Neonateology Flashcards

1
Q

What is the most frequent cause of severe early-onset (< 7 days) infection in newborn infants?

A

Group B streptococcus infection

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2
Q

What is caput succedaneum?

A

Caput succedaneum (caput) involves fluid (oedema) collecting on the scalp, outside the periosteum.

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3
Q

How does caput present and how is it resolved?

A

There is usually no, or only mild, discolouration of the skin. It does not require any treatment and will resolve within a few days.

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4
Q

What causes caput?

A

Caput is caused by pressure to a specific area of the scalp during a traumatic, prolonged or instrumental delivery.

The periosteum is a layer of dense connective tissue that lines the outside of the skull and does not cross the sutures (the gaps in the baby’s skull).

The fluid is outside the periosteum, which means it is able to cross the suture lines.

Fluid (oedema) collecting on the scalp, outside the periosteum.

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5
Q

What is Cephalohaematoma?

A

A cephalohaematoma is a collection of blood between the skull and the periosteum.

It is caused by damage to blood vessels during a traumatic, prolonged or instrumental delivery.

It can be described as a traumatic subperiosteal haematoma.

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6
Q

Cephalohaematoma vs caput?

A

In cephalohaematoma, the blood is below the periosteum, therefore the lump does not cross the suture lines of the skull. In caput the blood is above the periosteum so the lump does cross the suture lines.

Additionally, the blood can cause discolouration of the skin in the affected area in cephalohaematoma.

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7
Q

How does cephalohaematoma appear?

A

Head swelling, localised within suture boundaries, discolouration due to blood

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8
Q

Management of cephalohaematoma?

A

Usually a cephalohaematoma does not required any intervention and resolves without treatment within a few months.

There is a risk of anaemia and jaundice due to the blood that collects within the haematoma and breaks down, releasing bilirubin. For this reason the baby should be monitored for anaemia, jaundice and resolution of the haematoma.

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9
Q

Potential complication of cephalohaematoma and the subsequent required monitored?

A

There is a risk of anaemia and jaundice due to the blood that collects within the haematoma and breaks down, releasing bilirubin. For this reason the baby should be monitored for anaemia, jaundice and resolution of the haematoma.

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10
Q

Why might a neonate have facial paralysis?

A

Delivery can cause damage to the facial nerve.

Facial nerve injury is typically associated with a forceps delivery.

This can result in facial palsy (weakness of the facial nerve on one side).

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11
Q

Management/prognosis of facial paralysis?

A

Function normally returns spontaneously within a few months.

If function does not return they may required neurosurgical input.

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12
Q

Facial nerve injury in the newborn is most commonly the result of what?

A

Forceps delivery

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13
Q

Features of Erb’s palsy

A

Weakness of shoulder abduction and external rotation, arm flexion and finger extension.

This leads to the affected arm having a “waiters tip” appearance:

Internally rotated shoulder

Extended elbow

Flexed wrist facing backwards (pronated)

Lack of movement in the affected arm

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14
Q

What causes Erb;s palsy?

A

An Erb’s palsy is the result of injury to the C5/C6 nerves in the brachial plexus during birth

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15
Q

What is Erb’s palsy associated with?

A

It is associated with shoulder dystocia, traumatic or instrumental delivery and large birth weight.

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16
Q

Which nerves are involved in Erb’s palsy?

A

C5/C6 nerves in the brachial plexus

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17
Q

What might a clavicle fracture during birth be associated with?

A

The clavicle may be fractured during birth. A fractured clavicle can be associated with shoulder dystocia, traumatic or instrumental delivery and large birth weight.

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18
Q

Presentation of clavicle fracture in the newborn?

A

A fractured clavicle can be picked up shortly after birth or during the newborn examination with:

Noticeable lack of movement or asymmetry of movement in the affected arm

Asymmetry of the shoulders, with the affected shoulder lower than the normal shoulder

Pain and distress on movement of the arm

A fractured clavicle can be confirmed with ultrasound or x-ray.

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19
Q

Management of clavicle fracture in the newborn?

A

Management is conservative, occasionally with immobilisation of the affected arm.

It usually heals well.

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20
Q

Potential complication of fractured clavicle in the newborn?

A

The main complication of a fractured clavicle is injury to the brachial plexus, with a subsequent nerve palsy.

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21
Q

Components of immediate care of the neonate after birth?

