Week 10 Flashcards

emergencies, care in labour (364 cards)

1
Q

What would be unfavourable of likelihood of successful VBAC?

A
  1. PET or PIH
    1. LGA
    2. GDM
    3. Age over 35
    4. BMI >40
  2. Previous labour dystocia as indication for previous CS
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1
Q

What are the risks of VBAC?

A
  • Increased perinatal loss compared with ERCS at 39 weeks (1.8/1000 pregnancies vs ?ERCS)
  • Stillbirth after 39 weeks
  • Intrapartum death or neonatal death, related to scar rupture in labour
  • HIE risk (0.7/1000)
  • Increased morbidity of EmCS compared to ERCS if unsuccessful VBAC
    Pelvic floor trauma increased risk of apgars <7 at 5 minutes
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2
Q

What are the risks of elective CS?

A
  • Surgical morbidity and complications both with index pregnancy and further pregnancies
  • Increased risk of neonatal respiratory morbidity, low incidence >39 weeks gestation
    Associated with lower rates of initiating breastfeeding
    some risks of increased asthma and resp infection
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3
Q

What is the increase in perinatal mortality with VBAC and why?

A

1.8 per 1000 small amount due to rupture but mainly due to prolonging pregnancy

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4
Q

What is the increase in HIE with VBAC and why?

A

0.7 per 1000, some from rupture and some from hypoxia in labour

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5
Q

What is the risk of fetal injury at CS?

A

5 in 1000

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6
Q

Are breastfeeding rates lowest in Elective CS patients and what can be done?

A

yes, immediately skin to skin and support in OT and recovery to BF

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7
Q

Who is vaginal birth after cs not recommended for?

A
  1. Previous classical
    1. Previous inverted T or low vertical incision
    2. Previous uterine rupture
    3. Previous major uterine reconstruction eg full thickness myomectomy, cornual resection, mullerian anomaly
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8
Q

What use are risk calculators for VBAC?

A

high PPV low NPV, shouldn’t be used in isolation

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9
Q

If women have a non cephalic presentation and PPROM where should they be cared for?

A

inpatient

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10
Q

What should the category be for cord prolapse with normal FHR?

A

2 but need CFM on

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11
Q

what anaesthetic should be used for cord prolapse CS?

A

experience and patient factors

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12
Q

When is vaginal birth with cord prolapse okay to attempt?

A

full dilatation and able to delivery without impingement of cord

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13
Q

Can you do DCC after cord prolapse?

A

yes if the baby is well

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14
Q

Who should be offered elective admission at 37+0 due to risk o cord prolapse with ROM?

A

transverse, breech, oblique

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15
Q

What is the definition of cord prolpase?

A

descent of the umbilical cord alongside or past the presenting part in the presence of ROM

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16
Q

What is the overall incidence of cord prolapse and in breech?

A

0.1-0.6% breech 1%

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17
Q

What is the perinatal mortality or cord prolapse?

A

91 per 1000

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18
Q

What are the risks related to cord prolapse?

A

multiparity
lower BW <2.kg
PTL
congenital malformations
breech
trans verse or unstable like
second twin
poly
unengaged PP
LLP
ARM
vaginal manipulation of fetus
ECV
stabilisation ARM
large foley >180ml

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19
Q

how do you do manual elevation os a fetal head?

A

two fingers inside the vagina to lift PP upwards

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20
Q

At threshold of viability with cord prolapse what should be discussed?

A

continuation and conservative management or TOP

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21
Q

What is the definition of shoulder dystocia?

A

vaginal cephalic delivery that requires additional obstetric manoeuvres to deliver the fetus after the head has delivered and gentle traction has failed

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22
Q

what are the prelabour risk factors for shoulder dystocia?

A

previous SD
macrosomia >4.5kg
DM
BMI >30
IOL

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23
Q

What are the in labour factors associated with SD?

