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RANZCOG 2024 - Neonatal Edward > Birth Trauma and CP > Flashcards

Birth Trauma and CP Flashcards

1
Q

Discuss birth trauma
-Incidence (2)
-Risk factors (7)

A
  1. Incidence
    6-8:1000 live births
  2. Risk factors
    -LBW
    -LGA
    -Prematurity
    -Prolonged / rapid labour
    -Instrumental deliveries
    -Vaginal breech
    -Abnormal traction during delivery
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2
Q

Discuss cephalhaematoma
-Pathophysiology (4)
-Presentation (5)
-Management (2)

A
  1. Pathophysiology
    -Subperiosteal collection of blood.
    -Doesn’t cross suture lines so is self contained
    -Relatively common
    -Associated with prolonged labour or instrumental delivery
  2. Presentation
    Parietal usually.
    Can be bilateral
    Largest on second day.
    Boggy mass 48-72 hrs post delivery
    Exaccerbates jaundice
  3. Management
    Resolves in days to months
    Rarely needs drainage
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3
Q

Discuss subgaleal haemorrhage
-Pathophysiology
-Presentation
-Management

A
  1. Pathophysiology
    -Occurs between galea aponeurosis and periosteum
    -Associated with prematurity, ventouse (90%), may have underlying coagulopathy
    -40% associated with skull fracture, Intracranial haemorrhage
    Can hold up to 250mL (Almost all 3kg baby’s blood volume)
  2. Presentation
    -Boggy appearance and pitting skull oedema
    -Anterior displacement of the ears
    -Flick sign (Thrill or crepitus)
    -Fetal irritability
    -Periorbital oedema
    -Hypovolemic shock
  3. Management
    -Blood transfusion
    -FFP and coagulation factors
    -Phototherapy if Jaundice
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4
Q

Discuss cephalhaematoma
-Pathophysiology (4)
-Presentation (5)
-Management (3)

A
  1. Pathophysiology
    -Subperiosteal collection of blood.
    -Doesn’t cross suture lines so is self contained
    -Relatively common
    -Associated with prolonged labour or instrumental delivery
  2. Presentation
    Parietal usually.
    Can be bilateral
    Largest on second day.
    Boggy mass 48-72 hrs post delivery
    Exaccerbates jaundice
  3. Management
    Resolves in days to months
    Rarely needs drainage
    Photo therapy if jaundice
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5
Q

Discuss subgaleal haemorrhage
-Pathophysiology (5)
-Mortality rate (1)
-Incidence (2)
-Risk factors

A
  1. Pathophysiology
    -Occurs between galea/epicranial aponeurosis and periosteum
    -Potential space that can accommodate 250mL (90mL/kg babies blood volume)
    -Results from rupture of the emissary veins
    -40% associated with skull fracture, Intracranial haemorrhage
  2. Mortality rate
    -12-25%
  3. Incidence
    -0.6:1000 deliveries
    -6:1000 ventouse deliveries
  4. Risk factors
    -60-90% from ventouse deliveries
    -Nulliparity OR 4
    -Poor cup placement - over to one side, Not over flexion point
    -Failed vaccum extraction OR 16
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6
Q

Discuss facial palsy
-Pathophysiology
-Presentation
-Management

A
  1. Pathophysiology
    -Unilateral facial weakness.
    -Can be bilateral but then likely congenital cause
    -Associated with forceps delivery or pressure on maternal ischial spine
  2. Presentation
    -Unilateral facial weakness with ipsilateral eye remaining open
  3. Management
    -Eye drops if eye permanently open
    -Resolves in 1-2 weeks
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7
Q

Discuss facial palsy
-Pathophysiology (3)
-Presentation (1)
-Management (2)

A
  1. Pathophysiology
    -Unilateral facial weakness.
    -Can be bilateral but then likely congenital cause
    -Associated with forceps delivery or pressure on maternal ischial spine
  2. Presentation
    -Unilateral facial weakness with ipsilateral eye remaining open
  3. Management
    -Eye drops if eye permanently open
    -Resolves in 1-2 weeks
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8
Q

Discuss brachial plexus injury
-Types (2)
-Nerves affected in each type
-Incidence of each type
-Management
-Prognosis

A
  1. Types
    -Erbs palsy C5-6
    -Klumpke’s palsy C7-T1
  2. Incidence of each type
    -Erbs >90%
    -Klumpke’s <1%
  3. Management ad prognosis
    -Most heal without treatment in 3-4 months
    -Physiotherapy
    -Erbs 90% resolve
    -Klumpke’s 40% resolve
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9
Q

Discuss cerebral palsy
-Incidence (1)
-Definition (3)
-Cause (2)

A
  1. Incidence
    -2:1000 lie births
  2. Definition
    -Group of disorders characterised by motor and postural dysfunction
    -Permanent and non progressive
    -Commonly associated with cognitive impairment
  3. Causes
    -Many usually unidentified factors
    -More likely due to delivery event if preterm
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10
Q

