gland abscess
Either secondary to infected cyst, or a primary gland infection Usually polymicrobial Rarely caused by STIs
36
Epidemiology of Bartholin gland disease
2% of women of reproductive age will experience swelling of at least one Bartholin gland Typically in women 20-30y Rare in women >40y (malignancy should be considered)
37
Clinical presentation of Bartholins cyst
Painless (unless very large) labial swelling, usually unilateral No signs of surrounding cellulitis Discharge if has spontaneously ruptured will be non-purulent
38
Clinical presentation of Bartholin's Gland Abscess
Acute painful unilateral labial swelling Dyspareunia Pain with walking and sitting Sudden relief of pain followed by discharge (suggests spontaneous rupture) Can occur spontaneously or on history of a painless cyst Very tender with surrounding erythema and oedema may have surrounding cellulitis Purulent discharge if spontaneously ruptured
39
Management of Bartholin Gland Disease
Asymptomatic uncomplicated cyst: - Sitz baths 3x per day for several days (may induce resolution +/- rupture) Abscess: Incision and drainage +/- marsupialisation Antibiotics only required if significant surrounding cellulitis
40
Definitions of postpartum haemorrhage:
Traditionally primary postpartum haemorrhage = blood loss >500mL in first 24h Minor: 500-1000mL major: >1000mL (moderate 1000-2000mL, severe >2000mL) note that some centres consider PPH as >600mL following NVD or >750mL following LSCS
41
Risk factors for PPH
2/3 of women who have PPH have no risk factors identified Background risk: - PPH in previous pregnancy - grand multiparity (4+) - Nulliparity - Advanced maternal age (>35y) - known coagulopathies or liver disease - obesity - previous LSCS Antenatal complications: - multiple pregnancy - antepartum haemorrhage (esp placental abruption or previa) - known placenta accreta - anaemia - pre-eclampsia - macrosomia ``` Intrapartum: - need for/use of oxytocics - prolonged labour (especially 2nd stage) Pyrexia in labour operative delivery Episiotomy Placental retention Shoulder dystocia ```
42
Causes of PPH (general groups and %)
Tone (70%) Trauma (20%) Tissue (10%) Thrombin (<1%)
43
Atonic causes o PPH
Uterine atony (e.g. physiological or prolonged 3rd stage) Over-distended uterus (polyhydramnios, multiple gestation, macrosomia) Uterine muscle exhaustion (rapid labour, prolonged labour, high parity, augmentation with oxytocin) Intra-amniotic infection (PROM >24h) Drug-induced (magnesium, nifedipine, salbutamol, GA) Functional or anatomical distortion of the uterus (fibroids, placenta praevia, uterine abnormalities, bladder distention)
44
Tissue causes of PPH
Retained products Abnormal or adherent placenta Retained cotyledon or succenturiate lobe
45
Trauma causes of PPH
``` Lacerations to cervix, vagina, perineum (precipitous labour, operative delivery) Uterine rupture (high parity, fundal placenta) Extensions/lacerations at LSCS (malposition, deep engagement) ```
46
Thrombin causes of PPH
Non-obstetric abnormalities (Haemophilia, vWd, hereditary coagulopathies, liver disease) Acquired in pregnancy (ITP, PET, DIC, IUFD, severe infection, abruption, AFE) Therapeutic anti-coagulation (e.g. clexane for VTE)
47
Blood loss and signs of Class I hypovolaemic shock in late pregnancy
``` 15% (1000mL) RR: normal HR: <100 BP: Normal Mental state: anxious Urine output: normal ```
48
Blood loss and signs of Class II hypovolaemic shock in late pregnancy
``` 15-30% (1300mL) RR: 20-30 HR: >100 BP: Normal/increased diastolic Mental status: anxious/confused ```
49
Blood loss and signs of Class III hypovolaemic shock in late pregnancy
``` 30-40% (2000mL) RR: 30-40 HR: >120 BP: reduced systolic and diastolic Mental state: confused/agitated ```
50
Blood loss and signs of Class IV hypovolaemic shock in late pregnancy
``` >40% (2700mL) RR: >40 HR: >140 BP: decreased systolic and diastolic Mental state: lethargic Negligible urine output ```
51
Indications for intrapartum antibiotics (general)
- prevention of early onset GBS infection - women at risk of chorioamnionitis, or where infection is suspected (temp >38 on one occasion or >38.5 on two occasions) - women with cardiac lesions susceptible to infective endocarditis
52
Relative contraindications to amniotomy
1. Maternal HBV, HCV, HIV, HSV infection - minimise risk of vertical transmission to foetus 2. high and mobile presenting part
53
Factors to assess progress in the second stage of labour
Flexion Rotation Descent of head
54
Risk factors for pre-eclampsia (11)
``` Antiphospholipid syndrome Previous history of PET Pre-existing diabetes Nulliparity Multiple pregnancy Family history of PET Obesity (BMI >30) Systolic BP >130 <20/40 Diastolic BP >80 <20 weeks Age >40y Overweight (BMI 25-29.9) Underlying renal disease Chronic autoimmune disease Inter-pregnancy interval >10y ```
55
Early onset pre-eclampsia definition (i.e. gestation)
Onset <32 weeks
56
Systems which can be involved in pre-eclapmsia
``` Neurological Pulmonary Haematological Hepatic Renal Uteroplacental ```
57
Requirements for renal dysfunction in diagnosis of PET
Proteinuria >300mg/24h PR PCR >30 Creatinin >90 Oliguria <80mL/4h
58
Criteria for hameatological end organ dysfunction in diagnosis of PET
Platelets <100 Haemolysis (shistocytes or red cell fragments on film, raised bilirubin, raised LDH >600, reduced haptoglobin) Disseminated intravascular coagulopathy
59
Criteria for hepatic end organ dysfunction in diagnosis of PET
Increased transaminases | Severe epigastric and/or RUQ pain
60
Criteria for neurological end organ dysfunction in diagnosis of PET
``` Convulsions (=eclampsia) Hyperreflexia with sustained clonus Persistent, new headache Persistent visual disturbances (photopsia, scotomata, cortical blindness, posterior reversible encephalopathy syndrome, retinal vasospasm) Stroke ```
61
Criteria for pulmonary end organ dysfunction in diagnosis of PET
Pulmonary oedema
62
Criteria for uteroplacental end organ dysfunction in diagnosis of PET
Fetal growth restriction
63
Prophylaxis for women at risk of hypertensive disorders of pregnancy
``` Aspirin 50-150mg daily from diagnosis of pregnancy (aim for <16 weeks - 37 weeks) Calcium supplementation (esp if high risk and low calcium intake diet) 1.5g/day from <20/40 until delivery ```
64
Investigations in assessment for hypertensive disorders of pregnancy
Urine PCR CBE (Hb, PLT) EUC Urate (not actually in diagnostic criteria) LFTs Coagulation studies (depending on severity of presentation) USS: foetal growth, AFI, umbilical artery doppler assessment
65
Definition of SEVERE pre-eclampsia
BP >/= 160/110 with proteinuria ``` OR BP 140/90-159/109 with at least ONE of the following - severe headache - visual disturbances - severe pain below ribs OR vomiting - papilloedema - clonus (3+ beats) - liver tenderness - HELLP syndrome - PLT <100 - abnormal liver enzymes ```
66
Antihypertensives that can be considered during pregnancy
``` Methyldopa Labetalol Nifedipine XR Nifedipine IR Hydralazine ```
67
Antihypertensives for use in acutely lowering severe hypertension of pregnancy (and dose)
Nifedipine IR 10-20 mg repeated in 30 minutes if BP still above threshold Labetalol 200mg PO repeated in 30 minutes if not below threshold OR 20mg IV with repeat doses 40-80mg every 10 minutes until BP controlled (max 4 dose) Hydralazine f not controlled by nifedipine - 5mg IV bolus/5 minutes, repeated every 20 minutes until BP controlled (max 30mg)
68
Antihypertensives and doses for sustained BP control in pregnancy
Methyldopa 250-750mg every 8 hours Labetalol 100-400mg every 8 hours Nifedipine XR 30-60mg BD
69
Side effects of antihypertensives in pregnancy
Methyldopa: - depression - dry mouth - sedation - blurred vision Labetalol: - bradycardia (maternal and fetal) - bronchospasm - headache - nausea - scalp tingling ``` Nifedipine: - constipation - severe headache in first 24h - peripheral oedema tachycardia - flushing ``` Hydralazine: - flushing - headache - nausea - tachycardia
70
Onset of action of antihypertensives used to acutely lower blood pressure in pregnancy
Labetalol: peak effect within 5 minutes of each dose Nifedpine IR: onset 30-45 minutes Hydralazine: onset of action 20 minutes (Methyldopa only used for sustained BP control, has slow onset over 24 hours)
71
Contraindications to specific antihypertensives used in pregnancy
Methyldopa: depression Labetalol: Asthma/COAD Nifedipine: Aortic stenosis Hydralazine:
72
Treatment of severe pre-eclampsia
1. Stabilise - control BP (labetalol, nifedipine IR or hydralazine) - MgSO4 loading + maintenance dose) 2. Monitor - vital signs - urine output/strict fluid balance - neurological status - clotting factors - fetal conditions (CTG) 3. Plan for labour/birth
73
Indications for birth in women with pre-eclampsia (13)
Maternal: - >37/40 gestation - falling PLT count - intravascular haemolysis - HELLP syndrome - deteriorating LFTs - deterioration renal function - persistent neurological symptoms - persistent epigastric pain, nausea or vomiting with abnormal liver function - pulmonary oedema Fetal: - placental abruption - severe fetal growth restriction - non-reassuring fetal status
74
Additional considerations of management of PET
Thromboprophylaxis Monitoring of PLT at least daily (peripartum bleeding complications nor significantly increased until PLT <50) AND monitoring for intravascular haemolysis (CBE, blood film, LDH, haptoglobins)
75
Pregnancy complications associated with bipolar affective disorder (i.e. more likely in BPAD than in general population)
``` Pre-eclampsia Gestational diabetes Gestational hypertension Antepartum haemorrhage Severe fetal growth restriction Neonatal morbidity ```
76
Pregnancy complications associated with schizophrenia (i.e. more likely in pregnant schizophrenics than in general population)
Pre-eclampsia | Gestational hypertension
77
Pregnancy complications with a higher risk in borderline personality disorder
``` Gestational diabetes PPROM Chorioamnionitis VTE Caesarean section Preterm birth ``` High rates of substance abuse, referral to child protective services, anticipation of traumatic delivery and frequent request of early delivery
78
Optimising use of nitrous oxide
Start inhalation 30-50 seconds prior to contraction
79
Dosages of nitrous oxide
Start at 30% N2O, max of 70% N2O to prevent hypoxia
80
Adverse effects of nitrous oxide
If used with oxygen (as always should be in labour): - nausea - vertigo - megaloblastic anaemia N2O alone: - increased maternal heart rate - respiratory depression
81
Contraindications to nitrous oxide use
Inability to hold mouthpiece Impaired consciousness Impaired oxygenation (e.g. respiratory disease) Women who have received excessive amounts of other sedating medications Vitamin B12 deficiency (can cause megaloblastic anaemia) Recent ear surgery Hypersensitivity to N2O Any condition where air is trapped within a cavity and expansion may be dangerous (e.g. occluded middle ear, cysts, gross abdominal distension, maxillofacial injuries) Use >24h
82
Preconception management
(full history of woman and partner if possible - optimise any medical conditions) Imms: MMR, VZV, HBV Weight: reduce obesity BMI <30 ideal Nutrition: ?vegan/vego, assess and manage for nutritional deficiencies (B12, iron, VitD) Avoid excess caffeine (3-4 cup/day) CARD: cease all prior to conception. Aim for paternal smoking cessation pre-conception also Travel: avoid to areas particularly affected by Zika. mosquito and sexual protection if cannot avoid. Supplements: - Folic acid from 1/12 prior. 400mcg/day if low risk, 5mg/day if high risk (NTD hx, DM, AEDs, BMI >35, haemolytic anaemia) - Vit D if high risk group - B12 6mcg/day if vego/vegan or bariatric surgery - Calcium 1200mg/day if low dietary intake Iodine 150microg/day - iron if deficient, vego/vegan Genetic counselling: If high risk refer to geneticist, iff low risk, offer carrier screening e.g. Eugene (out of pocket currently)
83
Folic acid supplement dose in pregnancy/pre-conception
``` 400 microg/day if low risk 5mg/day if high risk: - DM - personal or FHx of NTD - BMI >35 - AEDs - multiple pregnancy - haemolytic anaemia ```
84
Vitamin B12 in pregnancy
6mcg/day if vegetarian/vegan/bariatric surgery
85
Immunisations to consider pre-conception
MMR VZV HBV
86
Risks of smoking in pregnancy
Pre-conception: - delayed conception by 2 months - 60% increased risk of female infertility - male infertility Obstetric: - Miscarriage - Preterm labour (2x) - placenta praevia (2x) - placental abruption (1.5x) - stillbirth (3x) - Ectopic (2.5x) - PPROM (2x) Fetal: - low birth weight (<2500g) (2x) - SGA (3x) - Birth defects (limbs, clubfoot, cleft palate, eye defects, GI defects) Postpartum: - less breastmilk production Child/adult: - SIDS (2.5x) - Behavioural issues (ADHD, CD, antisocial) - Respiratory disease (asthma, recurrent infection, reduced lung function) - Cognition (reduced academic performance) - T2DM - Obesity - HTN - Dyslipidaemia - Pyschiatric disorders early adulthood - Nicotine deopendence
87
Management of smoking in pregnancy
1. Counselling and QuitLine referral 2. NRT (1st line is intermittent short acting forms, if patches required make sure are removed at bedtime 16h patches) Champix and Bupropion not evidenced to be safe or effective in pregnancy
88
Risks of heroin use during pregnancy
``` IUGR Pre-term labour Placental abruption intrauterine passage of meconium Neonatal abstinence syndrome Foetal and neonatal death ``` Other associations: - inadequate antenatal care - poor nutrition - BBV exposure - overdose - financial hardship - unstable accommodation - pyschological instability