A

prolonged 2nd stage
secondary arrest
prolonged 1st stage
augentation
assisted

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24
what is the increase in risk of SD for DM or same weight?
2-4x
25
How is shoulder dystocia diagnosed?
axial traction
26
What are signs of shoulder dystocia?
turtle necking, difficult delivery of face to chin, failure of restitution, failure of shoulders to descend.
27
What is achieved with mcroberts?
hip flexion and abduction -> straightens the lumbosacral angle, rotates the maternal pelvis towards mother's head & increases relative AP diameter of the pelvis * Effective 90% of the time
28
How do you perform delivery of the posterior arm?
grasp fetal wrist and withdraw in a straight line from vagina. Associated with humeral fractures
29
What maternal injuries can occur with SD?
PPH & OASIS injury common, other reported complications: vaginal lacerations, cervical tears, bladder rupture, uterine rupture, symphyseal separation, sacroiliac joint dislocation, lateral femoral cutaneous neuropathy
30
What fetal injuries can occur with babies in shoulder dystocia?
BPI most important complications occurring 2.3-16%, other injuries: fractures of humerus and clavicle, pneumothoraces, hypoxic brain injury
31
what is the incidence of shoulder dystocia?
0.58-0.7% if vaginal deliveriesa
32
what is the incidence of OASI after shoulder dystocia?
3.8%
33
What is the risk of PPH after SD?
11%
34
what proportion of babies with SD weigh less than 4kg?
48%
35
when should elective CS be considered to prevent shoulder dystocia?
diabetes with EFW >4.5kg
36
How should shoulder dystocia be managed?
1. Diagnose shoulder dystocia 2. Tell mother to stop pushing & lie bed flat, remove pillows from back 3. Call for help 4. 'This is shoulder dystocia' to arriving team 5. McRobert's should be performed first 6. Suprapubic pressure to improve efficacy of McRobert's 7. Consider episiotomy only if access for internal manoeuvres difficult 8. Second-line: Internal manoeuvres or all-fours 9. Third-line: cleidotomy, symphysiotomy, Zavanelli manoeuvre 10. Prepare for PPH, neonatal resus & perineal trauma Debrief with parents
37
If the head to body delivery time is less than ? the risk of HIE is very low in SD?
5 minutes
38
How do you achieve rotation in shoulder dystocia?
pressure on posterior shoulder anterior or posterior. rotating into the wider oblique angle to free shoulder
39
Where can the shoulder be stuck with SD?
on symphysis pubis or sacral prominentry
40
why should women be recommended be at home for latent phase?
* Less likely to use an epidural in labour * Less likely to need oxytocin to augment their labour * No difference in CS birth, instrumental birth or amniotomy in the groups * More likely to evaluate their birth experience positively * No difference in Apgar scores No babies born before hospital admission
41
When should amniotomy and oxytocin be recommended in first stage?
when <2cm progress in four hours from 5cm
42
what maternal position is associated with less assisted birth?
standing
43
What is included int he perineal care bundle?
1. warm compress 2. hands on perineal support -counter pressure of fetal head, gentle traction to release anterior should and allow posterior shoulder to be release following the curve of Carus 3. episiotomy technique - when head crowning, 60 deg mediolateral angle, offer for primips with instrumental 4. assess tears with PR 5. grade tears with RCOG guideliness
44
per RANZCOG what is active first stage labour?
cervix 5cm or more until full dilatation
45
What is the recommendation on second stage?
1 hour for multip and 2 for primips however taking into consideration transfer time and access to resources it may be reasonable to give an additional hour
46
What is found in data about active management of first stage when progressing well and what is RANZOGs advice?
small reduction in CS, length of labour 1.5 hours shorter. Combined early amniotomy with use of oxytocin should not be used routinely
47
What does the RANZCOG guideline say about what the first stage of labour does not usually extend beyond?
15cm and beyond in nullip 18 hours and multip p12 hours
48
What is the data on length of second stage?
small RCT 78 showed extra hour reduces CS likelihood significantly without negative maternal or neonatal morbiditiy observational study 337k showed increased risk of PPH, chrio, enodmetritis, fevers, OASI, SD, NICU admission and sepsis for baby
49
What data is there on position of birth in labour?
standing reduces the likelihood of unassisted vaginal birth but not position reduces the risk of CS Epidural, position doesn't change out come 'consider left lateral'
50
what does the evidence show for DCC?
it improves the Hb small to moderate amount and possible increased jaundice risk
51
What is the ranxcog guidance on DCC?
offer for 60 seconds or until the cord is pulseless
52
what is the data for active management of 3rd stage show?
uncertain if reduces severe PPH RR 0.15 probably reduces need for other medications in 24 hours RR 0.15 Probably increases Hb May reduce primary blood loss of >500ml RR 0.33 may reduced RBC needs RR 0.3
53
What is the RANZCOG guidelines on active management of 3rd stage?
should be recommended to all women as reduces the risk of PPH by 50%
54
What is the best intervention we have for prevting OAIS?
warm compress RR 0.46
55
What improvement was found from the OASI care bundle in the UK?
reduction in OASI 3.3% to 3.0% in spontaneous vaginal birth 2.6% -2.2% primips 5.2-4.9% multips 1.7-1.5%
56
what is the RANZCOG statement on diet in labour?
safe to drink and remain hydrated and have a light diet in established labour unless risks for. GA are more likely
57
What is the definition of septic shock?
persistence of hypoperfusion despite adequate fluid replacement
58
What are the risk factors for antenatal sepsis?
* Obesity * Impaired glucose tolerance/diabetes * Impaired immunity/immunosuppressant medication * Anaemia * Vaginal discharge * History of pelvic infection * History of group B strep infection * Amniocentesis and other invasive procedures * Cervical cerclage * Prolonged SROM * GAS infection in close contacts/family members Black or other minority ethnic group origin
59
What is toxic shock caused by?
staphalococcal and streptococcol exotoxins
60
How does toxic shock present?
rash, pain out of proportion to clinical signs (necrotising fasciitis), N+V+D, watery discharge, conjunctival suffusion (redness)
61
what level of lactate is associated with tissue hypoperfusion?
>4
62
What is the sepsis bundle which should be given within 6 hours?
blood cultures broad spectrum IV ab within one hour serum lactate In the event of hypotension and/or lactate >4, give initial minimum of 20ml/kg fluid, if BP not responding give vasopressors for MAP>65mmHg If not responding to fluids ○ Achieve CVP >8mmHg ○ Achieve central venous oxygen saturation >70% or mixed venous oxygen saturation >65%