A

Skin to skin

Clamp the umbilical cord

Dry the baby

Keep the baby warm with a hat and blankets

Vitamin K

Label the baby

Measure the weight and length

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22
Q

Why do newborns require vitamin K?

A

Babies are born with a deficiency of vitamin K.

Vitamin K is an important part of normal blood clotting.

IM injection shortly after birth can have the helpful side effect of stimulating the baby to cry, which helps expand the lungs.

Vitamin K helps to prevent bleeding, particularly intracranial, umbilical stump and gastrointestinal bleeding.

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23
Q

How might vitamin K be delivered to the newborn?

A

Standard practice is to give all babies an intramuscular injection of vitamin K in the thigh shortly after birth.

Alternatively, vitamin K can be given orally, however this takes longer to act and requires doses at birth, 7 days and 6 weeks.

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24
Q

What is meant by skin to skin contact and what are the benefits?

A

Skin to skin contact involves putting the baby against the mothers chest immediately after birth. This has several potential benefits:

Helps warm baby
Improves mother and baby interaction
Calms the baby
Improves breast feeding

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25
Q

Normal care after birth following leaving the delivery room?

A

Initiate breast feeding or bottle feeding as soon as the baby is alert enough

The first bath is usually delayed until this baby is warm and stable. It can wait days without any issues.

Newborn examination within 72 hours

Blood spot test

Newborn hearing test

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26
Q

What conditions are screened for in Blood Spot Screening?

A

Sickle cell disease
Cystic fibrosis
Congenital hypothyroidism
Phenylketonuria
Medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
Maple syrup urine disease (MSUD)
Isovaleric acidaemia (IVA)
Glutaric aciduria type 1 (GA1)
Homocystin

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27
Q

What is Blood Spot Screening?

A

This is a screening test for 9 congenital conditions.

It is taken on day 5 (day 8 at the latest) after consent from the parent.

A heel prick is used to provide drops of blood.

The screening card requires four separate drops.

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28
Q

When does blood spot screening need to happen?

A

Ideally at day 5, by day 8 at the latest

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29
Q

How long does it take for blood spot screening results to come back?

A

6-8weeks

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30
Q

What is NAS?

A

Neonatal abstinence syndrome (NAS) refers to the withdrawal symptoms that happens in neonates of mothers that used substances in pregnancy. The symptoms and management is slightly different for each substance used in pregnancy. Mothers should be encouraged and supported with cutting back, and if possible stopping, substances that can affect the pregnancy.

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31
Q

What substances can cause NAS?

A

Opiates
Methadone
Benzodiazepines
Cocaine
Amphetamines
Nicotine or cannabis
Alcohol
SSRI antidepressants

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32
Q

In NAS, which substances can cause withdrawal symptoms from 3-72 hours following birth?

A

Most opiates
Diazepam
SSRIs
Alcohol

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33
Q

In NAS, which substances can cause withdrawal symptoms from 24 hours and 21 days following birth?

A

Most benzodiazepines other than diazepam
Methadone

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34
Q

CNS signs of NAS

A

Irritability

Increased tone

High pitched cry

Not settling

Tremors

Seizures

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35
Q

Vasomotor and respiratory signs of NAS

A

Yawning

Sweating

Unstable temperature and pyrexia

Tachypnoea (fast breathing)

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36
Q

Metabolic and GI signs of NAS

A

Poor feeding

Regurgitation or vomiting

Hypoglycaemia

Loose stools with a sore nappy area

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37
Q

NAS - what additional things should be considered after acute management?

A

Testing for hepatitis B and C and HIV

Safeguarding and social service involvement

Safety-net advice for readmission if withdrawal signs and symptoms occur

Follow up from paediatrics, social services, health visitors and the GP

Support for the mother to stop using substances

Check the suitability for breastfeeding in mothers with substance use

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38
Q

Management of NAS

A

Mothers that are known to use substances should have an alert on their notes so that when they give birth the neonate can have extra monitoring and management of NAS.

Babies are kept in hospital with monitoring on a NAS chart for at least 3 days (48 hours for SSRI antidepressants) to monitor for withdrawal symptoms.

A urine sample can be collected from the neonate to test for substances.

The neonate should be supported in a quiet and dim environment with gentle handling and comforting.

Medical treatment options for moderate to severe symptoms are dependent on the substance.
Neonates should be gradually weaned off oral treatment.
SSRI withdrawal does not typically require or benefit from medical treatment.

