Post-partum care Flashcards

1
Q

Physiology of post-partum

A

Uterine involution
- 10-14 days after delivery fundus should not be palpated abdominally
Internal os of cervix closed by 48h postpartum
Duration of lochia is variable
Fall in oestrogen causes atrophy of lower genital tract
Decreased secretions from glandular tissue
Ligament laxity resolves as progesterone and relaxin levels reduce
Divarication of the rectus abdominus muscle is common
Pulse rate and CO return to pre-pregnancy level by 6 weeks PP
Diuresis (3rd day PP) –> reduction in plasma volume –> increase in Hb levels

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2
Q

Cochrane - early skin-to-skin associated with:

A

Increased likelihood of breastfeeding in the first 1-4 months and increased breastfeeding duration
Less infant crying
Increased infant interaction with their mother
No harmful or negative outcomes

WHO recommends skin to skin immediately after birth for at least 1-2h
As little as 15-20 mins can be beneficial

Improves thermal regulation in the neonate and facilitates mother infant attachment

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3
Q

Incidence of PPH

Define

  • major
  • primary
  • secondary
A

incidence 5-15%

Major / severe PPH
>1000ml, complicates 1-5% of deliveries

Primary PPH - Within 24h of delivery

Secondary PPH - Between 24h and 6 weeks postpartum
Incidence 0.47% to 1.44%

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4
Q

Total blood volume at term

A

~100ml/kg
- Maternal blood volume may be approx 7L for a 70kg woman

Blood flow to the placental bed is approximately 750ml/min at term

Blood loss may be life-threatening with unreplaced volume loss of as little as 30%

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5
Q

Risk factors for atony

A
Uterine overdistension
Increasing parity
Functional or anatomical distortion of the uterus
- Prolonged labour
- Precipitous labour
- Fibroids 
- Uterine anomalies
- Placenta praevia
Intra-amniotic infection (chorioamnionitis)
Oxytocin withdrawal
Instrumental birth
Uterine relaxants
Previous PPH - 3-fold increase
IOL 
Iron deficiency anaemia
Bladder distension
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6
Q

Prevention of PPH

A

Active management of third stage with prophylactic oxytocics and CCT

  • Reduce risk of PPH by at least 50%
  • Cochrane review - reduction of 68%
  • Majority of PPH cases occur in the absence of known risk factors
  • Physiological third stage cannot be recommended
  • CCT should only be applied once uterus is well contracted and the placenta is separated

Uterine massage is of no benefit in the prophylaxis of PPH
Treat anaemia / iron deficiency antenatally
Determine placental site at anatomy scan
Fetal pillow for second stage CS - reduces the risk of uterine extension

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7
Q

With prophylactic uterotonic

A

Women without risk factors delivering vaginally - Oxytocin 10 iu IM

Women delivering by CS- Oxytocin 5 iu slow IV injection

Women with increased risk of PPH - Ergometrine-oxytocin

Women with increased risk of PPH, delivering by CS - Consider IV TXA

Meta-analysis compared oxytocin 5IU, 10 IU and syntometrine

  • Similar efficacy in preventing PPH >1000ml
  • Syntometrine associated with small reduction in risk of PPH of >500ml
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8
Q

Oxytocin

  • dose
  • mechanism of action
  • pros and cons
A

Direct relaxant effect on vascular smooth muscle
Structurally similar to vasopressin –> antidurectic effects

Caution if possibility of undiagnosed second twin (no USS in pregnancy) when using for active management

Adverse effects:

  • Rapid IV bolus can cause profound hypotension, esp if hypovolaemia
  • Antidiuretic effects can lead to water intoxication and hyponatraemia
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9
Q

Ergometrine

  • dose
  • mechanism of action
  • pros and cons
A

Syntometrine 1ml IM = oxytocin 5 units/ml + ergometrine 500mcg/ml

Alpha-adrenoceptor and dopamine receptor agonist –> strong sustained uterine contractions
Causes vasoconstriction

Contrainidcation:

  • Hypertension
  • Severe cardiac disease

ADR:
5-fold risk of adverse effects over oxytocin
Nausea and vomiting
HTN

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10
Q

Misoprostol

  • dose
  • mechanism of action
  • pros and cons
A

Less effective than oxytocin
Cheap, stable, can be used in under-resourced countries