63
What are common pathogens for chorio?
usually mixed gram + and -ve bugs
64
What bugs are most common in women dying of sepsis?
ecoli and group A strep
65
What is the gram stain of GAS?
Gram pos cocci in pairs or chains beta haemolytic, catalase negative, anaerobe
66
What acute disease can GAS cause?
* Sepsis * Skin and soft tissue infection causing necrotising faciitis, cellulitis * Bone and joint infection * LRTI - pneumonia, empyema * Toxic shock syndrome * Endomyometritis Meningitis
67
What long term complications can occur from GAS?
rheumatic heart disease, acute rheumatic fever and post streptococcal glomerulonephritis
68
What are the severe sequale of mastitis?
TSS, necrotitsing fasc, abscess
69
what are the four criteria to treat for GAS pharyngitis?
need 3 of: fever tonsillar exudate no couhgh tender anterior cervical lyphadenopathy
70
What does augmentin not cover?
MRSA, pseudomonas
71
What does metronidazole cover?
anerobes only
72
What does clindamycin cover?
most streptococcus and staph including MRSA stops exotoxin production not renally cleared or nephrotoxic
73
What does pip taz and carbapenem not cover? what is their relationship with the kidneys?
MRSA, renal sparing
74
When should IVig be considered? How does it work?
for severe invasive streptococcal or staphylococcal infection if other therapies have failed . Neutralises the effect of exotoxins and inhibits production of TNF?
75
What is the home birth rate in NZ and australia?
NZ 4% Australia 0.6%
76
What is the transfer rate from home birth in nullips and multips?
34% and 6%
77
What is the evidence of harm to baby from home birth?
no conclusive evidence
78
What is a low risk or women without identified risk factors?
Have had antenatal care Singleton cephalic fetus 37+1 - 41+0 Normally grown fetus No previous uterine scars No pre-existing medical conditions affecting woman of baby which may increase risk of adverse outcome during birth, pregnancy or PN period
79
What are the benefits of the woman for a home birth?
* Increased likelihood of intact perineum * Reduced likelihood of OASIS * Reduced likelihood of CS birth Reduced likelihood of instrumental birth
80
What are the reduced risks for the baby?
* Small reduction in risk for NICU admission * No increase in rates of early neonatal death (note that this outcome is very rare) No increase in rate of stillbirth (note that this outcome is very rare)
81
When should fetal cord gases be taken?
instrumental, FBS in labour, APGAR <4 at 1 minutes, <7 at 5 minutes
82
what is 1+ moulding?
bones are just touching
83
What is 2+ moulding?
reducible overlap
84
what is 3+ moulding?
irreducible overlap
85
What is the parietal decidua?
the lining of the uterus which doesn't have the placenta over it
86
What is the mechanic of a uterine contraction?
Contractions start at the uterotubal junction with waves meeting at the fundus and spreading downwards towards the cervix -> fundus becomes thicker while the lower uterus retracts
87
How do myometrial cells communicate?
intracellular channels called gap junctions
88
When and why do gap channels increase in number?
the onset of labour. Progesterone inhibits and oestrogen stimulates formation. Prostaglandins regulate and formation and function
89
When do oxytocin receptors reach peak levels?
by 34-35 weeks until labour(where they increase again). 12 fold increase from T1
90
What stimulates oxytocin receptor formation?
oestrogen
91
Where are the oxytocin receptors found and in what volume?
Myometrial receptor concentrations are highest in the fundus and the corpus with less in the lower uterine segment and the cervix has the lowest concentration
92
What nerve supplies the sympathetic nervous system to the uterus?
hypogastric nerve
93
What receptors on the uterus cause contractions?
alpha adreno receptors
94
What receptors on the uterus cause relaxation? What is this clinical relevance?
beta adreno receptors. Terbutaline is a beta agonist
95
How does nifedpine work to stimulate uterine relaxation?
Work on gap junctions to reduce myometrial activity but relies on calcium levels.
96
What physical changes occur in the cervix with cervical ripening?
* Increase in water content * Alteration in proteoglycan/glycosaminoglycan composition * Reduction in collagen concentration * Rearrangement and realignment of collagen
97
What are the two theories on what stimulates labour?
1. withdrawal of progesterone 2. increase in corticotrophin releasing hormone
98
How does the withdrawal of progesterone start labour?
Progesterone inhibits myometrial contractions and decreases gap junction formation, anti-inflammatory agent
99
How would CRH increase stimulate labour?
- CRH is secreted by trophoblasts - Usually the levels of CRH are kept low by CRH binding protein - 3 weeks prior to spontaneous labour there is a fall in the CRH BP in the maternal circulation and amniotic fluid level - CRH stimulates prostaglandins and from human amnion and decidua which stimulates oxytocin - higher CRH levels are associated with PTB
100
Where is CRH normally made and what does it do?
made in hypothalamus stimulates APG to release ACTH Which stimulates the adrenal glands to release cortisol
101
What are the six mechanisms of birth?
1. Cervical effacement & dilation 2. Descent, flexion & internal rotation (OT to OA/OP) 3. Extension (crowning) 4. Delivery of the head 5. External rotation (restitution) 6. Delivery of the shoulders & body
102
What is the definition of the first stage of labour?
defined from onset of regular uterine activity associated with effacement and dilation of the cervix and descent of the presenting part
103
What would be a prolonged third stage?
active management >30 minutes physiological >60 minutes
104
What is the friedman curve?
observational data in the 1950s on the progress of labour * Average progress during active phase of 1.1cm per hour Average length of labour * Nulliparous: 12 hours Multiparous: 6 hours Newer data saying progress can be 0.5cm per hour NICE says 2cm in 4hours
105
What are the three pelvic bones?
ilium, ischium, pubis
106
What makes up the pelvic inlet?
pubic symphysis ala of the sacrum sacral prominentry ileopectineal line
107
What is the shape of the pelvic inlet?
round. 13.5 trans and 11.5 AP
108
What is the mid pelvis? How big is it?
in line with the ischial spines, 10.5cm
109
What is another name for the ileopectineal lines?
arcuate lines
110
What is the subpubic arch?
convergence of the inferior rami of the ischium and pubis on either side, below the pubic symphysis.
111
What is the shape and the boundaries of the pelvic outlet?
diamond shaped boundaries are subpubic arch, ischial tuberosities, sacrotuberous ligaments (posterior from ischial tuberosity to sacrum) & coccyx