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39
Q

Medical management of moderate to severe NAS due to opiate withdrawl

A

Oral morphine sulphate for opiate withdrawal

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40
Q

Medical management of moderate to severe NAS for non-opiate substances

A

Oral phenobarbitone for non-opiate withdrawal

SSRI withdrawal does not typically require or benefit from medical treatment.

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41
Q

What conditions may arise in the neonate during to events in pregnancy?

A

Fetal Alcohol Syndrome
Congenital Rubella Syndrome
Congenital Varicella Syndrome
Congenital Cytomegalovirus
Congenital Toxoplasmosis
Congenital Zika Syndrome

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42
Q

Features of fetal alcohol syndrome?

A

Microcephaly (small head)
Thin upper lip
Smooth flat philtrum (the groove between the nose and upper lip)
Short palpebral fissure (short horizontal distance from one side of the eye and the other)
Learning disability
Behavioural difficulties
Hearing and vision problems
Cerebral palsy

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43
Q

Features of congenital rubella syndrome

A

Congenital cataracts

Congenital heart disease (PDA and pulmonary stenosis)

Learning disability

Hearing loss

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44
Q

When is the risk of congenital rubella syndrome highest

A

First trimester

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45
Q

Potential consequences VZV infection in pregnancy

A

More severe cases in the mother, such as varicella pneumonitis, hepatitis or encephalitis
Fetal varicella syndrome
Severe neonatal varicella infection if mum is infected around delivery

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46
Q

Symptoms congenital varicella syndrome?

A

Fetal growth restriction

Microcephaly, hydrocephalus and learning disability

Scars and significant skin changes following the dermatomes

Limb hypoplasia (underdeveloped limbs)

Cataracts and inflammation in the eye (chorioretinitis)

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47
Q

Congenital varicella syndrome occurs in around 1% of cases of chickenpox in pregnancy. It occurs when there is infection in which part of pregnancy?

A

first 28 weeks of gestation.

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48
Q

Congenital cytomegalovirus (CMV) infection symptoms?

A

Fetal growth restriction
Microcephaly
Hearing loss
Vision loss
Learning disability
Seizures

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49
Q

Classic triad of symptoms Congenital Toxoplasmosis?

A

Intracranial calcification

Hydrocephalus

Chorioretinitis

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50
Q

When is the risk of congenital toxplasmosis higher?

A

Infection with the Toxoplasma gondii parasite is usually asymptomatic. It is primarily spread by contamination with faeces from a cat that is a host of the parasite. When infection occurs during pregnancy it can lead to congenital toxoplasmosis. This risk is higher later in the pregnancy

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51
Q

Congenital Zika syndrome features?

A

Microcephaly

Fetal growth restriction

Other intracranial abnormalities, such as ventriculomegaly and cerebellar atrophy

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52
Q

What issues in early life can result from prematurity (birth before 37 weeks gestation)

A

Respiratory distress syndrome
Hypothermia
Hypoglycaemia
Poor feeding
Apnoea and bradycardia
Neonatal jaundice
Intraventricular haemorrhage
Retinopathy of prematurity
Necrotising enterocolitis
Immature immune system and infection

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53
Q

Long term affects of prematurity (birth before 37 weeks gestation)

A

Chronic lung disease of prematurity (CLDP)

Learning and behavioural difficulties

Susceptibility to infections, particularly respiratory tract infections

Hearing and visual impairment

Cerebral palsy

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54
Q

What is SIDS and when does it occur

A

Sudden infant death syndrome (SIDS) is a sudden unexplained death in an infant. It is sometimes referred to as “cot death”. This usually occurs within the first six months of life.

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55
Q

Risk factors for SIDS

A

Prematurity
Low birth weight
Smoking during pregnancy
Male baby (only slightly increased risk)

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56
Q

Measures to prevent SIDS?

A

Put the baby on their back when not directly supervised

Keep their head uncovered

Place their feet at the foot of the bed to prevent them sliding down and under the blanket

Keep the cot clear of lots of toys and blankets

Maintain a comfortable room temperature (16 – 20 ºC)

Avoid smoking. Avoid handling the baby after smoking (smoke stays on clothes).

Avoid co-sleeping, particularly on a sofa or chair

If co-sleeping avoid alcohol, drugs, smoking, sleeping tablets or deep sleepers

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57
Q

Support for parents who have lost a child to SIDS

A

The lullaby trust is a great charity to help support families affected.