89
Opioid substitution therapy in pregnancy
Methadone and buprenorphine both cross the placenta Methadone has been used for longer, more experience with it. >50% of exposed neonates will show signs of NAS Buprenorphine - only the mono therapy (without naloxone) is offered to pregnant women. Evidence suggests associated with fewer neonatal complications than methadone (less frequency, less severe NAS and less medication and admission durations) Concentrations in breastmilk are low, breastfeeding should be encouraged while on OST if no other contraindications
90
Features of neonatal abstinence syndrome
Develops within first 48-72 hours of birth - lasts from 1-several weeks depending on type of opioid use - difficulty feeding - central and autonomic hyperactivity - poor suckling - irritability - hyperactivity - sleep disturbances - high-pitched cry - seizures (in 5%)
91
Management of neonatal abstinence syndrome
``` Close monitoring in special care nursery for prolonged period Observation with standardised NAS scoring Oral morphine (dose and duration based on NAS scoring) ```
92
Complications of alcohol in pregnancy
``` Miscarriage Stillbirth Low birth weight Premature birth Brain damage Birth defects Foetal alcohol spectrum disorders ```
93
Common impact on child(and then adult) from alcohol used in pregnancy
``` Hyperactivity/inattention/impulsivity Aggression Impaired social interactions Antisocial personality traits Disrupted schooling Substance use disorders Mental health issues Employment/financial/independent living issues Criminal system contact ```
94
Advice for alcohol and breastfeeding
Safest not to use alcohol at all while breastfeeding Definitely no alcohol in first month postpartum and until BF established If chooses to drink after than, limit consumption as much as possible Avoid drinking immediately prior to breastfeeding Option to express prior to alcohol consumption
95
Diagnostic features of foetal alcohol syndrome
1. evidence of prenatal alcohol exposure 2. Growth deficiency (pre or post natal <10th centile) 3. Facial features (** = sentinel) - epicanthal folds - flat nasal bridge - short palpebral fissures** - upturned nose - smooth/flat philtrum** - thin upper lip ** 4. Neurological dysfunction - Structural: - -HC <10% - -structural brain abnormality on imaging - Neurological - -any neurological issues NOT due to postnatal event - Functional - -performance below expected for age
96
Foods to recommend avoiding during pregnancy
Risk of listeriosis: - pre-prepared salad vegies (e.g. salad bars) - raw, undercooked, chilled pre-cooked meats, pate and meat spreads - unpasteurised dairy, soft, semi-soft and surface-ripened cheeses Risk of salmonella - raw eggs/foods containing raw eggs Risk of mercury - shark/flake, marlin, broadbill/swordfish, catfish Risk of hepatitis A - frozen berries - bean sprouts Foods containing saturated fats, added salts and sugars
97
Recommended maximum daily caffeine intake per day during pregnancy
300g (3-6 cups coffee/tea per day)
98
Recommended water intake during pregnancy
750-1000mL above daily pre-pregnancy needs
99
Vitamin supplements that can be associated with harm if taken antenatally
``` Vitamin C (preterm birth, perinatal death, PPROM) Vitamin E (PPROM) Vitamin A (congenital malformation) ```
100
Physical activity advice in pregnancy
- Specifically designed programs can prevent pelvic girdle pain and reduce severity of back pain - Yoga associated with less stress, enhanced relationships, reduced back pain and less reported pain in labour - can prevent urinary incontinence - low-moderate intensity exercise is safe throughout pregnancy
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Impacts of pregnancy on oral health
Reduced immune system (increased risk of periodontal infections) Vomiting/reflux in pregnancy increases acidity -> enamel damage -> decay Frequent snacks/soft drinks and other cravings (often sweet) can increase risk of tooth decay
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Recommendations to reduce impact of pregnancy induced vomiting on oral health:
Rinse mouth with bicarb soda after vomiting Avoid tooth brushing directly after vomiting Use fluoridated mouthwash and toothpaste Small protein-rich non-cariogenic foods throughout the day Chew sugar-free gum (esp ones containing xylitol or CPP-ACP) after meals/sugar/acidic drinks
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Women in whom you should screen for haemoglobinopathies (pre-natal or antenatally)
- family history of anaemia or haemoglobinopathy - MCV <80 OR MCH <27 Following ethnic backgrounds: - Southern European - African - Middle Eastern - Chinese - Indian subcontinent - Central and SE asian - Pacific Islander/Maori - South American - Caribbean - Northern WA/NT ATSI communities
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What to include in a haemoglobinopathy screen
FBE (for MCV+MCH) Ferritin (exclude Fe def) Hb electrophoresis DNA testing if indicated (microcytosis with normal iron and Hb electrophoresis and risk of disease)
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Hb electrophoresis results in beta-thalassaemia
High HbA2 (>3.5%) Normal HbA2 with low MCV and normal ferritin may be alpha thalassaemia
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Diagnosing alpha-thalassaemia
Requires DNA analysis for definitive diagnosis. Suggested with low MCV and normal Hb eletrophoresis + ferritin level
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Hormones involved in the onset of labour
Progesterone - suppresses uterine contractility - systemic or functional withdrawal (due to reduced responsiveness due to inc. PR-A:PR-B intrauterine expression) leads to increased uterotonin production Prostaglandins: - stimulate contractions, cervical softening and rupture of membranes - synthesis is catalysed by COX-2 - increase the intrauterine PR-A:PR-B ratio-> feed forward mechanism
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Benefits of water immersion in labour
- more tolerable labour pains - lower use of pharmacological analgesia - lower augmentation rates - lower bleeding, reduced risk of PPH - shorter labour
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Definition of the puerperium
the 6 weeks following delivery during which woman's physiology returns to pre-pregnancy state
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Expected course on uterine involution postpartum
Fundus at level of umbilicus immediately post delivery By day 5-7 halfway between umbilicus and pubic symphysis By 2 weeks not palpable By 6 weeks almost back to pre-pregnancy state
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Cause of involution and lochia
Contractions and reduction of size of myometrial muscle (Cause of after pains) Thrombosis and hyalinisation of blood vessels -> decidual shedding
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Normal progress of lochia
Until day 5-6: lochia rubra Until day 10-12: lochia serosa (darker brown) Then becomes lochia alba (yellowish/white)
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Timing of return of ovarian function post partum
In non-lactating women usually by 10 weeks, can be as early as 4-6 weeks In lactating women highly variable Make sure to offer contraception from 4 weeks if sexually active
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Healing time of perineal injury
Most 1st/2nd and episiotomies will heal within 3 weeks
115
Care of perineal injuries
Keep dry and clean, clean from front to back Warm sitz baths Avoid constipation Advise to watch for excessive pain/PV discharge or malodourous discharge Abstinence for 6 weeks, advise may be some discomfort when resumes
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When to resume sexual activity postpartum
Advise abstinence for 6 weeks if any tears If no tears, as soon as desired/comfortable Lactating women can have vaginal atrophy and may require topical oestrogen (after BF established) or lubrication
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Diet and exercise recommendations postpartum
Regular diet ASAP Full ambulation ASAP Abdominal strength exercises after delivery pains have subsided (usually 1 day post NVD, 6 weeks post LSCS) - curl-ups while lying in bed (flexing knees and hips)
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Bladder changes postpartum
Massive diuresis can occur immediately post-partum due to withdrawal of oxytocin
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Cathartics use postpartum
Psyllium husk Docusate or Bisacodyl Should be given to all women with OASI injury postpartum, and to other women if BNO day 3 (or if otherwise desired)
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Managing breast engorgement postpartum
If plans to BF:Hand expression in warm shower or pump between feeds, regular feed schedule, wear comfy nursing bra ``` If not wanting to BF: Supportive bra (avoid gravity), avoid nipple stimulation or manual expression, tight binding of breasts (e.g. with tight sports bra), cold packs and analgesia PRN ```
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Post partum mental health changes
``` Transient depression is common in the first week - mood swings - irritability - anxiety - poor concentration - insomnia - crying spells Typically only mild and subsides by day 7-10 ```
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When to advise women to see their GP re: ?postpartum depression
- If depressive symptoms last >2 weeks post partum - if symptoms interfering with daily life - ANY suicidal or homicidal thoughts
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Family planning recommendations post partum
Obstetric outcomes are improved by delaying conception until 18 months post delivery MUST delay conception at least 4 weeks post live vaccines Avoid combined oestrogen/progesterone contraceptives while lactation is being established
124
Vulnerable groups who are statistically less likely to breastfeed (thus require more support)
``` Aboriginal and Torres Strait Islander Women Younger women (especially <20y) Less educated women Obese women Lower socioeconomic status ```
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Benefits of breastfeeding for the infant
- nutrients in perfect composition, bioavailability and readily absorbable state - active and passive immunity - improved visual acuity - improved psychomotor and cognitive development (higher IQ with longer durations of breastfeeding) Reduced risks of: - malocclusion - physiological reflux - pyloric stenosis - GI infections - respiratory illness - otitis media - urinary tract infections - meningitis - SIDS - NEC (in Prem babies) - Atopy (breastfeeding during time of antigen introduction facilitates development of tolerance) - Some childhood cancers - T1DM/T2DM - Coeliac diseae (if breastfeeding at time that gluten is introduced) - IBD - HTN, dyslipidaemia - obesity
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Maternal benefits of breastfeeding
- reduced risk of breast Ca - reduced risk of ovarian Ca - reduced risk of GDM women developing T2DM - Promotes uterine involution (less bleeding -> preservation of iron stores) - ?maybe helps return to pre-pregnancy weight
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What to discuss around breastfeeding antenatally
- importance of exclusive breastfeeding to 6 months and recommend breastfeeding to at least 12 months for nutritional and protective benefits - basic breastfeeding management - anticipatory guidance for coping with minor problems
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Factors that delay the initiation of lactation
- stressful delivery (due to reduced oxytocin release) - Caesarean delivery - Maternal T1DM (can delay lactation by 24h) - retained placental fragment (persistent progesterone release) - maternal obesity (higher levels of progesterone + attachment issues)
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Correct technique for breastfeeding
- Mum upright/semi-reclined with good back/feet/arm support - "C-hold" - if nipple erect, support outer area of breast, if flat/inverted should hold well behind areola from the bottom to shapebreast between thumb and index finger - Support infant behind shoulders, body flexed around mum, nose at level of nipple - Tease infant with underside of areola to encourage wide gape, then quickly bring INFANT to the BREAST - should be no clicking or sucking in of infants cheeks, slow even rhythm with deep jaw movements, pauses are normal - come off breast spontaneously
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Number of breastfeeds per day
8-12 typically | Typically will establish pattern within first week
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Absolute contraindications to breastfeeding
HIV infection (but discuss with specialist) Active TB Breast Ca treatment Breast syphilis Brucellosis Infant metabolic conditions requiring special formula (e.g. galactosaemia)
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Advice around smoking and breastfeeding
Ideally quit smoking during pregnancy and breastfeeding If unable to quit, reduced as much as possible COMPLETELY avoid smoking 60 minutes prior to feed (and during feed) Never smoke in same room as infant Champix and Zyban are not safe during pregnancy or lactation