ADR:
GI disturbance
Dizziness
Headache
Fever
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11
Q

Carboprost

  • dose
  • mechanism of action
  • pros and cons
A

0.25mg IM

Synthetic prostaglandin
Used when ergometrine is contraindicated or ineffective
Can repeat dose at 15 min intervals until total 2mg

Contraindications:

  • Asthma
  • Cardiac disease
  • Pulmonary disease
ADR:
Bronchospasm
Vasodilation
HTN
Increased risk of infection
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12
Q

Retained placenta

  • incidence
  • risk factors
A

3% of vaginal deliveries

Retained placenta diagnosed after:

- 1 hr of physiological management
- 30 mins of active management

Causes and risk factors:

- Full bladder
- Atony
- Previous uterine scar
- Fibroid uterus
- Other uterine abnormality
- Cervical constriction ring
- Placenta accreta spectrum
- Umbilical cord snapping
- Premature birth
- Stillbirth 

Associated with recurrence

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13
Q

Secondary PPH

A

Causes:

  • Endometritis
  • RPOC
  • Subinvolution of the placental implantation site
  • Rarely: Pseudoaneurysm, AVM

10% present with massive haemorrhage and require immediate attention

ERPOC associated with 1.5% risk of perforation

41% occur - 8-14 days

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14
Q

Balloon tamponade

for PPH

A

No clear evidence for duration to remain in
Tamponade controls atony in upper segment and placental bed bleeding in lower segment
Bakri balloon - usually requires 300ml saline, but has capacity for 500mls
In most cases 4-6 hours should be adequate to achieve haemostasis
- Most units 12-24h
Remove during daytime hours
Cover with antibiotics

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15
Q

Haemostatic brace suture for PPH

A

75% success in avoiding hysterectomy
B-lynch requires hysterotomy
Absorbable suture with large needle
Hayman suture (2 separate sutures)

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16
Q

Risk factors and common presentation of Sheehan syndrome

A

Risk factors:

- PPH
- T1DM
- Sickle cell disease

Common presentation:

- Failure to lactate post-delivery
- Amenorrhoea or oligomenorrhoea 

Can present with any of the manifestations of hypopituitarism, e.g. hypotension, hyponatraemia, hypothyroidism

If patient remains hypotensive after control of haemorrhage and volume replacement, evaluate and treat for adrenal insufficiency immediately
Evaluate for other hormone deficiencies at 4-6 weeks post-partum

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17
Q

Risk factors for uterine inversion

A
  • Accreta
  • Fundal placental insertion
  • Any condition that predisposes to atony and prolapse
  • CCT without countertraction in an uncontracted uterus
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18
Q

Management of uterine inversion

A

Goals:

  • Replace the fundus to correct position
  • Management PPH and shock
  • Prevent recurrent inversion

Discontinue uterotonic drugs
Do not remove the placenta
- Do after uterus is replaced as likely will increase blood loss
Immediately attempt to manually replace the inverted uterus - Johnson manoeuvre
- Once reverted, keep hand in uterus, and restart oxytocin
Transfer to OT for manual removal

If unstable after initial attempt, reasonable to proceed to laparotomy
If haemodynamically stable
- GTN
- Terbutaline

Can try hydrostatic pressure

Prevent recurrent inversion:

  • Uterotonic meds
  • Hold uterus in place
  • Prophylactic antibiotics

Documentation
Debrief

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19
Q

Perineal tear classification

A

1st degree = Injury to perineal skin and/or vaginal mucosa only
2nd degree = Injury to perineum involving perineal muscles but not anal sphincter
3rd degree = Injury to perineum involving anal sphincter complex

3A <50% of EAS torn
3B >50% of EAS torn
3C Both EAS and IAS torn

4th degree = Injury to perineum involving anal sphincter complex and anorectal mucosa

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20
Q

Preventing perineal trauma

A
Cochrane 2017
- Hands off vs. hands on - no difference
- Reduction in OASIS:
	○ Warm compresses during second stage
	○ Perineal massage during antenatal period (last month of pregnancy) - May also be beneficial in second stage 
- Further research needed

Evidence for the protective effect of episiotomy is conflicting
There is evidence that a mediolateral episiotomy should be performed with instrumental deliveries as it appears to have a protective effect on OASIS

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21
Q

Benefits of rapid absorbable suture for tear repair over standard synthetic absorbable