Discuss the correlation of apgar scores and development of CP

A

-5 minute APGAR <7 increased risk CP
-10 minute APGAR <4 - 5% of babies develop CP
-75% of babies who develop CP have normal APGARS

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11
Q

Discuss risk factors for cerebral palsy
-Fetal (3)
-Obstetric (4)
-Neonatal (3)

A
  1. Fetal risk factors
    -PTB <34/40 - 5%
    -LBW <1500g
    -Multiple pregnancy 5% of triplets 1% of twins
  2. Obstetric risk factors
    -Chorioamnionitis
    -Antepartum haemorrhage
    -Placental insufficiency
    -Perinatal asphyxia
  3. Neonatal
    -Intraventricular haemorrhage
    -Periventricular leucomalacia
    -HIE (Biggest RF)
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12
Q

Discuss the correlation of APGAR scores and development of CP

A

-5 minute APGAR <7 increased risk CP
-10 minute APGAR <4 - 5% of babies develop CP
-75% of babies who develop CP have normal APGARS

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13
Q

Discuss the correlation of APGAR scores and development of CP (3)

A

-5 minute APGAR <7 increased risk CP
-10 minute APGAR <4 - 5% of babies develop CP
-75% of babies who develop CP have normal APGARS

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14
Q

Discuss cerebral palsy presentation

A
  1. 95% have mild/moderate symptoms
    -Associated with muscle issues and movement, spacity, weakness and balance issues
    -Increased problems with cognition, social interactions, ADHD, anxiety
    -Becomes more obvious at school age
    -50% need additional educational assistance
  2. 5% have severe impairment
    -Difficulty living independently
  3. 92% live to >20
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15
Q

Discuss hypoxic ischemic encephalopathy
-Definition (3)
-Causes (1)
-Clinical manifestation (4)
-Incidence (1)

A
  1. Definition
    -No universal definition
    -Is a subset of neonatal encephalopathy
    -Requires evidence of hypoxia on cord gases, low apgars and early evidence of cerebral oedema on imaging.
  2. Causes
    -Results from intrapartum hypoxia and acidosis
    -Not all metabolic acidotic babies develop HIE
  3. Clinical manifestations
    -Abnormal level of conscience
    -Seizures
    -Difficulty with breathing - initiating and maintaining
    -Depression of tone and reflexes
  4. Incidence
    -1.5:1000 live births
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16
Q

Discuss hypoxic ischemic encephalopathy
-Grades
-Characteristics of each grade
-Prognosis of each grade

A
  1. Grade 1 - mild
    -Hyper alterness
    -Irritability
    -Jittery
    -Normal EEG
  2. Grade 2 - moderate
    -Obtundation
    -Hypotonia
    -Strong distal flexion
    -Multifocal seizures
    Prognosis:
    -20-30% death or major neurological sequalae
  3. Grade 3 - severe
    -Coma
    -Frequent seizures
    Prognosis:
    Majority of cases = death or severe neurological sequalae
  4. Overall prognosis
    -14% of HIE develop CP
17
Q

Discuss diagnosis for HIE (3)

A
  1. EEG
    -Do son after birth to look for seizure activity
    -Of prognostic value
  2. Cranial USS
    -Use to detect cerebral oedema
    -Can show brain lesions associated with CP (periventiricular leukomalacia, IVH)
  3. MRI
    -Gold standard
    -Early imaging before 96 hr helps to show cause of hypoxia
    -MRI around 10days shows full extent of brain injury
    -Good for prognosis
18
Q

Discuss cooling as management of HIE
-Method of cooling
-Who should be cooled
-Pathophysiology behind management
-Efficacy of cooling

A
  1. Method of cooling
    -Reduce temp to 34 degrees within 6hrs of birth and maintain for 72hrs with slow rewarming
  2. Who should be cooled
    -Moderate or severe HUE
    - >36/40
    -Evidence of acidosis pH <7 BE >16
    -APGAR <5
  3. Pathophysiology behind management
    -Ischemia causes primary neuronal death
    -Upon re-establishment of circulation there can be secondary neuronal death in a zone around the initial neuronal death.
    -Cooling aims to avoid / decrease this secondary neuronal death
  4. Efficacy
    -NNT in moderate HIE = 6
    -NNT in severe HIE = 7
19
Q

What are the poor prognostic markers for HIE (6)

A
  1. Persistent seizures
  2. Persistent abnormal neurological exam
  3. Poor feeding by 2 weeks of age
  4. Limited evidence of recovery on EEG
  5. Abnormal MRI findings suggesting basal ganglia changes or cerebral atrophy
  6. Poor postnatal head growth
20
Q

Outline the steps of neonatal resus

A
  1. Assess infant for tone, breathing, crying
  2. Dry and take to resus site - resusitare
  3. Keep warm
  4. If poor breathing effort or HR <100 start positive pressure ventilation with room air
21
Q

Discuss subgaleal haemorrhage
-Presentation (7)
-Management ()