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Signs to monitor if breastfeeding has established
- Content neonate after feed (though may cluster feed at certain period of each day) - time remaining on breast (should never be >60 mins) - passing urine at least 1x/day first few days (6+ times/day as volume increases) - transitional stools by 24-48h-> breastfed stools by day 3-4 - appropriate weight gain (averaged over 4 week period)
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What is lactogenesis stage I
After maturation of alveoli of breasts due to prolactin, progesterone and human placental lactogen -> breast able to secrete small amounts of specific milk components (e.g. lactose) - complete by mid pregnancy Milk production is inhibited in late pregnancy by high progesterone levels
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What is lactogenesis stage II
Rapid increase in milk production in the first 30-40h following delivery of placenta (due to progesterone withdrawal)
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Average breast milk production per day
800mL/day AVERAGE
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Milk ejection reflex
Sucking -> pulse of oxytocin from posterior pituitary -> contraction of myoepithelial cells surrounding alveoli -> milk ejected into ducts and lactiferous sinuses
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Symptoms women may get due to milk-ejection reflex
- No symptoms at all - tingling/prickling/pins and needles sensation - sudden feeling of fullness - increase in skin temperature - feeling of wellbeing/relaxation - pain or nausea - dripping/leaking from other breast - intense thirst - uterine contractions + gush of lochia - slow sucking of infant (approx 1/sec)
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Recommended nutrition for lactating women
- overall increased energy requirements - intake affects micronutrient composition of breastmilk only Vitamin D and iodine (150 microg/day supplementary) is recommended
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Advice to give vegan mothers who choose to raise infant on vegan diet
Breastfeed as long as possible (ideally 2+ years) If not, then soy-based formula for the first 2 years AND dietary advice Likely will require supplements especially for iron and B12
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Schedule of solids introduction in infants
From AROUND 6 months (4-6mo depending on infant signs) First introduce IRON-RICH foods (iron-enriched cereals, pureed meat/poultry/fish, cooked tofu and legumes) 6-8 mo: purees -> mashed -> minced -> chopped foods Ensure lumpy foods <9mo 8mo: finger foods 12mo: same foods as rest of family, continue iron-rich foods, small frequent servings of nutrient-dense foods
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Recommended drinks to offer infants/children
NOTHING other than breastmilk/formula first 6 months Cows milk: only with cereals etc <12mo, >24mo max of 500mL/day Water (after 12mo) Fruit juice, soft drinks, cordial should be avoided Tea, coffee, caffeinated drinks are unsuitable
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Foods to avoid in infancy
Honey - do not give <12months due to risk of botulism Animal milks - FSCM ONLY with cereals/custards etc. in first 12 months - goat's milk NEVER GIVE TO A CHILD - unpasteurised milk NEVER GIVE - plant based milks (only acceptable is soy follow-on formula) - nutrient poor, high fat/salt/suagr foods (e.g cakes, biscuits, chips, lollies etc)
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Definition of subgaleal haemorrhage
Bleeding into the space between the epicranial aponeurosis and the periosteum
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Cause of subgaleal haemorrhage
Rupture of emissary veins (which connect dural sinusess to scalp veins) Most commonly after vacuum delivery
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Potential consequence of subgaleal haemorrhage
Life threatening haemorrhage - up to 250mL (50-75% of neonatal blood volume) can bleed into subgaleal space, with only a 1cm increase in scalp thickness
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Mortality associated with subgaleal haemorrhage
12-25% in infants admitted to NICU
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Risk factors for subgaleal haemorrhage
- Instrumental delivery (esp vacuum) - nulliparous - 5 min apgar 7 or less - cup marks on sagittal suture - leadingedge of cup <3cm from anterior fontanelle - failed vacuum extraction (requiring forceps/LSCS) - high number of pulls/cup detachments/prolonged time from cup attachment to delivery
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Clinical features of subgaleal haemorrhage
Insidious onset Localised signs: - vague generalised scalp swelling - laxity of scalp - then becomes fluctuant - ballotable lesion crossing suture lines - pitting oedema over scalp/preauricular/periorbital Generalised signs: - 5 minute apgar 7 or less without asphyxia - irritable cry or evidence of pain with handling - haemodynamic instability (later sign) (tachycardia, tachypnoea, poor activity, pallor, anaemia, coagulopathy, acidosis, death)
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Clinical features of caput succadaneum
Can cross suture lines and midline | Size and firmness starts to reduce 1h post delivery
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Clinical features of cephalohaematoma
(bleeding between periosteum and underlying skull) more common after instrumental delivery Soft, fluctuant, localised swelling with well-defined outline Does NOT cross suturelines Canincrease in size over 12-24 hours
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Prevention of subgaleal haematoma
Promote neonatal IM vitamin K after instrumental delivery +++ Avoid vacuum when contraindicated Ensure correct placement of cup, correct traction, and abandonment if too many pulls/detachments/prolonged
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Early diagnosis guidelines for subgaleal haematoma
Surveillance of different levels for all infants post instrumental delivery If higher risk (ie lots of pulls/detachments etc, more difficult extraction, incorrect cup placement) should have regular formal observations for 12 h, and cord gas + Hb and platelets at delivery
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Management of possible subgaleal haemorrhage
Immediately discuss with neonatologist Prompt evaluation, resuscitation and supportive treatment - restore circulating blood volume (IVT, blood products) - circulatory support - correct acidosis or coagulopathy Transfer to NICU
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Definition of neonatal hypoglycaemia
Low BGL <2.6mmol/L (note that intervention thresholds may differ according to clinical situation e.g. preterm deliveries or at risk babies intervention threshold is lower at 2.0 due to expected drop in BGL)
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Risk factors for neonatal hypoglycaemia (14)
- nil by mouth - preterm birth - respiratory distress/TTN - LGA/macrosomia - IUGR - hypoxic-ischaemic events - systemic conditions e.g. infection - hypothermia (<36C) - inborn errors of metabolism - maternal medications (esp. beta blockers or valproate) - hyperinsulinaemia - maternal diabetes - congenital hyperinsulinaemic hypoglycaemia - iatrogenic hypoglycaemia
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Reasons- to check BGL in an infant not considered "at risk"
- disinterest in feeding for 8h or more from birth/last feed - hypothermia <36 - jitteriness
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Recommendations for neonatal hypoglycaemia screening
Screen all at risk neonates at 1 and 4h (SA PPG)
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Symptoms of neonatal hypoglycaemia
Mild- moderate: Neuro: irritability, jitters, tremors, hypotonia, lethargy, temperature instability, high-pitched cry Respiratory: tachypnoea CVS: tachycardia, diaphoresis Gastrointestinal: poor-feeding, vomiting SEVERE: Neuro: eye roll, seizures, altered conscious state Resp: hypoventilation, apnoea, cyanosis CVS: pallor
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Investigations to consider in neonatal hypoglycaemia
``` Serum glucose insulin Growth hormone Cortisol Ketone level (via UA or glucometer) ```
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Basic nursing management of neonatal hypoglycaemia
Check temp and manage as indicated Offer breastfeed/EBM or formula as soon as practical Alert medical team Recheck BGL in 30-60 min
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Management of neonatal hypoglycaemia
BGL 1.5-2.5 (or 2.0): - offer feed - consider 10% glucose infusion at 60mL/day esp if respriatory distress - repeat in 30-60 min aiming for >2.5 if enteral or >3.5 in IV replacement <1.5 at any time (or baby with major illness <2.5) URGENT MANAGEMENT REQUIRED - IV 10% glucose bolus 2ml/kg + infusion 90mL/day - IM glucagon if IV access delayed - repeat BGL in 30 min - Aim for >3.5mmol by 30-60 min Advice from paediatric team
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Risk factors for neonatal jaundice
Set up for haemolysis - previous child with antibody mediated HDN - FHx G6PD deficiency or inherited red cell membrane/metabolic defects (hereditary spherocytosis, PKD etc.) - +ve maternal blood group antibody screen and +ve cord DAT to antibodies associated with HDN - visible jaundice of any degree within first 24h Weight loss >10%/poor feeding Gestation 35-38 weeks Unwell infant OR Confirmed/likely haemolysis - in utero haemolysis on basis of fetal anaemia + pos maternal antibody screen - rate of rise of SBR >5 without PTx or continued rise despite PTx - baby with bilirubin above exchange level
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Maternal blood group antibodies associated with haemolytic diseaese of the newborn
Anti-D Anti-C Anti-kell Others including Anti-A or -B are less likely to cause haemolysis
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Recommended monitoring for neonatal jaundice
Daily clinical assessment for low risk babies prior to discharge - blanching of skin with finger tip in appropriate light OR - transcutaneous POC light reflectance meter higher risk babies requireblood bilirubin measurements
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Clinical assessment of neonatal jaundice
Extending below nipple line has high sensitivity for plasma levels >75th centile - therefore should be checked with bilimeter and/or SBR Clinical assessment is limited in dark skinned babies, therefore should be checked with bilimeter or blood level
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Bilimeter use and efficacy
Unaffected by gestation, postnatal age or skin pigmentation Underestimates total bilirubin level, especially at higher blood levels - therefore blood bilirubin should be checked if bilimeter result >75th%ile
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Use of hour-specific bilirubin charts in neonates
Only validated in well babies without haemolysis | Therefore should only be used in well babies >38 weeks chart, and well babies 35-37+6 weeks
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Indications of exchange transfusion
1. Rising bilirubin despite intensive PTx, approaching exchange line 2. anaemia with Hb <100, cardiac failure, or hydrops 3. Suspected kernicterus regardless of bilirubin level
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Definition of prolonged neonatal jaundice
>2 weeks in >35/40 gestation OR >3 weeks in <35/40 gestation Requires investigation, advise parents to present for medical review if any visible jaundice after 2 weeks, or if pale stools at any time
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Standard investigations for prolonged neonatal jaundice
1. Review NNST results 2. Total and conjugated bilirubin 3. Free T4 4. Urine culture If above all normal and healthy breast fed baby, reassure that breast milk jaundice, and will resolve over 2-3 months
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Follow up of jaundiced babies
HEARING: AABR for neonatal screening rather than usual test if: - jaundice due to haemolytic disease - bili >350 in term baby - bili >250 in sick term, of a preterm >32/40 - all babies <32/40 or 1500g BW Should be performed as close to discharge from hospital as possible. If passes, no routine audiology f/up required ANAEMIA: - if confirmed haemolysis, close f/up over 4-6 weeks to watch for late anaemia - Most likely with Rh isoimmunisation - weekly CBE and reticulocyte - folic acid supp where continued haemolysis suspected - if unusual haemolysis, haem advice ENCEPHALOPATHY - if any symptoms/signs or who have been unwell with jaundice require long-term follow-up with paediatrician
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10 significant viral infections in pregnancy:
1. CMV 2. Parvovirus 3. Rubella 4. Measles 5. Mumps 6. Varicella 7. HIV 8. Hepatitis A 9. Hepatitis B 10. Hepatitis C
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Most common manifestations of congenital cytomegalovirus infection
``` Deafness Mental disability Hepatitis Pneumonitis Blindness ```
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Transmission of cytomegalovirus
Transmitted through infectedblood, saliva, urine, breastmilk or through vertical transmission (in utero or intrapartum) or sexual contact