A

Reduced analgesia up to 10 days postpartum
Less suture material removal required
Increased superficial partial skin gaping
No difference in longer term outcomes

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22
Q

Continuous vs. interrupted

for perineal tear

A

Cochrane review
Continuous for all layers:
- Reduction in short term pain
- Reduction in suture removal

Continuous suture for skin:
- Reduction in analgesia
No difference in long term pain or need for resuturing

23
Q

Episiotomy should be considered where…

A

there is a high likelihood of severe laceration

Soft tissue dystocia
Requirement to accelerate birth of a compromised fetus
Need to facilitate operative vaginal birth
History of FGM

24
Q

Incidence of OASIS

A

UK incidence: 2.9% (range 0-8%)
Primiparae 6.1%
Multiparae 1.7%

25
Q

Risk factors for OASIS

A

However RF do not allow accurate prediction of OASIS

Nulliparity	
Asian ethnicity	
Birthweight >4kg	
OP position	
Shoulder dystocia
Prolonged second stage	
Instrumental delivery	
- Ventouse without episiotomy	OR 1.89
- Ventouse with episiotomy	OR 0.57
- Forceps without episiotomy	OR 6.53
- Forceps with episiotomy	OR 1.34

Midline episiotomy

26
Q

OASIS repair technique

A

Cochrane

  • at 1y f/u, overlap had reduced incontinence and urgency
  • at 36/12 - no difference

Anorectal mucosa repair - 3/0 vicryl (cont or interrupted)
IAS - 3/0 PDS interrupted or mattress without any attempt to overlap the IAS

EAS 3-0 PDS:

  • 3C - either overlapping or end-to-end technique
  • 3A or 3B - end-to-end technique
27
Q

Post-op management of OASIS

A

Document
Broad-spectrum antibiotics
- reduce the risk of post-op infections and wound dehiscence
Bladder catheterisation
Analgesia
Diet
Laxatives
- associated with earlier and less painful BM and early postnatal discharge
- To reduce the risk of wound dehiscence

Physiotherapy
GOPD follow up 6-12 weeks post-natal
- Manometry
- Endosonography

28
Q

6 week review for OASIS

A

Review symptoms
- 60-80% will be asymptomatic

Consider investigations

  • Anal manometry - balloon in rectum which is inflated to check the muscle function of the IAS/EAS
  • Endoanal USS - looks for defect in the muscle

Referral to General Surgeons if symptomatic or abnormal investigations
- If family complete would recommend secondary sphincter repair

Non-surgical management

- dietary advice 
- egulate bowels 
- Constipating agents e.g. loperamide 
- Pelvic floor exercises and biofeedback 

5-7% risk of sustaining another OASIS tear
- 17% of women will develop worsening faecal symptoms
If symptomatic –> c-section
If chooses vaginal birth then hands on delivery with experienced practitioner
Role of episiotomy in next pregnancy unclear - should have episiotomy if clinically indicated

29
Q

Risk factors for recurrent OASIS in subsequent pregnancy

A

Asian ethnicity

Forceps delivery

Birthweight >4kg

30
Q

Anatomy of the breast

A

Contain mammary glands which produce milk
Breasts composed of glandular tissue and fatty tissue
Cooper’s ligaments - anchor’s breast tissue to chest wall
15-25 lobes arranged radially with interposed fat

Composed of lobules and alveoli - alveoli synthesise milk
Each alveoli has a draining duct
Contractile unit made up of myoepithelial cells which eject breastmilk into ducts
Each alveoli is drained by a duct which joins to form a single large duct for each lobe
Lacteriferous duct open separately on the nipple

Areola / Montgomery glands secrete lipoid fluid which moisturisers the nipple and also has a scent to attract baby

31
Q

Blood and nerve supply of the breast

A

Blood supply from the internal mammary and lateral thoracic arteries

Innervated by the intercostal nerves of the 4th and 5th intercostal spaces

32
Q

Lactogenesis

A

Lactogenesis I:

  • Human placental lactogen –> breast growth
  • Begins at 15-20/40 - breast develops capacity to secrete milk components
  • Prolactin stimulates mammary cells to produce milk, nipple growth
  • High levels of progesterone inhibit lactation
  • Mammary fat pads decrease in size and are replaced by developing ducts and alveoli