112
What is the size of the pelvic outlet?
AP 9.5-11.5cm Transverse 11cm
113
What is the bregma on the skull?
where the coronal and sagittal sutures meet
114
What are the anatomical landmarks presenting in a face presentation and what is the width?
submento bregmatic 9.5cm
115
What are the anatomical landmarks presenting in a brow presentation and what is the width?
mento vertical (vertex) 13.5cm
116
What are the anatomical landmarks presenting in a deflexed OP presentation and what is the width?
occipito posterior 11cm
117
What are the anatomical landmarks presenting in a vertex presentation and what is the width?
This is optimal fetal position sub occipital bregmatic 9.5cm
118
Which face presentation can deliver vaginally?
mento anterior
119
What do you do with an engaged brow?
CS
120
What are the three stages on CTG of fetal hypoxia development in labour?
1. stress - presence of decelerations without rise in baseline or reduction in variability 2. stress to distress - loss of accelerations --> rise in baseline --> loss of variability 3. distress to collapse - rise in BR, marker reduction in variability, no accelerations may be born with acidosis and hypoxia. if ignored may get terminal brady cardia
121
Why do chronically hypoxic fetuses not always have a BR rise?
unable to increase HR
122
what would make you concerned about the fetal status in a bradycardia?
reduced variability prior
123
What is the 3, 6, 9, 12 rule in bradycardia?
3 minutes - medical attention 6 minutes - start preparing for expediting delivery. eg move to theatre 9 minutes - expedite delivery 12 minutes - ideally baby should be delivered
124
What occurs if the fetal baseline rate is less than the deceleration time?
fetus is unable to replenish it's oxygen levels and excrete CO2. risk of fetal acidosis and hypoxia
125
in IA how often should you listen?
Listen for 1 minute first stage, every 15 minutes after contraction second stage, either after every contraction or every five minutes
126
How regularly should you do obs in labour?
every four hours in first stage every hour in second stage
127
What is the MOTHERS acronym for fetal acidosis?
Meconium oxytocin temperature hyperstimulation /haemorrhage epidural rate of progress scar
128
How does anaerobic metabolism cause acidosis?
lactic acid is a by product. H+ ion on lactic acid is poorly buffered by fetal circulation --> tissue damage and toxicity
129
What is the energy efficiency of anaerobic metabolism?
95% less efficient
130
What is the chance of fetal hypoxia base on CTG alone?
50%
131
What pH reflects acidosis on FBS?
<7.2
132
What FBS lactate reflects fetal acidosis?
>4.9
133
What are the CI to FBS?
maternal refusal, fetal bleeding disorders (haemophilia, NAIT, chronic immune thrombocytopenia), <34 weeks maternal infection - HIV, Hep B, Hep C, active genital herpes
134
How much can left lateral tilt increase CO by?
20-25%
135
What fluid bolus had been shown to reduce hypoxia in fetus?
500ml over 20 minutes
136
Why is maternal oxygen for fetal hypoxia not used?
causes fetal harm through creation of free radicals
137
What is measured in APGARs?
appearance (colour) pulse grimace (reflex irritability) activity (muscle tone) respiratory rate
138
Why do we take an arterial and a venous cord gas?
artery - provides most accurate information about fetal and new born acid base status vein provides maternal and venous info
139
What pH and base deficit are substantially associated with neonatal mortality and morbitidity and CP?
pH <7 and base def <12
140
what do lactic acid in the brain and hypoxia cause?
edema and tissue necrosis
141
What are the CI to FSE?
* Maternal infection - HIV, Hep B, Hep C, active genital herpes, chorio * History of genital herpes - avoid if possible * <34 weeks * Face, brow or uncertain presentation * Bleeding disorder - haemophilia, fetal thrombocytopenia, known maternal AI thrombocytopenia
142
What is the rate of uterine rupture in women planning vaginal birth after CS?
1 in 122 to 500
143
What is the risk of RBC transfusion for planning vaginal birth vs ERCS?
higher in plnning vaginal birth OR 2.8 but only one RBC for every 125-248 women planning vaginal birth
144
What is the risk of perpueral sepsis for planning vaginal birth vs ERCS?
higher in planned vaginal birth only 1 in 1000
145
What is the risk of surgical injury for planning vaginal birth vs ERCS?
higher in planned vaginal birth 1 in 1250
146
What is the risk of OASI in planned vaginal birth after CS?
OR 1.27
147
What is the risk of RDS for planning vaginal birth vs ERCS?
reduced in planned vaginal birth group OR 0.32
148
What is the risk of apgars <7 at 5 minutes for planning vaginal birth vs ERCS?
four fold higher in planned vaginal birth but still only 1 in 98-112
149
What is the risk of perinatal death and NICU admission for planning vaginal birth vs ERCS?
conflicting data
150
What are the maternal variable which can change success rates for planned vaginal birth?
* Obstetric history * IPI - <18 months of >35 months may slightly increase risk of EmCS * Medical hx - GDM, HTN may increase risk of EmCS * Age - increased risk of emCS with advancing age 35-39 RR 1.49 and >39 RR 2.08 * BMI - if >30 RR 0.5, >40 RR 0.42 * Fetal and neonatal characteristics - SGA and breech and LGA increase risk of emCS. Gestation no difference
151
What cut off for IPI does RANZCOG use for increased risk for uterine rupture?
<21 months
152
what variables does grobmans model for the MFMU calculator use?
1. Maternal age 2. Pre pregnancy weight 3. Height 4. Previous labour dystocia 5. Obstetric history * No vaginal birth * Previous vaginal birth before CS * Previous VBAC 6. Treated chronic HTN
153
What is the reduced likelihood of successful VBAC with induction vs spont. labour?
OR 0.86
154
What is the documented rate of uterine rupture with planning vaginal birth after 2 CS eg 1 per*?
1 per 327
155
What is the rate of perinatal death related to uterine rupture in VBAC per 1000?
0.4-0.7
156
What is the rate of neonatal acidosis <7 related to uterine rupture in VBAC per 1000?
1.5
157
what was the perinatal related death number in 2021?
11.2 per 1000 births (highest since 2010). increased TOPs >20 weeks
158
What trend are we seeing with perinatal death rates?
stable
159
What are the two most common causes of perinatal death?
congenital anomalies 28% spontaneous PTL with ROM <37 weeks 17%
160
What are the high risk groups for perinatal death?
maori pasifika indian age <20 and >40 low SES
161
What is the increase in risk of perinatal death with COVID in pregnancy?
7 x higher
162
What trend is there in NE rates in NZ?
small, upward trend SS
163
What is the leading cause of maternal mortality in NZ?
suicide 40%
164
What is the increase in suicide of maori in maternal death rates?
3 x