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Risk of CMV infection in pregnancy transmitting to neonate
In primary infection - 50% | In reactivated disease: only 1% transmission rate
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Features associated with symptomatic fetal infection (11)
``` Microcephaly Ascites Hydrops fetalis Oligo or polyhydraminos Hepatomegaly Pseudomeconium ileus hydrocephalus IUGR pleural or pericardial effusion Intracranial calcification Abdominal calcification ```
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Rate of symptomatic congenital CMV in babies to mothers who develop infection in pregnancy
50% transmission in PRIMARY infection - 10% of infants will be born symptomatic 90% of these infants will develop sequelae (10-30% mortality rate, 18% hearing loss, neurological conditions - microcephaly, intellectual impairment, seizures, chorioretinitis)
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Diagnosis of CMV in pregnancy
Maternal: CMV serology and repeat 2-4 weeks (if IgG -ve to positive OR rising then primary infection)
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Management of CMV in pregnancy
Supportive management of mother Check for fetal infection (amniocentesis for PCR/viral culture and serial USS) Counsel mother re: option to continue pregnancy v terminate Counsel re: risk of congenital CMV up to 4y following seroconversion (1% risk in 4th year)
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Management of newborn with known congenital syphilis
Paeds at delivery for detailed examination Test: - ophthal examination - cranial USS ?hydrocephaly - CT brain - intracranial calcification, verntriculomegaly, cerebral atrophy Labs <3weeks: - CMV IgM serology - PCR for viral detection +/- viral culture (blood, urine, NPA) Consider ID input ?antivirals Paeds review every 3-6 months if asymptomatic, likely more if symptomatic depending on presentation
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Main pathophysiology behind congenital CMV
Fetal infection causes cytolysis leading to areas of focal necrosis and healing by fibrosis and calcification
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Transmission of parvovirus
Direct contact with respiratory secretions and hand-mouth contact Vertical transmission Most infectious from 1 week after exposure to before rash onset (likely not infectious after that)
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Clinical features of parvovirus
30-40% subclinica Fever, myalgias and malaise which settle prior to rash onset (slapped cheek/reticular macular rash) Arthralgia or arthritis common adults, can develop few weeks after infeciton Can cause aplastic crisis in people with thalassaemia or sickle cell anaemia
185
Advice to pregnant women to avoid parvovirus
Standard precautions Susceptible pregnant HCW avoid caring for women with known parvovirus Routine screening not recommended
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Complications of fetal parvovirus infection
``` Spontaenous miscarriage/stillbirth - 13% risk <20/40 - 0.5% risk >20/40 Hydrops fetalis - 3% risk if maternal infection 9-20/40 - on average 5 weeks after maternal infection ``` No evidence of congenital anomalies or long term sequelae for infant
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USS findings of hydrops
Ascites Skin oedema Pleural and pericardial effusions Placental oedema
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Management of pregnant women exposed to parvovirus
Check IgG and IgM - if IgG positive = immune, no further management - if IgG negative monitor in 2-4 weeks ?seroconversion If infection confirmed, serial USS every 1-2 weeks to assess for hydrops, if any signs, refer to MFM
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Epidemiology of varicella in pregnancy
up to 4% of pregnant women NOT immune VZV in pregnancy is complicated by pneumonia in 10% of cases 20-30% risk of transmission to neonate
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Transmission of varicella
- through airborne/respiratory droplets and direct contact with vesicle fluid - contagious from 2d before rash until all lesions crusted over (approx 1 week after onset)
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Risk of foetal varicella syndrome in maternal varicella infection
0.5% risk in 1st trimester 1.4% risk in 2nd trimester Nil in 3rd trimester (but may be at risk of neonatal disease if around time of delivery)
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Consequences of foetal varicella syndrome
``` Skin scarring Eye and limb abnormalities IUGR/LBW Prematurity Cortical atrophy, intellectual disability Decreased sphincter control Early death ```
193
Risk of severe neonatal varicella infection secondary to maternal infection
If primary CHICKENPOX disease onset in mother >7 days before delivery, neonatal infection is mild (as maternal IgG is protective) If <7days before or 2 days after, risk of severe infection No risk if shingles infection - shingles in otherwise healthy pregnancy is not associated with intrauterine infection
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Definition of significant varicella exposure for pregnant woman
Same household as someone with active varicella Direct face-to-face contact with a person with varicella for at least 5 minutes Same room for at least 1 hour
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Prevention of foetal varicella syndrome
Preconceptual varicella serology+/- immunisation If <96h post exposure and seronegative, give zoster immunoglobulin and seek medical care immediately if develop chicken pox If >96h post exposure consider oral antivirals if >20 weeks, lung disease, immunocompromised or active smoker
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Management of maternal varicella infection in pregnancy
Isolate If <24h since appearance of rash- oral antivirals If >24h since onset of rash: - no antivirals - monitor at home unless underlying lung disease, ISS, or active smoker (in which case monitor in hospital) Complicated varicella infection (respiratory, haemorrhagic o neurological symptoms, fever >6 days, newpox developing after 6 days) - 7-10 days aciclovir 10mg/kg for 7-10 days (iV then oral)
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Management of neonates exposed to varicella
Maternal chickenpox >7 days before delivery: No interventions unless <28/40 or <1000g then IV aciclovir Maternal chickenpox <7 days before to 2 days after delivery: ZIG 200IU <24h after birth ideally (up to 72h) no isolation req, still breastfeed Maternal chicken pox 2-28 days after delivery (or other exposure when mumw as seronegative): Consider ZIG <96h Maternal shingles - no risk
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Varicella zoster immunoglobulin doses
Neonates: 200iu IM (1x vial) Adults: 600IU I (3 vials)
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Risk of vertical transmission of herpes simplex
40-50% risk in women with primary infection + active lesions at time of vaginal delivery/ROM 1-3% risk if lesions associated with recurrent infection (thought HSV1 higher at 15%, HSV2 <0.01%)
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Risk factors for intrapartum neonatal infection with herpes simplex
Maternal PRIMARY infection Multiple lesions Premature delivery Premature rupture of membranes
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Management of HSV in pregnancy
If pre-existing: - consider suppressive antiviral therapy from 36/40 if multiple recurrent lesions or sooner if frequent symptomatic recurrences - careful speculum in early labour to check no active lesions If first episode in pregnancy: - obtain type specific HSV serology and PCR/culture from swab (if both positive for same type then likely recurrent infection) - if confirmed new primary <28 weeks, counsel as per pre-gestaional - if diagnosis >28/40, consider suppressive therapy from 36 weeks + caesarean delivery regardless of active lesions If first episode diagnosed during labour: - LSCS - HSV type specific PCR on genital swab
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Neonatal management of HSV exposure
Asymptomatic low risk neonate (e.g. maternal seroconversion >6 weeks before birth) - normal postnatal care - at 24h post birth collect surface swabs (eye, throat, umbilicus and rectum) for HSV1/2 PCR - collect urine for HSV1/2 PCR - observe for signs of infection Asymptomatic high risk infant (i.e. maternal HSV close to birth or born through active HSV disease and no previous history of genital HSV) - paeds at birth, complete exam for signs of HSV - neonatal care unit - urine for HSV 1/2 PCR - CBE (?low PLT) - LFT - coags - HSV PCR on bloods - LP - commence IV aciclovir - surface swabs 24h after birth Symptomatic infant - Above tests - IV aciclovir 14-21 days - repeat LP after 7h if initially negative with signs of CNS disease - repeat LP near end of treatment completion to confirm clearance
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Clinical signs of neonatal HSV (9)
Vesicular skin lesions, atypical pustular or bullous lesions (especially on presenting part) - ulcers involving buccal mucosa - corneal ulcer, conjunctivitis, keratitis - seizures - unexplained fever or sepsis with negative blood cultures, not responding to antibiotics - low PLT - elevated LFTs - DIC - respiratory distress 24h after birth
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Clinical features of rubella infection
Asymptomatic in 25-50% May have: - low grade fever - transient erythematous rash - cephalocaudal spread with caudocephalic resolution within 3 days - arthritis and arthralgia (most commonly in women of child-bearing age) - neuro disorders, thrombocytopaenia (rare)
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Infectious period of rubella
1 week before until 4 days after onset of rash
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Incubation period of rubella
14-23 days
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Potential (general) outcomes of a maternal rubella infection
``` No effect on fetus Placental infection only Placental/fetal asymptomatic infection, but can affect organs IUFD/miscarriage Congenital rubella syndrome ```
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Risk of congenital rubella complications by gestation
- 90% of fetuses <8 weeks will be affected - 50-80% fetuses 8-12 weeks will be infected, half of these will have fetal defects - 12-16 weeks 30% fetuses infected, 10%overall risk of fetal defect (sensorineural deafness most likely) - >16 weeks fetal manifestations rare Maternal reinfection in immune women very low risk of fetal damage
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Potential features of congenital rubella syndrome
Sensorineural deafness CNS dysfunction (intellectual impairment, developmental delay, microcephaly) Eye abnormalities (cataracts, retinopathy, glaucoma, strabismus, micropthalmos) Cardaic abnormalities (PDA, PA stenosis) IUGR, short stature Inflammatory lesions of brain, liver, lungs and bone marrow
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Women who require post natal MMR vaccination
Anyone with Rubella IgG <10 OR 10-20 if born in Australia or the Western world Should receive a second dose of MMR 4 weeks after the first **ensure to inform NOT to get pregnant within 28 days of vaccination
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Diagnosis of maternal rubella
Test rubella specific IgG and IgM for any pregnany woman with contact with OR clinical features of rubella If both positive - possible recent infection, repeat test to confirm (4-fold increase in IgG titre is indicative of recent infection) If both negative - susceptible - repeat serology if <3 weeks since contact or <7 days since onset of illness - if no seroconversion, requires postnatal immunisation - if seroconversion occurs, then consistent with maternal infection IgG negative, IgM positive - possible recent infection - repeat - if no IgG seroconversion occurs may be false positive IgM (occurs especially in presence of rheumatoid factor) IgG positive, IgM negative - past infection or immunisation
212
Counselling women re: seroconversion that indicates maternal rubella infection
Counsel regarding risks relevant to gestation - termination should be offered if infection occurs in first trimester - consider fetal testing if maternal infection in 2nd trimester (CVS may be appropriate in 1st trimester if couple are uncomfortable about termination based solely on risk of fetal infection) i. e. rubella PCR, culture and fetal IgM through CVS, amniocentesis or fetal blood sampling
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Pre-pregnancy management of woman with HIV
Refer to HIV physician, sexual health physician and high risk obstetric consultant for discussion and screening Ensure CST up to date (within last 12 months)
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Management of HIV positive woman in pregnancy
Routine antenatal bloods+ serology for CMV, VZV, HSV, toxoplasmosis, cryptococcus, candida - CBE, CD4 count, lymphotcyte subsets - HIV viral load and resistance testing (unless already known) - baselineLFT, EUC, amylase, lactate, HLA B5701 Refer to tertiary centre for MDT management with HIV specialist, ID specialist and High risk/MFM obstetrician
215
Intrapartum management of HIV positive woman