Lactogenesis II:

  • Onset of copious milk production
  • Begins 30-40h after birth, complete by day 8 PP
  • Delivery of placenta –> rapid drop in progesterone and estrogen –> increased levels of prolactin –> breast milk biosynthesis

Lactogenesis III:

  • Maintenance of milk production
  • “Supply and demand”
33
Q

WHO’s baby friendly initiative and 10 steps to successful breastfeeding

A
  1. Having a written breastfeeding policy that is routinely communicated to all health care staff
  2. Training all health care staff in skills necessary to implement this policy
  3. Informing all pregnant women about the benefits and management of breastfeeding
  4. Helping mothers initiate breastfeeding within a half hour of birth
  5. Showing mothers how to breastfeed, and how to maintain lactation even if they should be separated from their infants
  6. Giving newborn infants no food or drink other than breastmilk, unless medically indicated
  7. Practicing rooming in - allowing mothers and infants to remain together 24h a day
  8. Encouraging breastfeeding on demand
  9. Discouraging the use of artificial teats or pacifiers in breastfeeding infants
  10. Fostering the establishment of breastfeeding support groups and referring mothers to them on discharge from the hospital
34
Q

The value of breastfeeding - for infants

A

Decreased infant mortality
Enhanced immunity and decreased risk and severity of infections
Decreased risk of asthma, eczema and allergies
Decreased risk of SIDS
Decreased risk of obesity, diabetes, hypercholesterolaemia
Enhanced cognitive development
Decreased risk of childhood cancers
Decreased risk of certain chronic diseases

35
Q

The value of breastfeeding - for mothers

A

Enhanced psychological bonding
Decreased PP bleeding and rapid uterine involution due to the action of oxytocin
Decreased risk of breast, ovarian and endometrial cancer
Earlier return to pre-pregnancy weight

36
Q

Causes of decreased milk supply

A
RPOC
PPH
Maternal diabetes
Hormonal issues 
- Hypopituitarism - Sheehan's syndrome
- Thyroid disease
Stress
Inadequate or infrequent nipple / breast stimulation
Separation from infant
Medications
Anatomic issues, e.g. previous breast surgery
Systemic infection
Mother-infant separation
CS
37
Q

Management of low supply

A
Assess attachment
Increase feeds including waking infant
Express
Increase skin to skin time
Domperidone 
- Acts by increasing prolactin
38
Q

Breast engorgement

A

May occur within first few days of established breastfeeding
Result of interstitial oedema, increased blood flow and accumulation of milk in the breast
Usually bilateral pain, redness, hardness of breasts

As for low supply
- check position and attachment
- If above current, then express for comfort
Treat by unlimited, frequent feeding

39
Q

Lactational Mastitis

A

Flu-like symptoms, rigors, red and tender breasts
May be localised area of tenderness = blocked milk duct
If symptoms persist more than a few hours after management for blocked duct, evaluate ? infective mastitis (Symptoms do not improve, or are worsening, after 12-24h despite effective milk removal)
Only 4% of mastitis is infective

40
Q

Blocked duct

A
Causes build up and inflammation
Tender and palpable lump
Management:
- Encourage mother to feed on affected side first
- Position infants chin towards blockage
- Massage when feeding / expressing
- May progress to mastitis
41
Q

Risk factors for mastitis

A
Poor breastfeeding technique 
Failure to alternate between breasts 
- Can cause nipple fissures, cracks (inconclusive evidence), sores 
Not wearing a well-fitting maternity support bra
Abrupt discontinuation of breastfeeding
Past history of mastitis
Primip
Maternal fatigue
Infrequent or interrupted feeding
Mixed bottle and breastfeeding
Delayed initiation of feeding 
Time limited feeds
Incomplete emptying 
Late shift from colostrum to milk production
42
Q

Incidence of mastitis

and common pathogens

A

Acute mastitis in 2-3% of postpartum women
Lactation mastitis in 10-33%
Breast abscess in untreated mastitis is ~3%

Common pathogens:
- Staphylococcus aureus
- Staphylococcus epidermidis
If recurrent - mixed flora including anaerobes

Beta haemolytic strep A B F
Haemophilus influenzae
E. Coli

43
Q

Physiological changes in pregnancy affecting CPR

A

Difficult to intubate - breast enlargement, laryngeal oedema, weight gain
–> Secure airway early