165
What is the definition of maternal death?
death of a person while pregnant of withing 42 days after the end of the pregnancy (6 weeks) from any cause related to or aggravated by the pregnancy or it's management.
166
What are causes of maternal mortality broken down into with the PMMRC?
direct indirect unknown coincidental (unrelated to pregnancy)
167
What is does direct causes in the PMMR for maternal mortality mean?
complications of pregnancy, labour or puerperium
168
What is does indirect causes in the PMMR for maternal mortality mean?
underlying medical conditions exacerbated by pregnancy
169
What are some examples of direct causes of pregnancy related death?
Suicide AFE Hypertensive disorders of pregnancy Haemorrhage VTE Sepsis
170
What is the HELPERR acronym stand for?
H Call for help E Evaluate for episiotomy L Legs into mcroberts P Suprapubic pressure E Enter rotational movements R Remove the posterior arm R Roll onto hands and knees
171
What is the definition of asphyxia?
a condition of impaired gas exchange which can lead to hypoxia and hypercapnia
172
What is the definition of ischaemia?
low perfusion in the tissue bed
173
What is the definition of hypoxia?
tissue concentration of oxygen that is less than normal
174
What is base deficit?
Base deficit is the amount of base in mmol/L that would be required to get the pH back to normal 7.40 at standard temperature and PaCO2
175
What are the neonatal signs of acute birth asphyxia?
Apgar <5 at 5 and 10 minutes cord artery <7 or base excess equal or more than 12 neuro imaging evidence of acute brain injury presence of multi organ failure consistent with HIE cerebral palsy - spastic quadriplegia or dyskinetic CP are most common
176
In chronic hypoxia where do fetuses redistribute blood flow?
heart, brain, adrenals
177
What do babies with chronic hypoxia normally has problems with when born?
temperature control due to decreased energy stores eg brown fat and glycogen metabolic issues eg hypoglycemia, lipid metabolism may show periventricular leukomalacia and develop spastic CP
178
What are the kinds of hypoxia?
chronic chronic partial hypoxia acute asphyxia
179
What causes cerebral injury in acute asphyxia?
ischaemia related to acute period of hypotension
180
What period of asphyxiation is associated with fetal death?
25 minutes
181
What are the causes of fetal hypoxia?
maternal - hypotension, hypoxia placental - insufficiency, abruption cord - occlusion, prolapse
182
What is the modified Sarnat criteria?
Criteria used to classify NE into mild, moderate and severe based on examination findings to guide prognosis and management including cooling.
183
What is a assessed in the modified sarnat criteria?
seizures - if present at least moderate LOC spontaneous activity when awake posture tone primitive reflexes autonotic system
184
What infants are eligible for cooling?
MSC NE stage II and III less than 6 hours of age evidence of perinatal hypoxia >35 weeks
185
What is the definition of NE?
a clinically defined syndrome of disturbed neurological function in the earliest days of life in the term infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, sub normal level of consciousness and often seizures
186
What are moderate NE features?
hypotonia, reduced LOC, decreased spontaneous movements +/- seizures
187
What are mild NE features?
uninhibited moro and strecth refelexes symptahetics effects normal EEG duration <24 hours of hyper alertness
188
What are severe NE stage features?
stupor - deeply unresponsive flaccid seizures suppressed brain stem function EEG abnormal
189
what areas of the brain with changes on MRI are associated with high risk of cerebral palsy?
basal ganglia, thalami
190
What is the best predictor on MRI of the ability to walk at two years with HIE?
signal enhancement of the posterior limb of the internal capsule
191
What are chronic changes of HIE on MRI?
cortical atrophy and thinning, and multicystic encephalomalacia
192
What is cerebral palsy?
Group of heterogenous conditions involving permanent non-progressive central motor dysfunction, affecting muscle, tone and movement
193
What are other symptoms associated with CP?
intellectual disability, communication & behavioural difficulties, seizure disorders, MSK complications, altered sensation or perception
194
What is the prevalence of CP?
2 in 1000 live births
195
What is the rate per 1000 of CP in infants <28 weeks?
82 per 1000
196
what proportion of CP is caused by perinatal hypoxia in near term/term innfants?
<10%
197
What are the 4 Hs in cardiac arrest?
hypoxia hypothermia hypoglycemia hyper/hypokalemia
198
What are the 4 ts in cardiac arrest?
tension PTx toxins thrombus tamponade
199
What % of reduction in CO do you get from aortocaval compression?
30-40%
200
What % of CO is uterine flow?
10%
201
Why is oxygen requirement different in resus in pregnancy ?
dilutional anaemia reduced functional residual capacity increased O2 consumption from the uteroplacental unit
202
When should PMCS be complete by?
5 minutes
203
What are risk factors for AFE?
poly hydramnios, uterine rupture, abruption, AMA
204
When does AFE normally occur by?
labour or within 30 minutes
205
What physiological response occurs in AFE?
1. pulmonary hypertension from systemic vaso constriction 2. coagulopathy due to release of plasminogen activation inhibitor 1 and massive fibrinolysis and procoauglant tissue factor causing consumptive coagulopathy 2. anaphylactoid response from histamine release
206
what are the serious sequelae of AFE?
arrythmia pulmonary edema ARDS coagulopathy cardiac failure
207
What should you give in local anaesthetic toxicity?
intra lipid bolus (1.5mg/kg) then infusion (15mg/kg/hr)
208
how do you manage anaphylaxis?
1. raise feet up 2. 0.5ml of 1:1000 IM adrenaline, can be given 5 minutely 3. hydrocortisone 100mg IM or slow IV 4. Can be biphasic monitor for 6 hours 5. Typtase levels start, one hour and 24 hours 6. refer to allergy clinc
209
what is the preferred mode of delivery for women with cardiomyopathy?
vaginal birth without active pushing
210
What are clinical signs of aortic dissection?
Tachycardia, different or absent peripheral pulses and variations in blood pressure between the limbs New heart murmur on auscultation
211
how do you diagnose aortic dissection in pregnancy?
echo
212
What medication needs to be given in cardiomyopathy?
clexane
213
What % of deliveries have a shoulder dystocia?
0.6-1%
214
What % of SD will have a brachial plexus injury?
4-16%
215
what % will have a permanent disability after a brachial plexus injury?
<10%
216
What occurs with erbs palsy?
injury of C5-6 internal rotation and adduction of should with extension elbow and pronation of wrist
217
What is the recurrence rate of shoulder dystocia?
1-25%
218
What is the shoulder dystocia risk of a GDM vs non GDM baby >4.5kg