If SROM, consider augmentation If PPROM 34-37 weeks, immediate delivery (with antibiotic and steroid cover) If <34 week PPROM- MDT discussion and planning If viral load undetectable at or after 36 weeks, can have vaginal delivery without intrapartum zidovudine If viral load <400 - intrapartum zidovudine and consider LSCS If viral load >400 intrapartum zidovudine and plan LSCS
216
Factors which increase risk of maternal to child transmission of HIV
>70% occurs in labour Risk increased by: - advanced maternal illness - high viral load - poor maternal immune status (e.g. low CD4 count) - ROM >4h before birth - Preterm birth - breastfeeding - procedures that may damage integrity of natural barriers (e.g. FSE, vigorous suctioning, injections through unwashed skin, invasive testing such as CVS)
217
Tests performed in HIV screening
Screening test with ELISA for HIV antibody -if positive, then confirmed with Western Blot (if indeterminate, discuss with reference lab + virologist)
218
Risk of perinatal hepatitis B transmission
If mother is HBeAg positive risk is 70-90% of developing HBV infection by 6 months (if does not have HBIG and postpartum Hep B immunisation) Risk with administering HBIG and Hep B reduces to 5-10% If acute HBV in 1st or 2nd trimester, risk of transmission to newborn 10%, if in 3rd trimester, risk approx 75%
219
Recommended antenatal screening for hepatitis B
HBsAg to ALL pregnant women - positive = infection with Hep B Can have false negatives though due to mutation in HBsAg therefore all women in HIGH RISK groups should also be screened with HBcAB
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Further tests recommended if pregnant woman found to be HBsAg or HBcAb positive
HBeAg (positivity indicates high infective status) HBeAb (positivity indicates lower risk of spreading HBV infection) HBcAb LFTs (and repeat at 28 weeks) CBE HBV viral load (repeat before 32 week gestation)
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Management of HBV in pregnancy
Refer to ID specialist and high risk obstetric unit. If high viral loads may be considered from approx 32 weeks (or 28) to reduced risk of perinatal transmission(not indicated if very low viral laod)
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Postpartum management of neonate born toHBV positive mother
HBIG 100 units AND HBV vaccine given within 12 hours - skin should be cleaned prior to injection - continue with normal childhood HBV schedule Follow up at 8-12 months (2 months post completion of primary schedule) for HBsAg, HBsAb - if antigen positive, refer to paeds gastro or ID Breastfeeding encouraged
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Risk of perinatal transmission in HCV RNA positive women
approximately 5% - transmission is 3-4 x more likely in event of co-infection with HIV
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Postpartum management of neonate born to HCV positive mother
Clean skin with soap and water if visible blood OR with alcohol wipe prior to injections HBV vaccination within 12 hours of birth If co-infection with HBV, also requires 100IU of HBIG Test for HCV Ab at 18 months of age
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Risk of fetal transmission and congenital abnormalities of toxoplasmosis
Depends on gestation at maternal seroconversion 1st trimester - low risk of vertical transmission (5-15%) but high risk of abnormalities (60-80%) 2nd trimester - moderate risk vertical transmission (25-40%), low risk of congenital abnormalities (15-25%) 3rd trimester - 30-75% risk of vertical transmission (higher rates closer to term), 2-10% risk of abnormalities
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Abnormalities associated with congenital toxoplasmosis (9)
- Chorioretinitis/retinal scarring - Hydrocephalus - Intracranial calcification - Mental retardation - Hepatosplenomegaly - Pneumonia - Thrombocytopaenia - Lymphadenopathy - Myocarditis
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Clinical features of toxoplasmosis
``` Most patients will be completely asymptomatic Potential symptoms in mild illness: - flu-like symptoms - malaise - myalgias - Swollen lymph glands ``` ``` Severe disease (more likely in immunocompormised) - ocular toxoplasmosis (blurred vision, photophobia, red eye, tearing) ```
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Diagnosis of toxoplasmosis
Consider testing toxoplasmosis serology in pregnant women with acute symptoms (e.g. malaise, fever, lymphadenopathy) If IgG and IgM positive indicates POSSIBLE recent infection - IgM can remain positive for years - IgA, rising AigG and/or low IgG avidity are more specific for recent infection - if both are positive, repeat serology for IgM, IgA and/or IgG titre and avidity - if on repeat, High IgM, positive IgA and low IgG avidity consistent with recent toxoplasmos infection
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transmission of toxoplasmosis
Faecal-oral route - undercooked, contaminated meat (esp. pork, lamb or venison) or shellfish - contaminated water - accidental ingestion through contact with cat faeces (e.g. cleaning cat's litterbox, touching or ingesting anything that has come into contact with cat faeces, accidentally ingesting contaminated soil)
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Management of toxoplasmosis in pregnancy
Further investigations to determine risk to fetus: - USS to detect abnormalities - amniocentesis for PCR/culture at 18-20 weeks or >4 weeks after maternal infection If both above are negative, consider pharmacological treatment if maternal infection is fairly certain In 1st trimester: counsel woman/partner re: termination if amniocentesis PCR is positive 2nd trimester: Counsel re: termination if USS abnormal Spiramycin, atavaquone or azithromycin if medication indicated (unknown efficacy) 3rd trimester (as above medical treatment, termination not advised)
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Intra-/Postpartum management of toxoplasmosis in pregnancy
Paeds at delivery Newborn assessment for congenital toxoplasmosis - ophthal examination and cerebral ultrasound required - placenta for histo/PCR - infant whole blood for PCR, serology for specific IgM and/or IgA, persistent IgG - infant CSF for PCR Majority of infected babies will be asymptomatic Manage with spiramycin oral syrup for first 12 months - repeat IgG at 6 months - regular paeds/ID review
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Presentation of listeriosis in pregnancy
*always obtain a dietary history from pregnant women with febrile, flu-like ilness, myalgia, headache or diarrhoea Often asymptmatic Can mimic pyelonephritis due to loin pain
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Risks of listeria in pregnanct
In early pregnancy: fetal infection can cause miscarriage In 2nd and 3rd trimesters, if untreated maternal infection, associated with 40-50% fetal mortality (septicaemia, multi end organ damage, still birth, neonatal death) Neonatal infection: pneumonia, sepsis or meningitis Mortality rate 3-50%
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Management of maternal listeriosis infection in pregnancy
Mild: PO amoxicillin Severe: IV amoxicillin + gentamicin (if penicillin allergy, consider bactrim PO or IV if >12/40)
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Presentation of neonatal listeriosis
Variable, but most commonly: - respiratory distress - rash - fever - jaundice - lethargy Suspicious findings include: - placental, cord, or post-pharyngeal granulomas - multiple small skin granulomas, papular or pustular skin rash - Meconium stained liquor <34 weeks - purulent conjunctivitis
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Pathophysiology of UTIs in pregnancy
1. Obstructed urinary flow -> stasis -> increased risk of asymptomatic bacteriuria becoming pyelo 2. Smooth muscle relaxation secondary progesterone -> reduced bladder and ureteral tone, dilatation of renal pelvices and ureters -> increased bladder volume, urinary stasis, residual volume and VUR 3. pregnancy-induced changes in urine pH, osmolality, glycosuria and aminoaciduria may facilitate bacterial growth
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Asymptomatic bacteriuria in pregnancy statistics
occurs in 5-10% of pregnancies 30% will develop acute pyelonephritis if untreated Associated with preterm birth, LBW Antibiotics associated with reduced preterm delivery and LBW infants
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Pathogens involved in asymptomatic bacteriuria in pregnancy
E coli >80% second most common is staphylococcus saprophyticus
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Indications for antenatal MSSU
Routine MSSU at booking Repeat after contaminated specimen History of recurrent infections outside of pregnancy Structural abnormality of the urinary tract
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Gestation of highest risk of UTI in pregnancy
Risk begins at 6/40 and peaks 22-24/40
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Risk factors for UTI in pregnancy
``` Low SES Sickle cell trait DM Neurogenic bladder retention History of previous UTIs Structural abnormality of urinary tract Renal stones ```
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Diagnosis of asymptomatic bacteriuria/UTI in pregnancy
>100,000 bacteria/mL - <20 white cells (in AB) - if 2+ organisms usually contamination and should be repeated + clinical findings in acute cystitis
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General considerations for management of acute cystitis or asymptomatic bacteriuria in pregnancy
- 5 day course antibiotics (10-14 days for pyelo) - at least 48h IV if bacteraemia - increase fluid intake +/- IVT - monitor urine output - urinary alkalinisers are safe, but DO NOT USE WITH NITROFURANTOIN (will reduce efficacy) - only commence antibiotics for asymptomatic bacteriuria AFTER culture and sensitivities (not empirical based on UA)
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Antibiotics for uncomplicated UTI (empirical) in pregnancy
Cephalexin 500mg BD for 5 days OR Nitrofurantoin 100mgBD for 5 days OR Augmentin DF BD for 5 days (only if <20/40) OR Trimethoprim 300mg daily for 5 days (only if>12/40)
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Antibiotic options for asymptomatic E coli bacteriuria
1. cephalexin 500mg BD 5 days 2. nitrofurantoin 100mg BD 5 days (but don't use Ural) 3. trimethoprim 300mg daily for 5 days 4. ADF BD for 5 days
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Augmentin duo forte use in pregnancy
Only use if <20 weeks Associated with increased risk of necrotising enterocolitis, functional impairment and cerebral palsy, therefore only use inf no alternative
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Antibiotics options for staph saprophyticus asymptomatic bacteriuria in pregnancy
1. Cephalexin 500mg BD 5 days OR 2. Amoxicillin 500mg TDS for 5 days
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Antibiotics for pseudomonas asymptomatic bacteriuria in pregnancy
Norfloxacin 400mg BD 5 days | Repeat MSSU 48h after treatment completed
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Management of GBS asymptomatic bacteriuria in pregnancy
``` Penicillin V 500mg BD 5 days OR cephalexin 500mg BD 5 days OR clindamycin 450mg TDS 5 days ``` (dependent on allergies) THESE WOMEN NEED GBS PROPHYLAXIS IN LABOUR
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Management of acute pyelonephritis in pregnancy
48h minimum IV antibiotics IVT+ monitor urine output Antipyretics PRN Monitor for preterm labour Amoxicillin 2g 6 hourly IV+ gentamicin 5mg/kg daily OR ceftriaxone 1g IV daily Step down to oral antibiotics after >24h apyrexia, clinically improving. Base on susceptibilities. (doses same as for UTI except cephalexin 500mg QID) and continue for 10 days
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Indications for antibiotic prophylaxis for UTIs in pregnancy
2+ documented separate episodes of CYSTITIS (not asymptomatic bacteriuria) OR Single episode pyelonephritis
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UTI prophylaxis options in pregnancy
Nitrofurantoin 50mg nocte (be careful using close to term) OR cephalexin 250mg nocte OR trimethoprim 150mg nocte (avoid 1st trimester or in women concerned about folate)
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Indications for tuberculosis screening in pregnancy
HIV positive mothers OR recent contact with infectious TB (e.g. household) Not otherwise performed as usually treatment would be deferred until 2-3 months postpartum in latent infection
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Amphetamine effects on pregnancy
``` Amphetamines: - cardiac malformations - ?other malformations such as cleft palate - IUGR (impaired placental function) Methamphetamines(ice/speed): - preterm labour - placental abruption ``` MDMA/Ecstasy: - little evidence of obstetric complications or teratogenicity, but likely confounding effect as multi-drug users Risk of neonatal abstinence syndrome with all, lower than risk with opioids. 50% will have some withdrawal but only 5% of infants will require treatment
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Effects of marijuana in pregnancy
Crosses the placenta - may cause withdrawal syndrome in neonates of heavy users Some evidence of association with IUGR
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Definition of polyhydramnios