Bereavement services and bereavement counselling should be available for affected families.

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58
Q

What is NEC?

A

Necrotising enterocolitis (NEC) is a disorder affecting premature neonates, where part of the bowel becomes necrotic.

It is a life threatening emergency.

Death of the bowel tissue can lead to bowel perforation.

Bowel perforation leads to peritonitis and shock.

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59
Q

Risk facotrs for NEC

A

Very low birth weight or very premature

Formula feeds (it is less common in babies fed by breast milk feeds)

Respiratory distress and assisted ventilation

Sepsis

Patient ductus arteriosus and other congenital heart disease

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60
Q

Presentation of NEC

A

Intolerance to feeds
Vomiting, particularly with green bile
Generally unwell
Distended, tender abdomen
Absent bowel sounds
Blood in stools
When perforation occurs there will be peritonitis and shock and the neonate will be severely unwell.

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61
Q

Blood tests in NEC

A

Full blood count for thrombocytopenia and neutropenia

CRP for inflammation

Capillary blood gas will show a metabolic acidosis

Blood culture for sepsis

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62
Q

Investigations for NEC

A

Abdominal xray is the investigation of choice for diagnosis in the supine position

Bloods (FBC, CRP, blood culture)

CBG

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63
Q

Management of NEC

A

Neonates with suspected NEC need to be nil by mouth with IV fluids, total parenteral nutrition (TPN) and antibiotics to stabilise them.

A nasogastric tube can be inserted to drain fluid and gas from the stomach and intestines.

NEC is a surgical emergency and requires immediate referral to the neonatal surgical team.

Some neonates will recover with medical treatment. In others, surgery may be required to remove the dead bowel tissue.

Babies may be left with a temporary stoma if significant bowel is removed.

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64
Q

NEC: complications

A

Perforation and peritonitis

Sepsis

Death

Strictures

Abscess formation

Recurrence

Long term stoma

Short bowel syndrome after surgery

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65
Q

What is apnoea of prematurity?

A

Apnoea are defined as periods where breathing stops spontaneously for more than 20 seconds, or shorter periods with oxygen desaturation or bradycardia.

Apnoea can occur in neonates of all gestational ages. They are often accompanied by a period of bradycardia.

Apnoea is very common in premature neonates. They occur in almost all babies less than 28 weeks gestation and the incidence decreases with increased gestational age. In term infants apnoea usually indicate underlying pathology.

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66
Q

Causes of apnoea in the neonate

A

Apnoea occur due to immaturity of the autonomic nervous system that controls respiration and heart rate.

This system is more immature in premature neonates.

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67
Q

Apnoea in the neonate are often a sign of developing illness, such as what?

A

Infection

Anaemia

Airway obstruction (may be positional)

CNS pathology, such as seizures or haemorrhage

Gastro-oesophageal reflux

Neonatal abstinence syndrome

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68
Q

Management of neonatal apnoea?

A

Neonatal units attach apnoea monitors to premature babies.

These make a sound when an apnoea is occurring.

Tactile stimulation is used to prompt the baby to restart breathing.

Intravenous caffeine can be used to prevent apnoea and bradycardia in babies with recurrent episodes.

Episodes will settle as as the baby grows and develops.

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69
Q

What is retinopathy of prematurity and why is screening important?

A

Retinopathy of prematurity is a condition affecting preterm and low birth weight babies.

It typically affects babies born before 32 weeks gestation.

Abnormal development of the blood vessels in the retina can lead to scarring, retinal detachment and blindness.

Treatment can prevent blindness, which is why screening is so important.

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70
Q

Babies born before what gestation are typically affected by retinopathy of prematurity

A

Babies born before 32 weeks

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71
Q

Pathophysiology of retinopathy of prematurity

A

Retinal blood vessel development starts at around 16 weeks and is complete by 37 – 40 weeks gestation.

The blood vessels grow from the middle of the retina to the outer area.

This vessel formation is stimulated by hypoxia, which is a normal condition in the retina during pregnancy.

When the retina is exposed to higher oxygen concentrations in a preterm baby, particularly with supplementary oxygen during medical care, the stimulant for normal blood vessel development is removed.

When the hypoxic environment recurs, the retina responds by producing excessive blood vessels (neovascularisation), as well as scar tissue.

These abnormal blood vessels may regress and leave the retina without a blood supply. The scar tissue may cause retinal detachment.

72
Q

How is retinopathy of prematurity assessed?