50% vs 22%
219
what % of shoulder dystocia will mcroberts resolve?
90
220
how do you complete delivery of the posterior arm?
grasp wrist and withdraw arm in a straight line from vagina
221
What is the perinatal mortality rate of cord prolapse?
1%
222
what idd the big baby trial find?
a RR of 0.62 in shoulder dystocia in PPA with IOL at 38-38+4 no difference in neonatal composite outcomes of injury or prematurity related maternal outcomes of CS and composite of OASI, PPH tears reduced with IOL
223
What nerve level should be blocked for CS or trial?
T4-S4
224
What nerve level should be blocked for an epidural?
T10-S4
225
What level should be blocked for perineal repair?
S2-S4
226
Why don't be use pethidine anymore?
crosses the placenta much more readily than morphine
227
Why is remifenatnil used in labour?
rapid acting <1 minutes, doesn't accumulates, lipophilic and minimal crossing of placenta as rapidly degraded
228
Who is should you be cautious with remifent for?
asthma, sleep apnoea, addrenocortical insuff.
229
What is the maximum you should use entonox for and why?
24 hours, bone marrow suppression
230
Where does the pundendal nerve arise from?
S2-4
231
What is the motor and sensory innervation of pudendal nerve?
motor - muscles of perineum sensory - vestibule and external genitalia
232
What are the three branches of the pudendal nerve?
1. dorsal nerve clitoris 2. perineal branch 3. inferior haemorrhoidal branch
233
What level do eidural and spinals go in at?
L4 tuffiers line (iliac crests)
234
Where is the epidural space?
potential space outside the dura mater, contains small blood vessels, lymphatics, loose fatty tissue and spinal nerve roots. Go through the ligamnetum flavum and a loss of resistance it is outside the dura mater
235
What space does the spinal spacemedication go into?
subarachnoid space (CSF)
236
What are indications for epidural?
* Patient request * Patients at high risks for GA (aiming to use the epidural in theatre) * Cardiac, cerebrovascular or severe respiratory disease * Extreme obesity * Previously noted or anticipated difficult airway * Malignant hyperthermia or other known reactions to anaesthetics Medical comorbidity where felt to be beneficial
237
What level does the spinal cord terminate?
L1-2
238
What are CI to epidural?
* Maternal refusal * Coagulation disorders - plts >75 * Local/generalised sepsis - concern about memningitis, spinal safe * Hypovolaemia * Fixed cardiac output - valve stenosis * Raised ICP - in case of accidental dural puncture and coning * Allergy to local anaesthetics Lack of available trained staff to care for patient post procedure
239
What are potential complications of epidrual?
need for other analgesia (1 in 8) significant BP drop (1 in 50) severe headache nerve damage epidural abscess meningitis epidural haematoma severe injury (1 in 250,000)
240
Why do you get hypotension with spinal?
blocks sympathetic vasomotor function, vessel dilatation
241
What can be done for dural headache?
rest, hydration, caffeine, blood patch
242
when adrenaline is used with local anaesthetic what does it do?
prolonged duration of action by 60%
243
What determines potency of LA?
lipid solubility
244
What determines duration of action of LA?
protein binding
245
What is bupivocaine used for?
spinals has available form with heavy solution to get gravity to asssist, long acting, slow onset
246
What is prilocaine used for?
short acting spinal eg repair or MROP
247
What is LAST?
local anaestehtics systemic toxicity
248
What are the symptoms of LAST?
Early features: perioral tingling, tinnitus, slurred speech, tremor, changed mental status (confusion, agitation, generalised convulsions) Late features: coma, respiratory depression
249
What is the maximum mg/kg of lidocaine without adrenaline?
3mg/kg (7 with adrenaline)
250
How much lidocaine in 10ml of 1%?
100mg
251
How long does aspirin and clopidogrel need to be stopped pre op?
7 days
252
what INR do you want for spinal?
<1.5
253
how can you reverse warfarin?
vitamin K prothrombin complex concentrartes FFP
254
How does heparin work?
increases antithrombin thrombin complex formation, inhibiting clotting factors and platelets
255
How do you monitor heparin effect?
APTT
256
How long should you wait after prophylactic LMWH prior to spinal or epidural?
12 hours
257
How long should you wait after treatment dose LMWH for spinal or epidural?
24 hours
258
How long should you wait after epidural removal or spinal to give clexane?
4-6 hours
259
what is the definition of APH and its prevalence?
bleeding from genital tract >20 weeks 2-5%
260
What are the contraindications to giving tocolytic in APH?
fetal compromise, mum unstable, major APH. in other situations if giving involve SMO
261
if APH beyond term what should occur?
IOL
262
What is the definition of placental abruption?
Premature separation of the placenta form uterine wall prior to delivery
263
what is the most predictive risk factor for abruption?
previous 1 previous 4.4% recurrence
264
What is the pathophysiology of abruption?
multifactorial UP ischaemia, and insufficiency from implantation inflammation and disruption of cells causing detachment can get blood extending into myomterium and then rupture.
265
What is the name of when blood tracks back into myometrium in abruption?
couvelaire uterus
266
How is abruption diagnosed and confirmed?
clinically, then on histology
267
What are common features of abruption?
bleeding, pain, contractions, fetal distress 60%, IUFD, DIC, shock
268
What are risk factors for abruption?
* PET/hypertension * FGR * Polyhydramnios * Advanced maternal age * Multiple pregnancy * Multiparity * Intrauterine infection * PPROM: earlier the PPROM = higher risk of abruption (50% if PPROM <20/40) * Thrombophilia, especially factor V Leiden and heterozygote prothrombin 20210A * Non-vertex presentations * First trimester bleeding * Low BMI * Assisted reproduction techniques * Abdominal trauma Smoking & drug misuse (particularly cocaine & amphetamines)
269
What is the incidence of abruption?
0.5-1%
270
What bloods should be done for abruption?
FBC, G+ cross match, creat, electrolytes, LFTS (HELLP), coags, kleihauer
271
What are complications of abruption?
* Infection * Anaemia * Hypovolaemic shock secondary to haemorrhage * Coagulopathy/DIC * ARF/ATN * Ischaemic necrosis of distal organs: adrenal, pituitary * Couvelaire uterus * PPH * Feto-maternal haemorrhage Psychological sequelae
272
What proportion of women will have a LLP in the second trimester?
2-28%
273
What is the rate of placenta praeveia at term?
0.5%
274
What % of LLP will resolve by term?
90%
275
What is the utility of cervical length in PP?
if <25mm RR of massivae haemorrhage at CS is 7.2
276
When should you consider classical in placenta praevia?
fetal malpresentation or <28 weeks
277