AFI >20cm (used to be 24cm) | OR Maximal vertical pool >8cm
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Amniotic fluid production
Mostly produced by amniotic membrane covering placenta and cord >20 weeks also contribution by fetal kidneys
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Composition of amniotic fluid
Same composition as maternal plasma for first half of pregnancy Then hypotonic compared to fetal and maternal plasma, with more urea and creatinine than plasma
259
Prevalence of polyhydramnios
Affects 1% of pregnancies
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Causes of polyhydramnios
1. Impaired swallowing - anencephaly - CNS abnormalities - myotonic dystrophy - oesophageal atresia - tetralogy of fallot 2. Reduced absorption - gut atresias 3. increased production from fetal membranes - spina bifida - anencephaly 4. Excessive urination - cardiac overload (high output cardiac failure, fetal anaemia) 6. Increased placental area - multiple pregnancy - diabetes - placental tumour (rare)
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Complications associated with polyhydramnios
Maternal: - overdistention -> PROM - pain - unstable lie - cord prolapse - abruption - PPH Fetal/neonatal: - associated fetal anomalies - asphyxia from cord prolapse - prematurity
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Clinical features of polyhydramnios
- SFH large for dates - tense abdomen - difficulty palpating fetal parts - reduced fetal movements
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Investigations to consider in polyhydramnios
USS (to confirm) - detect fetal structural anomalies Diagnostic amniocentesis Exclude treatable causes (fetal anaemia, cardiac failure)
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Oligohydramnios definition
Varies with gestational age, but generally: AFI <5cm Deepest pool (MVP) <2cm
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Causes of oligohydramnios
MATERNAL: - PROM - poor placental diffusion - drug effect FETAL: - hypoxia - fetal anomalies (renal agenesis, renal dysplasia, urethral valve anomalies)
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Complications associated with oligohydramnios
High risk pregnancy Fetal anomalies IUGR Fetal hypoxia (related to poor placental function) Early severe oligohydramnios associated with pulmonary hypoplasia and fixed deformities of flexion
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Risks associated with poor glycaemic control in pregnancy
- congenital malformations - pregnancy complications (macrosomia, IUGR, preterm birth, PET, shoulder dystocia, IUFD) - operative delivery or LSCS - Neonatal complications (hypoglycaemia, jaundice, respiratory distress)
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Hypoglycamic agents safe in pregnancy
Metformin Insulin All else have limited evidence and should be discontinued prior to pregnancy
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Pre-conception counselling for pre-existing diabetes
- Discuss risks of poor glycaemic control in pregnancy - plan reviews with woman's GP, endocrinologist/physician, DNE - delay attempts of conception until BGL optimised (HbA1c <75, ideally <6.5% - change to pregnancy safe hypoglycaemics (metformin, insulin) - If T1DM, consider change to continuous subcut pump (refer to diabetes service) - folate 5mg daily for 6 weeks prior to conception
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Antenatal care specific for women with pre-existing diabetes
- refer to high risk clinic + DNE - aspiring 100mg nocte - weekly DNE monitoringofBGL - 2-4 weekly specialist appointments ADDIT investigations: - booking: HbA1c, TFTs, early morning spot urine ACR - UA for protein every visit - confirm dates with dating scan - consider early 16/40 morphology if appropriate - If HbA1c >10%, fetal echo at 20-22 weeks - Consider growth scans in third trimester BGL MONITORING: - change monitoring to include fasting+ 2h post-prandial measurements REFER: - ophthal - high risk clinic, obs med, endo, DNE
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Timing of birth for women with T1DMor T2DM
Should always occur <40+6 (but only if BGL within target, normal growth and AFI and otherwise uncomplicated pregnancy) Induction at 38+6 if: abnormal AFI, difficulty maintaining target BGL at 38/40, macrosomia or IUGR, HTN/PET developing IF birth likely <37+0, consider steroids for fetal lung maturity, admitfor additional glucose monitoring and increased insulin at direction of obs med/endocrine
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Method of birth for women with pre-existing diabetes
Vaginal birth is safe if EFW <4kg - discuss risks of IOL and potential shoulder dystocia
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Intrapartum care for women with T1DM
CTG Consul with physician Avoid prolonged labour and water overload If ordered, give oxytocin with NORMAL SALINE (not Hartmann's) to prevent hyponatraemia Insulin infusion as per protocol, with hourly BGL monitoring
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Intrapartum care for women with T2DM
Continue pre-existing insulin regimen until labour is established, or no later than midnight on day of admission for IOL Continue metformin until labour established Hourly BGL (if >8 over 2h period and birth not imminent, to commence insulin infusion) Continuous CTG If giving oxytocin, give with normal saline Beware of risk of shoulder dystocia Cease dextrose/insulininfusionimmediately after birth
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Management of neonates born to women with T1/T2DM
Paediatrician aware of birth Feed within 60 minutes (ideally BF) First BGL <1h of age Most babies need close observation in nursery for hypoglycaemia, polycythaemia, jaundice, hypocalcaemia, RDS
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Postpartum care for women with non-gestational diabetes
Send placenta for histopath Review hypoglycaemic therapy early (risk of hypos) Appropriate contraception Encourage breastfeeding for minimum 2 months Ensure appropriate hypoglycaemic agents for breastfeeding
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Hypoglycaemics safe in breastfeeding
Insulin (all forms) Metformin Glibenclamide and glipizide (NOT gliclazide or glimeprimide) NOT SAFE: - glitazones, acarbose, DDP-4 inhibitors (-gliptins), GLP1 antagonists and SGLT-2 inhibitors
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Target BGLs in pregnancy
Fasting <5 Postprandial (2h) <6.7 If 2 or more of the same reading is elevated in one week, step up in management
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How to administer OGTT in pregnancy
``` 75g glucose load Fast from food for at least 8h Drink glucose over 10-15 minutes Remain seated and non-smoking for duration of test Blood at fasting, 1h, and 2h ```
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Contraindications to OGTT
Gastric bypass surgery | gastric banding usually okay
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When to perform an early OGTT in pregnancy (8)
In women who are at risk for OVERT diabetes in pregnancy (FBG >7 or 2h BGL >11) - previous hyperglycaemia (including in pregnancy) - maternal age >40y - ethnicity: Asian, Indian subcontinent, ATSI, Pacific islander, Maori, Middle eastern, non-white African - Family history of DM (1st degree relative with DM OR sister who had GDM) - pre-pregnancy or booking BMI >30 - Previous macrosomic baby (>4.5kg or >90th centile) - PCOS - Medicated with steroids or antipsychotics
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Statistics of DVT in pregnancy
90& occur in LEFT leg | >70% are iliofemoral (higher risk of embolisation than calf DVT)
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Management of VTE in pregnancy
LMWH 1mg/kg BD 3 months if uncomplicated distal DVT OR 6 months for PE or proximal DVT If therapy finished before end of pregnancy, prophylactic dose should continue until 6 weeks postpartum
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Postpartum options for pharmacological treatment or prevention of VTE
LMWH - safe in breastfeeding Warfarin - safe in breastfeeding NOT SAFE IN PREGNANCY NOACs unsafe in pregnancy AND breastfeeding
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Management of uncomplicated superficial thrombophlebitis in pregnancy
Aspirin 100mg for 5-7 days + TEDS + analgesia | If not resolved, for enoxaparin 40mg for 7-10 days, if not resolved for ultrasound
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Features which complicate superficial thrombophlebitis in pregnancy (and indicate management with enoxaparin from outset)
Previous episodes in current pregnancy Length >20cm Previous personal or family history (1st degree) of DVT
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Incidence of VTE in pregnancy
0. 5-2/1,000 pregnancies affected - 25% are PE - 1 in 40 PE in pregnancy is fatal
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Increased risk of VTE in pregnancy and postpartum period
5-10 fold increased risk antenatally | Further 15-25-fold increased risk postpartum
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Factors in assessing women with history of VTE for antenatal prophylaxis
If on previous long-term anticoagulation (therapeutic dose LMWH) 2 or more previous VTE (prophylactic or intermediate dose LMWH) 1 previous unprovoked or oestrogen related VTE (prophylactic dose) 1 previous VTE provoked by non-oestrogen transient risk factor (surveillance)
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Consideration of antenatal VTE prophylaxis in women with family history of VTE
If 1st degree relative with VTE NOT in setting of active malignancy - clinical vigilance or prophylactic LMWH if significant clinical risk factors
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Antenatal VTE prophylaxis for women with known thrombophilias
Protein C or S deficiency OR FVL heterozygote: clinical vigilance FVL homozygotes, prohrombin gene mutation homozygotes, double heterozygote FVL/PGM or antithrombin deficiency: clinical vigilance may be appropriate if no family history of VTE, if family history prophylactic LMWH at least
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Side effects of long term LMWH
``` Bruising and pain at injection site Allergic skin reaction (rare) Thrombocytopaenia (HIT uncommon) Reversible osteoporosis Rise in ALT ```
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Contraindicationsto LMWH use in pregnancy
History of HIT Actively bleeding High risk (e.g. placenta praevia) Delivery expected within 24h Intracranial haemorrhage or ischaemic stroke within past 4 weeks Uncontrolled hypertension (SBP>200 or DBP>120) Precautions: CrCl <30 PLT <80 Coagulopathy
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Peripartum LMWH considerations
Therapeutic LMWH - no regional analgesia for 24h Prophylactic LMWH- no regional analgesia for 12h No LMWH within 4h of spinal or removal of epidural
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Causes of thrombophilias
``` Inherited: PROGOACULANT factor abnormalities - FVL mutation (causes activated protein C resistance) - prothrombin gene mutation - plasminogen activator inhibitor ``` DEFICIENCIES of endogenous proteins in coagulation cascade: - Protein C deficiency - Protein S deficiency - Antithrombin deficiency ACQUIRED: - lupus anticoagulant - antiphospholipid antibodies - anticardiolipin antibodies MIXED inherited/acquired: - hyperhomocystinaemia
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epidemiology of thrombophilias in pregnancy
15% of Western populations are affected with inherited thrombophilia Inherited disposition can be identified in 60-70% of women presenting with DVT
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Indications for investigating a woman for thrombophilia
- Strong family history of VTE in 1st and 2nd degree relatives (only check for inherited conditions) - recurrent (3+) first trimester miscarriages - Second trimester fetal loss - any previous history of VTE - stillbirth - Early onset PET <34 weeks - IUGR delivered <34 weeks
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Investigations to consider in thrombophilia screen
``` Lupus anticoagulant Protein C and S (Protein S should not be measured in pregnancy) Activated protein C resistance (APCR) Factor V leiden Prothrombin gene MTHFR homocysteine Anticardiolipin antibody ```
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Antenatal management of women with thrombophilias
Refer to obs med/physician/obstetrician with expertise Arrange ongoing care in level 2-3 hospital Antenatal aspirin Increased feto-placental surveillance antenatally Consider if LMWH heparin necessary
300
Factor V Leiden statistics
Heterozygosity present in 20-40% of non-pregnancy people with VTE Homozygosity carries 80-fold increased risk for VTE Occurs in 5-15% of European populations (rare in Asian or African populations) Risk of VTE in pregnancy for FVL carriers is 0.2% (due to low prevalence in pregnancy overall)
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Obstetric risks associated with factor v Leiden disease
``` Second and third trimester fetal loss Severe IUGR Abruption Severe early onset PET Preterm delivery Increased risk of pathological Doppler measurements ```
302
how to screen for factor V leiden disease
Screen with abnormal phenotype (Activated protein C resistance/APCR)