A
  1. Presentation
    -Mean onset 1-6hrs post delivery
    -Diagnosis is clinical. Don’t delay for imaging
    Generalised signs:
    -associated with blood loss and low 5 min apgar in setting of no asphyxia
    Localised signs:
    -Generalised skull swelling and scalp laxity, pitting oedema infront of ears
    -Ballotable lesion that crosses suture lines
    -Anterior displacement of the ears and periorbital oedema
    -Crepitius or fluid thrill - flick test +
    -Hypovolemic shock
  2. Management
    -Medical emergency.
    -Involve senior paeds immediately
    -Serial head measures may be useful but shouldn’t be considered reassuring
    -Blood transfusion and aggressive fluid resus
    -FFP and coagulation factors
    -Phototherapy if Jaundice
22
Q

Discuss prevention strategies for subgaleal haemorrhage
-Appropriate patient selection (3)
-Proper technique (10)
-Medical prophylaxis (1)

A
  1. Appropriate patient selection
    -Absolute contra-indication if <34/40
    -Relative contraindication if <36/40
    -Absolute contra-indication in infants with bleeding disorders
  2. Proper technique
    -Should be done by someone with adequate training or with supervision
    -Cup should be placed on flexion point
    -Cup should be /3cm (ideally 6cm) from anterior fontanelle
    -Cup should be placed evenly across sagittal suture
    -Steady traction with contractions and maternal effort only
    -Good decent of head
    -Avoid prolonged traction
    -Abandon if time longer than 20mins and not delivered (consider changing tact after 15mins)
    -Abandon if more than 3 pulls and head not yet on perineum (Can do more if birth imminent)
    -Abandon if > 3 pop offs
  3. Medical prophylaxis
    -IM Vit K for all neonates with instrumental delivery
23
Q

Discuss neonatal surveillance for subgalial haemorrhage
-Levels of neonatal surveillance (3)
-Indication for monitoring at each level (3)
-What each level requires in terms of surveillance

A
  1. Intensity of surveillance should be based on perceived risk of SGH
  2. Level 1 neonatal surveillance
    Indaction:
    Minimum surveillance level for all infants delivered by instrumental or second stage CS
    Monitoring
    -Baseline obs and activity at 1 hr of age
    -Structural assessments at 1-6hrs then at 24hrs post birth
    -Avoid hats so changing head size and appearance can be noted
    -If signs of SGH then escalate to level 2 surveillance
    -If concern secondary to neonatal behaviour (irritable, poor feeding, pallor) escalate to level 2
  3. Level 2 neonatal surveillance
    Indication:
    -Total extraction time >20mins, >3 pulls, >2 pop offs
    -5 min apgar <7
    -At clinical request
    -Level one surveillance causing concern
    Monitoring:
    -Take cord bloods
    -Check Haemocrit and plts
    -Continue formal neonatal SGH obs for 12 hrs - hrly x 2 then 2 hrly
  4. Level 3 neonatal surveillance
    Indications:
    -Clinical suspicion following delivery
    -Abnormalities noted on level 2 surveillance
    Monitoring:
    -Review by paeds with consideration for admission to NICU for ongoing investigation and management
24
Q

Discuss responsibility of neonatal resus
-Who should attend low risk births (3)
-Who should attend high risk births (3)
-Who decides who should be there

A
  1. Who should attend low risk births
    -There should always be someone who is trained in neonatal resus
    -Staff members trained in basic neonatal resus
    (Resus steps up to CPR)
    -Health practitioners with advanced resus skills should be available but not required at the birth
  2. Who should attend high risk births
    -Health practitioners with advanced resus skills (Intubation, vascular cannulation, use of drugs and fluids)
    -The health practitioner should only be responsible for care of the baby (not the mother)
    -More than one experienced health practitioner with training should be at the birth.
  3. Who decides who should be there?
    -The responsibility falls to the accoucher managing the birth to decide based on RF
25
Q

Discuss the responsibilities of medical practitioners at neonatal resus
-Who decides on skill level required
-What should skill levels requirement be based on
-What should happen if ongoing care is needed post resus

A
  1. Who decides
    Requirement for staff skilled in advanced resus is at the discretion of the medical staff
  2. Things to consider for need of skills
    -Fetal risk factors
    -Maternal risk factors
    -Intrapartum risk factors
    -Whether a skilled practitioner can be there urgently if required. If not then should be in attendance as a precaution or tx woman
  3. Ongoing care post resus
    -The responsible clinician should be free from other responsibilities
    -There should be a clear hand over of duty and information
26
Q

What are the criteria which suggests intrapartum CP (6)

A
  1. Low apgar scores
  2. High umbillical arterial lactates / low pH <7.0 BE >12
  3. Early onset of HIE grades 2 and 3
  4. Early imaging supporting an acute non-focal cerebral anomaly
  5. Spastic quadraplegic or dykinetic CP
  6. No other reason for CP

RANZCOG 2024 - Neonatal Edward (3 decks)

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