what is the increase in risk of RBC requirement in Placenta praevia?
12x
278
What is the nitabuch layer?
band of fibrinoid between decidua and fetoplacental trophopblast. invaded with PAS
279
What is the risk of placenta acreta after 1, 2, 3, 4, 5+ CS?
1 - 0.3% 2 - 0.6% 3 - 2% 4 - 2.3% 5 - 6.7% much higher if praevia present
280
how often is PAS undiagnosed?
1/2-2/3
281
What features of PAS would you see on MRI?
* Abnormal uterine bulging * Dark intraplacental bands on T2-weighted imaging * Heterogenous signal intensity within the placenta * Disorganised vasculature of the placenta * Disruption of the uteroplacental zone
282
What is median blood loss with PAS?
2-7.8L
283
When should you consider admission for PAS?
34 weeks
284
What is fetal survival rate in vasa praevia if diagnosed antenatally vs not?
97% vs 44%
285
What is fetal blood volume at term?
80-100ml/kg
286
What is uterine scar dehiscence?
partial rupture not extending beyond visceral peritoneum
287
What is the risk of recurrence of uterine rupture?
5%
288
What are risk factors for uterine rupture?
* Previous CS 1:200, increases to 0.9-1.9% with oxytocin augmentation * Previous classical CS * Previous uterine rupture * High parity * Previous uterine surgery that broached the cavity * IOL or augmentation of labour * Hyperstimulation * Malpresentation * Macrosomia * Uterine abnormalities * Trauma
289
When should CTG start in VBAC?
onset of regular contractions
290
IOL or augmentation increase risk of scar rupture by?
2-3x
291
What is the utility of kleihauer in diagnosing abruption?
it is not sensitive
292
What are the antenatal risk factors for CTG use to do with the placenta?
marginal cord, 2VC, velamentous cord insertion
293
What is listed in 'correct reversible causes' in labour for abnormal CTG?
maternal position change correct hypotension if suspected hyperstimulation remove PG or stop oxytocin, consider tocolysis screen for sepsis if temp at or more than 38.0 and treat abs consider VE to rule out cord prolapse reposition toco and consider FSE
294
What are the RANZCOG antenatal risk factors for CTG monitoring in labour with a strong evidence base?
APH, breech, GDM on treatment or with macrosomia, PIH, PET, previous intrapartum still birth, velamentous cord insertion. there are several other recommended
295
What are the RANZCOG intrapartum risk factors for CTG monitoring in labour with a strong evidence base?
abnormal bleeding, clinical chorio, meconium, PTL, prolonged first stage, excessive UA. there are several other recommended
296
What are the CTG features unlikely to be associated with fetal compromise when in isolation?
a. BR 100-109 b. Reduced variability 3-5bmp for up to 40 minutes duration c. Absence of accelerations ?for an hour d. Early decelerations Uncomplicated variables
297
What are the CTG features which may be associated with fetal compromise and need further action?
a. BR >160 b. Rising FHR c. Complicated variables d. Late decels Prolonged decels >90 secs
298
What are the CTG abnormalities which are likely to be associated with fetal compromise and require immediate management?
a. Bradycardia b. Absent baseline variability c. Increased variability d. Sinusoidal pattern e. Complicated variables with reduced or absent variability Later decels with reduced or absent variability
299
What are the contraindication to tocolysis?
allergy, suspected abruption, suspected uterine rupture, medical conditions, fluid overload
300
What are contraindications to FBS?
a. Fetal bleeding disorder b. Non vertex presentation c. Maternal infection - HIV, untreated syphilis, hep B and C, primary active herpes , HTLV-1 d. Gestation <34 weeks
301
When should FBS not be performed?
a. Abnormal CTG likely associated with fetal compromise b. Evidence of sepsis c. Evidence of serious sustained fetal compromise or contraindication
302
What is RANZCOG statement on when you should do cord gases?
1. Paired cord gases should be performed where there is evidence of fetal compromised intrapartum or poor neonatal condition 2. Suggests paired cord gases are considered as routine at all births 3. Indications for selective cord gases
303
What are indications for selected cord gases?
a. Abnormal CTG which did not normalise prior to birth b. Apgars <4 at 1 minute c. Apgars <7 at 5 minutes d. FBS in labour e. Assisted birth f. AN or IP complications
304
how do you correctly do IA in labour? What is it called
1st stage every 15 to 30 minutes 2nd stage with each contraction for 1 minute immediately after a contraction document as a single number of beats observed over a minute not a range Take maternal HR each time to check different assessment of FM assessment of UA ASIA framework
305
What is the definition of an acceleration per RANZCOG?
a transient increase in the featl heart rate
306
What is the definition of active labour per RANZCOG?
regular painful uterine contractions a substantial degree of cervical effacement and cervical dilatation of 5cm of more to full dilation
307
What is the definition of baseline FHR per RANZCOG?
mean level of FHR when stable, excluding accelerations, decelerations, contractions. over 5-10 minutes
308
What is the definition of baseline variability per RANZCOG?
minor fluctuations around the baseline FHR assessed by estimating the difference in bpm between the highest and the lower of fluctuation in one minute segment between contractions
309
What is the definition of an early deceleration per RANZCOG?
uniform, repetitive decrease in FHR, slow onset and recovery by the end of the contraction
310
What is the definition of a variable deceleration per RANZCOG?
repetitive or intermittent decreasing FHR with rapid onset and recovery. may have a variable relationship with the contraction but commonly occurs simultaneously with contractions
311
What is the definition of a late deceleration per RANZCOG?
uniform repetitive decreasing of FHR slow onset, mid to end of the contractions and nadir more than 20 seconds after the peak, ending after the contraction. when variability is reduced this baseline drop doesn't need to be >15 bpm
312
What is metabolic acidosis?
low pH due to an increase in lactic acid which reflects the severity of impaired gas exchange
313
What is neonatal encephalopathy as per RANZCOG?
defined syndrome of disturbed neurological function in the earliest days of life in the infant born beyond 35 weeks. Manifested by decreased LOC or seizures. no specific tests. lies on a number of complex multifactorial causal pathways to CP
314
What symptoms often accompany NE?
difficulty initiating and maintaining respiration, depression of tone and reflexes.
315
What causes NE?
hypoxic events non hypoxic events can be intra partum or not
316
What is sinusoidal pattern on CTG?
smooth, regular oscillation around the baseline. typically 2-5 per minute