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Prevalence of Prothrombin gene mutation
2-5% prevalence | More prevalent in Caucasian women
304
Obstetric risks associated with prothrombin gene mutation
3-fold increased risk VTE ?PET (controversial association) IUGR Placental abruption
305
Which thrombophilia screens are altered in pregnancy
Protein S - there is a marked physiological decrease in pregnancy, therefore should not take until at least 8 weeks postpartum
306
Prevalence of protein C and S deficiency
PC: 0.3% PS: 0.1%
307
Obstetric risks associated with protein C and S deficiency
``` VTE Stillbirth Fetal loss (PS deficiency associated with recurrent loss) PET Abruption IUGR ```
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Epidemiology of antithrombin deficiency
Rarest of inherited thrombophilias but MOST thrombogenic- only thrombophilia that will ALWAYS require thromboprophylaxis in antenatal and postnatal period Prevalence 1 in 1,000-5,000
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Definition of antiphospholipid syndrome
Autoimmune disorder defined by associated of vascular thrombosis and/or pregnancy morbidity with specified levels of antiphospholipid antibodies (either Lupus anticoagulant or anticardiolipin antibody)
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Epidemiology of antiphospholipid syndrome
Most common acquired thrombophilia in pregnancy Predominantly affects young women Prevalence in pregnancy approx 2%
311
Who to screen for antiphospholipid syndrome and how
ANF and ACA in women with history of: - early onset(<32w) PET and/or IUGR - fetal death - placental abruption
312
Obstetric risks associated with antiphospholipid syndrome
``` Recurrent early pregnancy loss (<10 weeks) PET Thrombosis Abruption IUGR preterm birth ```
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Diagnosis of antiphospholipid syndrome
Lupus anticoagulant detected on 2 or more occasions at least 6 weeks apart Anticardiolipin antibodies with moderate-high IgG or or IgM antibodies on 2 occasions at least 6 weeks apart
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Antenatal management of women with antiphospholipid syndrome
Aspirin 100mg/day - if history of late fetal loss or IUGR - early dating scan - close BP and UA surveillance - uterine artery dopplers at 20 and 24 weeks(if abnormal, consider 2-3 weekly scans) - 4 weekly scans to assess growth and AFI if uterine arteries normal - consider heparin
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Contributors to hyperhomocystinaemia
``` Deficiencies in Vit B12, folate, B6 GI malabsorption Renal disease Thyroid deficiency Smoking Coffee and alcohol consumption ```
316
Risks associated with hyperhomocystinaemia
- early onset PET - placental abruption - neural tube defects - stillbirth - IUGR - Vascular disease - recurrent VTE (if severe) - fetal loss
317
most common gene mutation causing hyperhomocystinaemia
MTHFR
318
Antenatal management of women with hyperhomocystinaemia
``` Avoidsmoking, alcohol, coffee Well balanced diet Folic acid Early dating scan + 12 weeks scan for neural tube defect Close PET surveillance Regular growth and wellbeing ultrasound ```
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Prevalence of hyperthyroidism in pregnancy
0.2% | 95% of these cases are due to Graves' disease
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Management of Graves' disease in pregnancy
Refer to endocrinologist + obstetrician Anti-thyroid therapy (propothiouracil likely as less fetal effects) - on lowest maintenance dose to keep free T4 in high normal range - check T4 and TSH 6-weekly - monitor for fetal tachycardia Propanolol 40mg TDS if symptomatic
321
Obstetric complications of untreated hyperthyroidism
Preterm birth Perinatal mortality Fetal and neonatal thyrotoxicosis Risk of thyroid storm triggered by stressof infection, labour, or operative delivery (high risk of maternal and fetal morbidity and mortality)
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Antenatal management of hypothyroidism
Optimise T4 and TSH pre-conceptually Increase thyroxine by 30% immediately in first trimester (2 extra doses per week) Check TFT 4 weekly in T2, then 6-8 weekly Aim for TSH 0.5-2.5 Postpartum, return to pre-pregnancy dose and re-check 6-8 weeks postnatally
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Timing of prophylacitc anti-D in Rh negative pregnant women
28 and 34 weeks
324
Sensitising events which indicate prophylactic anti-D in pregnancy Rhesus negative women
First trimester: - miscarriage - termination of pregnancy - ectopic pregnancy - Chorionic villus sampling Second & Third trimester: - Amniocentesis/cordocentesis - Fetal death - Abdominal trauma significant enough to cause fetomaternal haemorrhage - Antepartum haemorrhage - External cephalic version
325
Antii-D dose
Multiple pregnancy: 625IU Sensitising event <12 weeks: 250IU Sensitising event >12 weeks (or routine prophylaxis): 625IU
326
How much Rh positive fetal RBCs will anti-D dose neutralise
250IU:2.5mL fetal RBC 625IU: 6mL fetal RBC
327
Rationale for routine anti-D prophylaxis
Silent transplacental haemorrhages will lead to very small amounts (0.1mL) of fetal RBC accessing maternal circulation, this usually occurs after 28 weeks and especially around time of delivery
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Management of pregnant women with preformed anti-D antibodies
Discuss with MFM specialist Assess monthly until 28 weeks, then every 2weeks in 3rd trimester Non-invasive fetal genotyping (cell-free DNA) If significant rise, maternal anti-D titre >1/16, or history of Rh disease in previous pregnancy fetal monitoring with MCA PSV
329
Requirements of RBCs use in fetal intrauterine transfusion
- O group (or ABO identical with fetus) - leucodepleted - CMV negative - irradiated (to prevent graft v host disease) - Plasma reduced - <5 days old - Rh and Kell negative - Indirect antiglobulin test crossmatch compatible with mother's plasma
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Physiological changes to the renal system during pregnancy
Increased renal blood flow (due to increased cardiac output), increasing GFR by up to 50% - fall in serum creatinine, urea, calcium and bicarbonate - tubular capacity to resorb glucose and protein is exceeded -> proteinuria + glycosuria Size of kidney increases due to increased blood flow (R>L due to dextrorotation of uterus) Dilatation of pelvicalyceal system R>L, up to 15-20mm, due to progesterone activity on relaxing smooth muscle Increased renin and aldosterone secretion -> sodium and water retention, fall in serum albumin and osmolality Increased EPO and vit D secretion
331
Diagnostic criteria for GDM
OGTT results: Fasting BGL 5.1-7 1h BGL 10-11 2h BGL 8.5- 11 (any one of these results = diagnosis) Below this range is normal Above this range is OVERT diabetes
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Epidemiology of PROM and PPROM
PROM occurs in 10% of all pregnancies PPROM occurs in 2-3% of pregnancies, but is associated with 40% of preterm deliveries
333
Risk factorsfor PPROM
- Past history of PPROM/preterm delivery - urogenital tract infection/colonisation - APH - cigarette smoking - past history of cervical surgery - amniocentesis in current pregnancy (PPROM in this setting associated with more favourable outcomes) - cervical length <25mm - positive fetal fibronectin - nutritional deficiencies - lean maternal body mass - multiple pregnancy - polyhydramnios
334
Risks associated with PPROM
Maternal: - infection (chorio, endometritis, septicaemia) - increased risk of operative delivery and associated risks Fetal: - preterm delivery (most deliver within 1 week of PPROM) - associated neonatalmorbidities (HMD, IVH, periventricular leukomalacia, neurological sequelae, infection - sepsis, pneumonia, meningitis, NEC, retinopathy) - pulmonary hypoplasia - MSK/facial deformities - malpresentation - cord events incl. prolapse - placental abruption - perinatal mortality
335
Investigations to perform in PPROM
``` HVS MCS LVS MCS GBS PCR +/- STI screen MSSU ``` USS: fetal growth, +/- dopplers, CRP + CBE daily for 3 days (then twice weekly if expectant management) If expectant management, weekly HVS MCS
336
Management of PPROM (general principles regardless of gestation)
Antibiotics: - prophylactic: IV benzylpenicillin 3g loading then 1.2g 4 hourly for 48 hours PLUS PO erythromycin 250mg QID for 10 days - if signs of chorio: amox 2g IV 6 hourly, gentamicin 5mg/kg IV daily, metronidazole 500mg IV BD (total 5 days treatment - can change to PO postnatal if afebrile) Tocolytics; - NEVER GIVE if signs of chorio - if contractions present but not in established labour, nifedipine can be given to prolong pregnancy for 4h while obtain steroid cover Corticosteroids - 11.4mg IM betamethasone in 2 doses 24h apart Magnesium sulphate: - if delivery anticipated within 24h, 24-30/40 gestation Aim to deliver >34/40 if GBS positive OR >36/40 if GBS negative However if any contraindicationsto expectant management (APH, fetal compromise, signs of chorioamnionitis, established labour), delivery when indicated
337
Surveillance required in expectant management of PPROM
- CTG daily for first 3-6 days then twice per week unless indicated - CBE + CRP daily for 3 days then twice weekly - HVS swab weekly
338
Statistics of preterm labour
- >50% of women who present in preterm labour will continue their pregnancy - occurs in 5-10% of all deliveries - prematurity is the cause for 75% perinatal deaths
339
Risk factors associated with spontaneous preterm labour (12)
- previous preterm birth - multiple pregnancy - polyhydramnios - urogenital tract infection - previous cervical surgery - uterine anomalies - periodontal disease - bleeding in 2nd trimester - extremes of age - smoking - low pre-pregnancy weight - pregnancies achieved through ART
340
Strategies for prevention of preterm labour
No population based interventions, but following may be suitable in at risk women: - cervical length assessment at 20/40 (mean is 42mm, intervention considered if <25mm) - supplemental progesterone (Cxlength10-20mm) - Cervical cerclage (history of cervical incompetence, length <25mm at <24/40)
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Factors to consider when using fetal fibronectin
Should be undetectable from 22-35 weeks (>35 weeks less valuable) Must use STERILE water as lubricant - as intravaginal lubricants or disinfectants may interfere with antibody reaction and cause false negatives False positive can occur with blood or semen
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Management of pre-term labour:
Antibiotics- IV benzylpenicillin 3g loading, 1.2g 4hrly (only if active preterm labour, reduces maternal infection rate, no benefit to fetus) Tocolytics - if need to transfer to another unit/give time to cover with steroids Corticosteroids: if gestation age 23-34+6 and risk of imminent preterm birth or planned/expected within next 7 days Mode of Magnesium sulphate: 24-30/40 gestation for neuroprotection where birth is anticipated within 24h Mode of delivery: If breech and viable -> caesarean If cephalic, aim for vaginal If <26/40 multiple, caesarean Attendance of paeds/neonatologist at delivery. Dual vessel cord blood gas, sent placenta for histopath + swab
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Definition of small for gestational age, IUGR, or low birthweight
SGA: weight OR abdo circumference <10th percentile for GA IUGR: Evidence of growth restriction or arrest with EFW or birthweight<10th centile Low birthweight: <2500g Very low BW: <1500g Extremely low BW <1000g
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Normal growth velocity of the fetus
5g/day 14-15/40 10g/day 20/40 30-35g/day 32-34/40 Growth rate decreases >34 weeks (growth rate lower in multiples than singletons)
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Factors commonly associated with SGA (not IUGR)
``` Race Maternal size Female fetus Nulliparity History of baby with SGA Matrilineal tendency ```
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Common factors assocaited with fetal growth restriction
MATERNAL: - multiple pregnancy - smoking, alcohol, amphetamines, cocaine - Low SES - DV - PET - previous stillbirth - obesity - Chronic HTN - Connective tissue disorders - Thrombophilias - diabetes - cardiac disorders - hypotension (<60mmHg diastolic) - respiratory disease e.g. severe asthma - anaemia - renal disease - medications (narcotics, chemo) - poor nutrition FETAL FACTORS: - fetal infection - malformations - chromosomal defects PLACENTAL FACTORS: - abruption - praevia - placentitis/vasculitis - chorioamnionitis - Placental cysts - decreased uteroplacental blood flow UTERINE FACTORS: - fibroids - morphological abnormalities (especially uterine septum)
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Causes of SGA/IUGR
CCPP acronym Constitutional Chromosomal Perinatal infections Placental insufficiency
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Aetiology of asymmetric v symmetric IUGR
Symmetric (20-30%) - all organs decreased proportionally - due to impairment of early fetal cellular hyperplasia Asymmetric (70-80%) - Relatively greater decrease in abdominal size (liver and subcut fat) than HC - due to fetal adaptation to hostile environment, redistribution of blood flow in favour of vital organs
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Percentage of SGA babies who are constitutionally small