A

The retina is divided into three zones:

Zone 1 includes the optic nerve and the macula

Zone 2 is from the edge of zone 1 to the ora serrata, the pigmented border between the retina and ciliary body

Zone 3 is outside the ora serrata

The retinal areas are described as a clock face, for example “there is disease from 3 to 5 o’clock”. The areas of disease are described from stage 1 (slightly abnormal vessel growth) to stage 5 (complete retinal detachment).

“Plus disease” describes additional findings, such as tortuous vessels and hazy vitreous humour.

73
Q

Which babies should be screened for ROP?

A

Babies born before 32 weeks or under 1.5kg should be screened for ROP

74
Q

When should screening for ROP start?

A

30 – 31 weeks gestational age in babies born before 27 weeks
4 – 5 weeks of age in babies born after 27 weeks

75
Q

When ROP screening is required, how often should it happen and when can it be stopped?

A

Screening should happen at least every 2 weeks and can cease once the retinal vessels enter zone 3 (outside the ora serrata), usually at around 36 weeks gestation

76
Q

ROP- examination

A

All retinal areas need to be visualised. Screening involves monitoring the retinal vessels as they develop and looking for plus disease.

77
Q

Management of ROP

A

Treatment involves systematically targeting areas of the retina to stop new blood vessels developing.

First line is transpupillary laser photocoagulation to halt and reverse neovascularisation.

Other options are cryotherapy and injections of intravitreal VEGF inhibitors.

Surgery may be required if retinal detachment occurs.

78
Q

Hypoxia during labour and delivery and the consequences

A

Hypoxia is central to neonatal resuscitation. Normal labour and birth leads to hypoxia. When contractions happen, the placenta is unable to carry out normal gaseous exchange, leading to hypoxia.

Extended hypoxia will lead to anaerobic respiration and a subsequent drop in the fetal heart rate (bradycardia).

Further hypoxia will lead to reduced consciousness and a drop in respiratory effort, in turn worsening hypoxia.

Extended hypoxia to the brain leads to hypoxic-ischaemic encephalopathy (HIE), with potentially life-long consequences in the form of cerebral palsy.

79
Q

Resuscitation issues unique to neonates?

A

Babies have a large surface area to weight ratio, and get cold very easily

Babies are born wet, so they loose heat rapidly

Babies that are born through meconium may have this in their mouth or airway

80
Q

Principals of neonatal resuscitation

A

Warm the baby
Calculate the APGAR Score
Stimulate breathing
Inflation breaths
Chest compressions

81
Q

What is an APGAR score and when is it done?

A

This is done at 1, 5 and 10 minutes whilst resuscitation of the neonate continues

This is used as an indicator of the progress over the first minutes after birth

It helps guide neonatal resuscitation efforts

82
Q

Warming the neonate during resuscitation

A

Get the baby dry as quickly as possible.

Vigorous drying also helps stimulate breathing.

Keep the baby warm with warm delivery rooms and management under a heat lamp

Babies under 28 weeks are placed in a plastic bag while still wet and managed under a heat lamp

83
Q

How to stimulate breathing in the neonate

A

Simulate the baby to prompt breathing, for example by drying vigorously with a towel

Place the baby’s head in a neutral position to keep airway open. A towel under the shoulders can help keep it neutral.

If gasping or unable to breath, check for airway obstruction (i.e. meconium) and consider aspiration under direct visualisation

84
Q

When are inflation breaths given?

A

Inflation breaths are given when the neonate is gasping or not breathing despite adequate initial simulation.

85
Q

How to give inflation breaths to the neonate?

A
  • Two cycles of five inflation breaths (lasting 3 seconds each) can be given to stimulate breathing and heart rate
  • If there is no response and the heart rate is low, 30 seconds of ventilation breaths can be used
  • If there is still no response, chest compressions can be used, coordinated with the ventilation breaths
86
Q

Air vs oxygen in neonatal resuscitation

A

When performing inflation breaths, air should be used in term or near term babies, and a mix of air and oxygen should be used in pre-term babies.

Oxygen saturations can be monitored throughout resuscitation if there are concerns about the breathing. Aim for a gradual rise in oxygen saturations, not exceeding 95%.

87
Q

Chest compressions in neonatal resuscitation

A

Start chest compressions if heart rate remains below 60 bpm despite resuscitation and inflation breaths (see protocol)

Chest compressions are performed at a 3:1 ratio with ventilation breaths

88
Q

Resuscitation of the neonate severe situations

A

Time is precious during neonatal resuscitation. Prolonged hypoxia increases the risk of hypoxic-ischaemic encephalopathy (HIE).