317
What are the risks of an admission CTG for low risk women?
* More likely to have a CS RR 1.2 * More likely to have a FSE in labour RR 1.3 * Morel likely to have FBS RR 1.28 * No difference in assisted, epidural, augmentation or amniotomy No difference in any fetal outcomes
318
What is the data on CTG intrapartum for low risk women?
* Increased likelihood of caesarean section RR 2.06 * Decreased likelihood of babies having neonatal seizures RR 0.36 * Little to no difference in assisted birth Uncertain evidence about perinatal mortality
319
What is the advice for CTG vs IA in labour in low risk women ?
IA should be discussed as an appropriate method of monitoring for women without risk factors, CTG can be offered but has similar fetal outcomes and increased risk of CS
320
What does the cochrane review for women with identified risk factors say for intrapartum fetal surveillence?
* Probably more likely to have a CS RR 1.91 * little or no difference in assisted * little or no difference in neonatal seizures * little or no difference perinatal death * May be more likely to cerebral palsy very wide confidence intervals - from a small study of PTB 28-32 weeks. 70% of CP occur before labour
321
What are the limitations on data on IA vs CTG in women with risk factors?
most data is prior to 1994. Now difficult to study as CTG has become the minimum level of care in these women studies exclude women at high risk of adverse outcomes unknown childhood outcomes beyond 18 months
322
When should women with risk factors of intrapartum fetal compromise call the birthing unit?
early labour
323
A cord pH of <7.2 is associated with?
neonatal mortality OR 16 HIE OR 13 IVH or periventricular leucomalacia OR 2.9 cerebral palsy OR 2.3
324
What is the strongest association of pH and base deficit with adverse outcomes?
pH <7.00 and base deficit >16
325
What gestation does variability reach normal?
30 weeks
326
what gestation do accelerations become similar to that of term fetuses?
32 weeks
327
What what gestation are variable decelerations less frequent?
28-32 weeks
328
What are the ways fetal oxygen supply can be impaired?
1. low maternal oxygenation 2. reduced maternal CO or uterine hypoperfusion 3. uterine blood flow to placental bed 4. poor gas exchange at placenta 5. umbilical cord compression
329
How much does lateral positions increased fetal oxygenation?
29%
330
How long does terbutaline effect last?
15-30 minutes
331
What are contraindications to terbutaline?
hypotension cardiac conditions suspected abruption suspected uterine rupture fluid overload allergy
332
What doses of GTN can you give for tocolysis?
sublingual 400mcg or 50mcg IV
333
What is a positive response to fetal scalp stim?
increase in variability or FHR
334
What do studies show about the NPV and PPV of FSS and FBS?
low PPV and high NPV so if negative for compromise very reasurring eg reponse of normal FBS if abnormal not as useful as reasonable number will still be normal
335
What are the benefits of lactate over pH from scalp?
less chance of failure as reliable less blood needed cheaper machine POC
336
When studied what is the benefit of FSS over FBS?
lower risk of CS with similar neonatal outcomes no adverse events can cause a vagal response causing decel
337
What are the down sides to FBS?
can cause delay in OT possibly worsening APGARs can only be done when cervix 3cm or more no evidence reduces CS or seizures potential for fetal injury
338
What is the level FBS or lactate needing expedited delivery?
lactate 4.8 or more pH 7.2 or less
339
What is borderline FBS and pH?
4.1-4.7 7.21 to 7.24
340
What benefit does FSE have on outomes ?
may reduce CS
341
What is the risk of abdominal only CTG?
may increase risk of NE and severe acidemia
342
What is the pH cut off for CP, epilespy, intellectual disability and SN defect at 4 years?
7.10
343
What is the argument against universal cord blood sampling?
have not been shown to predict adverse neonatal outcomes medicalises birth may impact DCC is of little importance is neonate is vigorous
344
How can you know if cord gases are A and V?
pH difference of 0.02 or more
345
From the cochrane review what does work in labour for analgesia?
epidural, CSE, inhaled anaesthesia
346
From the cochrane review what may work in labour for analgesia?
non opioid drugs (sedatives), water immersion, accupuncture, massage, relaxation, LA nerve blocks,
347
From the cochrane review what is there sufficient evidence to make judgement on for labour analgesia?
TENS parenteral opioids aromatherapy sterile water injection hyponosis biofeedback
348
What does the cochrane reveiw about analgesia in labour say about epidural ADRs?
increased fever, instrumental, CS for fetal distress but no different in CS overall, hypotension, urinary retention
349
What is morphine very effective for in labour?
visceral pain
350
What area on the vulva is not covered by a pudendal nerve block?
anterior labia, clitoris
351
What are the two kinds of pain experienced in labour?
visceral (early and late labour) somatic pain (late labour)
352
What kinds of pain do unmyelinated C fibres carry?
visceral pain, slow, dull, aching
353
What kinds of pain do myelinated A delta nerves carry?
somatic pain, fast, sharp
354
How do visceral pain signals get from the cervix/uterus to the brain?
Travel through uterine, cervical and inferior hypogastric nerve plexus into the main sympathetic chain -> posterior nerve roots -> enter spinal cord at the level of T10 to L1 --> synapse on the dorsal horn and run in the spinothalamic tract
355
Where does visceral T10-L1 pain refer to in early labour?
abdominal wall, lumbosacaral region, iliac crests, gluteal area and thighs
356
When do you experience somatic pain in labour? what causes it
transition and second stage. vaginal and perineal stretching
357
What somatic nerves are involved in labour?
pudendal and perineal branches of the posterior cutaneous nerve of the thigh S2-4 ilioinguinal and genitofemoral nerve L1-2
358
What path does the pudendal nerve take?
Arises from the sacral nerve plexus S2-S4. Course: * Exits the pelvis through the greater sciatic foramen * Under and around the sacrospinous ligament near the spinous process * Enters pelvis via the lesser sciatic foramen Then travels in the pudendal canal, made by the fascia of the obturator internus muscle
359
What kind of nerve is the pudendal nerve?
motor and sensory
360
What are the motor innervations of the pudenal nerve?
innervates external urethral sphincter and external anal sphincter, the bulbospongiosus, ischiocavernosus, levator anii
361
What does the perineal branch of the pudenal nerve innervate?
perineum, labia majora and minora, posterior scrotum
362
What does the inferior rectal branch of the pudenal nerve innervate?
perianal skin and lower third of anal canal
363