70% | Healthy fetuses with no long term morbidity
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Risks associated with babies who have IUGR
``` Still birth Birth hypoxia Neonatal complications Impaired neurodevelopment T2DM and hypertension in long term ```
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Chromosomal causes of IUGR
(20% of IUGR/SGA) Usually EARLY and SYMMETRICAL <5th%ile - aneuploidy - multiple deletions - gene mutations - placental mosaicism
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Perinatal infections which can cause IUGR
(5% of IUGR due to infection) - CMV most common - rubella - toxoplasmosis - varicella - syphilis
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Placental insufficiency causes of IUGR
Many causes, often recurrent | e.g. PET, abruption etc. manifestaitions
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"Other" causes of IUGR
Non-genetic congenital abnormalities (2%) - hypoxaemia (e.g. cyanotic heart disease, severe anaemia) Multiple gestation - nutritional - complications e.g. twin-twin, PET Maternal factors - reduced placental blood flow (HTN, DM, collagen disease, lupus, obstetric causes) - smoking - toxins e.g. warfarin, AEDs
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Prevention strategies for SGA/IUGR
``` Smoking cessation Nutritional advice - well balanced - severe dietary restriction associated with LBW - low fasting BGL associated with LBW ```
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Most sensitive measurements for detecting SGA/IUGR
AC is most sensitive SINGLE measurement (EFW also good) Serial RELATIONSHIP between HC and AC, along with AFI interpretation is most useful for identifying growth pattern - i.e. reduced AC growth with maintained HC growth, associated with oligohydramnios = IUGR ** oligohydramnios without an obvious cause is associated with high perinatal mortality
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Investigations to perform in a fetus thought to be IUGR
``` Bloods (if early <32/40): - Hb - ?thrombocytopaenia - TORCH screen If severe early IUGR, consider: - thrombophilia screen - karyotype ``` USS: - AC/HC/AFI - UA Doppler surveillance (if increased resistance, repeat in 2 weeks, if absent or reversed diastolic flow, admit and steroid load, usually needs delivery within days)
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Management of late onset growth restriction (>32 weeks)
Usually reflects mild-moderate uteroplacental dysfunction Serial growth and AFI every 2 weeks
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Delivery planning for growth restricted fetuses
Depends on aetiology, severity and gestation If moderate: - consider IOL if cervix favourable >36/40 - delay until >37/40 if normal surveillance If significant: - Aim to delivery 34-36 weeks - if very preterm, delay until imminent signs of fetal compromise - delivery if>34/40 and AREDF - If IUGR and oligohydramnios >36 weeks, deliver **If associated with AREDF, almost always requires LSCS delivery
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Neonatal recommendations for low birthweight babies on discharge
Routine iron supplement for all babies <2500g | - 2mg/kg/day from approx 8 weeks to 12 months of age
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Procedure for instrumental delivery
A: abdo palp (No fetal head palpable), address woman, analgesia, assistants B: bladder empty C: cervix check (fully, membranes ruptured) D: determine position, station and pelvic adequacy E: equipment- inspect vacuum cup, pump and tubing, check pressure. OR check correct forceps, blades match and lock F: FLEXION POINT- position cup 3cm anterior to posterior fontanelle and using Finger to clear maternal tissue FORCEPS: apply blades (left first) G: Gentle traction H: HALT - stop vacuum if no progress with 3 pulls, 3 pull offs or no significant progress after 20 minutes HANDLE ELEVATED: elevate forceps handles in axis of birth canal I: Incision - consider episiotomy J: Jaw - remove cup/forceps when jaw is reachable or delivery assured
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Indications for operative vaginal delivery
Maternal: - inability to push - Prolonged 2nd stage (3h with epidural, 2h without) - Cardio or vascular conditions - neurological or muscular disease - significant vaginal bleeding Fetal: - suspected compromise - malposition with relative dystocia (e.g. OP/OT)
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Contraindications to operative vaginal delivery
- operator inexperience - incompletely dilated cervix - unknown fetal position - unengaged head - malpresentation (e.g. face or brow) - suspected CPD - GA <36/40 (for vacuum only) (Relative:) - fetal predisposition to fracture e.g. OI - fetal bleeding disorder (e.g. haemophilia) - Maternal bloodborne virus
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Postpartum care following caesarean
- analgesia - early removal of IDC (within 24h) - early mobilisation and hydration - deep breathing and coughing exercises +/- physio - diet as tolerated - debrief on birth and impact on future pregnancies - observe for postop complications (ileus, UTI, URTI, DVT, wound infection)
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Criteria for confirmed miscarriage
- evidence of intrauterine fetal pole (CRL) >6mm on TV scan with absent heartbeat - Gestation sac >15mm without fetal pole - successive scans of gestation sac <15mm fail to show change in size over 10-14 days - substantial tissue within uterus >15mm with a history of blood loss and possible passage of tissue (incomplete miscarriage) - Small fetal pole seen and bHCG is falling
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Expectant management of miscarraige
- 70% will resolve spontaneously - contents <15mm likely to resolve spontaneously - 20% will need subsequent D&C especially if contents >15mm - Complete resolution may take weeks - less likely to be successful if there is an intact non-viable fetus and gestation sac Need review 7-10 days after diagnosis, consider repeat ultrasound if there were previously contents noted
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Risks of D&C when managing miscarriage
Bleeding Infection Perforation (1 in 300) Asherman's syndrome (1:1000) - less likely with suction curette GA risks Small risk of repeat procedure in presence of ongoing bleeding
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Most common sites for ectopic pregnancy
``` Tubal (95%) - Ampullary (55%) - Isthmic (25%) - fimbrial (17%) - Interstitial (2%) Other (5%) - Cervical - ovarian - peritoneal - C-section scar ```
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Epidemiology of ectopic pregnancy
in developed countries: Approx 1% of pregnancies are ectopic (1% of ART pregnancies are heterotopic, 1 in 30,000 spontaneous conceptions are heterotopic) - most common in 25-34yo - mortality rate in developed countries 0.2% - 10% recurrence risk after a single ectopic
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Risk factors for ectopic pregnancy
- PID (7-fold increased incidence) - smoking (impairs tubal motility) - tubal surgery - previous ectopic pregnancy - POP, emergency pill, IUD (lower risk than those NOT on contraception, but higher risk than COCP users as progesterone reduces tubal mobility) - ART - endometriosis - Abnormal embryo
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Investigations to confirm ectopic pregnancy
- inappropriately rising quant serum bHCG (though up to 1% will have hCG levels <25 therefore neg on UPT_ - no intrauterine sac seen with HCG levels suggestive that should be visible ultrasonographically (PUL, not confirmed ectopic) - fluid in pouch of douglas if ruptured, may have adnexal mass Laparoscopy - gold standard for diagnosis
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At what hCG level should an intrauterine pregnancy be visible on USS
TV scan: 1000-1500 | TA: 1800-2000
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Indications for surgical management of ectopic pregnancy
- Significant pain - Adnexal mass >35mm - fetal activity on USS - hCG 5000IU or higher - no availability for follow up of medical management - maternal preference or seeking permanent contraception - subsequent ectopic pregnancy in ipsilateral tube after previous medical management
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Options for surgical management of ectopic pregnancy
- Salpingectomy (ideally laparoscopic, especially if haemodynamic compromise Salpingotomy - if other risk factors for infertility (i.e. already had other tube removed) - 5% risk of persistent ectopic, 20% risk of further treatment, higher rates of recurrent ectopic Local injection of MTX, KCl or prostaglandins - high risk of persisting
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Contraindications for medical management of ectopic pregnancy
- haemodynamic instability - fetal cardiac activity - hCG >5000 - mass >35mm - no access to emergency facilities within 30 minutes of home - heterotopic pregnancy - immunodeficiency - free fluid in pelvis - sensitivity to MTX pre-existing liver, haematological, pulmonary or peptic ulcer disease
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Method of medical management of ectopic pregnancy
- Cease folate supplements - 50mg/m2 TBSA methotrexate single dose IM - Avoid UV light and high FODMAP foods to avoid side effects - paracetamol (+/- NSAIDs if safe)- can get separation pain approx day 3-4 - quant hCG on day 0(+baseline bloods), 4 and 7 - if fails to fall more than 15% between days 4 and 7, will need second dose - avoid pregnancy for 3 months Consider if anti-d required (all Rh negative women)
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Predictors that medical management of ectopic pregnancy will be successful
- lower serum hCG - slow-risking plateau or falling hCG prior to treatment - falling hCG by day 4
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Presentation of a female with Kallmann syndrome
Delayed or absent puberty with an impaired sense of smell +/- colour blindness (Autosomal dominant condition, causing GnRH deficiency (hypothalamic hypogonadotrophic hypogonadism)
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Further defining the cause of hypogonadotrophic hypogonadism
GnRH test - administer GnRH, if LH response is appropriate = hypothalamic failure - if absence of LH response = pituitary failure
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Causes of abnormal UTERINE bleeding
PALM COEI N PALM = visually objective structural COEI = unrelated to structural anomalies N = not yet classified (e.g. AV malformations etc. ) Polyps Adenomyosis Leiomyoma (i.e. fibroids) Malignancy Coagulopathy Ovulatory disorders Endometrial Iatrogenic keep in mind women may have NON-uterine causes of vaginal bleeding (urethral, vulvar, vesical, vaginal, cervical and recto-anal)
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Clinically significant maternal red cell antibodies
Anti-D Anti-c Anti-kell ``` Anti-S Anti-s Anti-u Anti-dia Anti-Coa ```
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Acceptable antibody titres for clinically significant maternal red cell antibodies
Levels <1:32 are reasonable UNLESS - >2-fold increase in titre OR - Anti-kell antibodies (even low titres are at risk for HDFN)
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Mechanism for significant fetal/neonatal disease with maternal anti-kell antibodies
``` Suppressed erythropoiesis PLUS haemolysis PLUS peripheral sequestration of red cells ```
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Monitoring pregnancies with clinically significant red cell antibodies
4 weekly titres until 28 weeks, then every 2 weeks If titre >1:32 then needs weekly MCA PSV (through MFM department)
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Causes for maternal collapse (12)
Vasovagal syncope Postural hypotension Haemorrhage (PPH, APH, Splenic artery aneurysm rupture, hepatic rupture) Thromboembolism Amniotic fluid embolism Epilepsy Eclampsia Intracranial haemorrhage Cardiac disease (MI, aortic dissection, cardiomyopathy, arrhythmia) Drug toxicity/overdose (MgSO4, Local anaesthetic, illicit drugs) Anaphylaxis
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When should perimortem caesarean section be performed?
If there is no response after 4 minutes of correctly performed CPR in a woman >20 weeks
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Amniotic fluid embolism "cause"
Can occur in any trimester Caused by changes in the normal relationship between the membranes, placenta and uterine wall -> disruption of the integrity of the uterine blood vessels amniotic fluid/debris is deposited in maternal lungs -> pulmonary vasoconstriction (?anaphylactic-type reaction)
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Clinical presentation of amniotic fluid embolism
Sudden collapse during labour/delivery or immediate postpartum associated with: - dyspnoea - pink frothy sputum - cyanosis - Cardiorespiratory failure - convulsions (10-20% of cases) HYPOTENSION HYPOXIA with respiratory failure DIC COMA OR SEIZURES
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Presentation of regional anaesthesia toxicity
Onset almost immediately (within up to 20 mins max) of administering local anaesthetic - complain of metallic taste, tinnitus, confusion and disorientation - respiratory muscle paralysis and cardiac arrest may occur