High risk of aspiration - reduced oesophageal tone, raised intra-abdominal pressure from gravid uterus, decreased gastric motility
–> Secure airway early, PPI in labour

Rapid development of hypoxia - dilutional anaemia, reduced FRV from increased minute ventilation and diaphragm splinting, increased O2 consumption from uteroplacental unit
–> Give early, high-flow O2

Chest compressions more difficult - breast hypertrophy and a raised diaphragm –> decreased chest wall compliance

Reduced venous return and CO by 30-40% –> Do uterine displacement for CPR

Predisposition to haemorrhage and hypovolaemia
–> Aggressive fluid resuscitation

Dilutional anaemia - Plasma volume increased by up to 50% in pregnancy
–> Treat anaemia antenatally

44
Q

Stages of DIC

A

Stage 1 = Hypercoagulable state
- Activation of clotting factors and development of microthrombi
Labs: decreased clotting, increased platelet adherence

Stage 2 = Consumptive hypercoagulable state
- Increased consumption of platelets and clotting factors –> bleeding
Labs: Increased clotting, decreased platelets and fibrinogen

Stage 3 = Secondary fibrinolytic state
- Substantial formation of fibrin degradation products and plasmin –> Marked bleeding
Labs: Increased thrombin time, decreased clot lysis time, increased fibrin degradation products

45
Q

Perimortem C-section

A

Should be carried out within 4 mins or as soon as possible after loss of spontaneous circulation in gestations >20/40
12-15% of circulating blood volume at term supplies the uterus
Trigger the massive obstetric haemorrhage protocol in an undelivered woman at the time the decision to proceed with peri-mortem CS is made

Delivery should be achieved within 5 mins of cardiac arrest
- Maximises maternal survival and reduces risk of long-term neurological impairment

46
Q

AFE diagnosis

A

Clinical diagnosis of acute hypotension or cardiac arrest, acute hypoxia and coagulopathy in the absence of any other potential explanation
Or diagnosed on post-mortem with presence of fetal debris in the pulmonary circulation

47
Q

AFE Incidence

A

5.4 cases per 100,000 women giving birth (Au/NZ)
Case fatality rate of 15%
If the AFE occurs in utero, neonatal mortality up to 40%

48
Q

Pathophysiology

of AFE

A

Poorly understood
Amniotic fluid enters maternal circulation via breach of barrier between maternal circulation and intact fetal membranes

Immune-mediated mechanisms suggested
Anaphylactic type reaction
Obstruction to pulmonary vessels
Complement activation - clotting problems

49
Q

Risk factors

of AFE

A
Given low incidence, no change to clinical practice warranted 
AMA
Placenta praevia
Placental abruption
Operative delivery 
Caesarean section 
Polyhydramnios
IOL 
Trauma
Multiple gestation
Multi parity
50
Q

Anaphylaxis presentation / pathophys

A

Rapidly developing

Airway, breathing, circulation problem

  • Significant intravascular volume redistribution –> decreased CO
  • Acute ventricular failure and myocardial ischaemia can occur
  • Upper airway obstruction from angioedema, bronchospasm, mucous plugging of smaller airways

Skin signs present in up to 90%

51
Q

Management of anaphylaxis

A

Remove trigger
Call for help
Lay patient flat with legs raised to combat vasodilation effects on circulation, unless prominent upper airway swelling

0.5ml (0.5mg) adrenaline 1:1000 IM at 5 minute intervals
STAT fluids
High-flow oxygen
Support with antihistamine and hydrocortisone

Blood tests for tryptase level
- Start of event, at 1 hour, and at 24h

Some patients can have a biphasic reaction so monitor for at least 6 hours

52
Q

Management of toxicity of MgSO4

A

calcium gluconate (10mls of 10%)

53
Q

Causes of cardiac arrest

A

4 Hs and 4 Ts

- Haemorrhage
- Hypoxia
- Hypo/hyperkalaemia 
- Hypothermia
- Thromboembolism
- Toxicity including sepsis
- Tamponade
    - Tension pneumothorax

Also intracranial haemorrhage and eclampsia

54
Q

RANZCOG management considerations

for PPH

A
  1. Recognition
  2. Communication and teamwork
  3. Resuscitation
  4. Monitoring and investigation
  5. Management of PPH