In severe situations, IV drugs and intubation should be considered.

Babies near or at term that have possible HIE may benefit from therapeutic hypothermia with active cooling.

89
Q

What is included in the APGAR score?

A

The APGAR score is measured out of 10. The lowest score is 0 and the highest is 10.

The included findings are:
Appearance (skin colour)
Pulse
Grimmace (response to stimulation)
Activity (muscle tone)
Respiration

90
Q

APGAR score: appearance

A

0: Blue / pale centrally

1: Blue extremities

2: Pink

91
Q

APGAR score: pulse

A

0: Absent

1: < 100

2: > 100

92
Q

APGAR: Grimmace (response to stimulation)

A

0: No response

1: Little response

2: Good response

93
Q

APGAR score: activity (muscle tone)

A

0: Floppy

1: Flexed arms and legs

2: Active

94
Q

APGAR score: respiration

A

0: Absent

1: Slow / irregular

2: Strong / crying

95
Q

When to clamp the umbilical cord in the neonate

A

Current guidelines from the resuscitation council UK state that uncompromised neonates should have a delay of at least one minute in the clamping of the umbilical cord following birth.

Neonates that require neonatal resuscitation should have their umbilical cord clamped sooner to prevent delays in getting the baby to the resuscitation team. The priority will be resuscitation rather than delayed clamping.

96
Q

Pros and cons of delayed cord clamping

A

After birth there is still a significant volume of fetal blood in the placenta.

Delayed clamping of the umbilical cord provides time for this blood to enter the circulation of the baby.

This is known as placental transfusion.

Recent evidence indicates that in healthy babies, delaying cord clamping leads to improved haemoglobin, iron stores and blood pressure and a reduction in intraventricular haemorrhage and necrotising enterocolitis.

The only apparent negative effect is an increase in neonatal jaundice, potentially requiring more phototherapy.

Neonates that require neonatal resuscitation should have their umbilical cord clamped sooner to prevent delays in getting the baby to the resuscitation team. The priority will be resuscitation rather than delayed clamping.

97
Q

Potential causes of neonatal sepsis?

A

Group B streptococcus (GBS)
Escherichia coli (e. coli)
Listeria
Klebsiella
Staphylococcus aureus

98
Q

Risk factors for neonatal sepsis

A

Vaginal GBS colonisation

GBS sepsis in a previous baby

Maternal sepsis, chorioamnionitis or fever > 38ºC

Prematurity (less than 37 weeks)

Early (premature) rupture of membrane

Prolonged rupture of membranes (PROM)

99
Q

Clinical features of neonatal sepsis?

A

Fever

Reduced tone and activity

Poor feeding

Respiratory distress or apnoea

Vomiting

Tachycardia or bradycardia

Hypoxia

Jaundice within 24 hours

Seizures

Hypoglycaemia

100
Q

Neonatal sepsis - red flags

A

Confirmed or suspected sepsis in the mother

Signs of shock

Seizures

Term baby needing mechanical ventilation

Respiratory distress starting more than 4 hours after birth

Presumed sepsis in another baby in a multiple pregnancy

101
Q

Treating for presumed neonatal sepsis

A

If there is one risk factor or clinical feature, monitor the observations and clinical condition for at least 12 hours

If there are two or more risk factors or clinical feature of neonatal sepsis start antibiotics

Antibiotics should be started if there is a single red flag

Antibiotics should be given within 1 hour of making the decision to start them

Blood cultures should be taken before antibiotics are given

Check a baseline FBC and CRP

Perform a lumbar puncture if infection is strongly suspected or there are features of meningitis (e.g. seizures)

102
Q

First line antibiotics for neonatal sepsis

A

benzylpenicillin and gentamycin

103
Q

Neonatal sepsis ongoing management

A

Check the CRP again at 24 hours and check the blood culture results at 36 hours:

Consider stopping the antibiotics if the baby is clinically well, the blood cultures are negative 36 hours after taking them and both CRP results are less than 10.

Check the CRP again at 5 days if they are still on treatment:

Consider stopping antibiotics if the baby is clinically well, the lumbar puncture and blood cultures are negative and the CRP has returned to normal at 5 days.

Consider performing a lumbar puncture if any of the CRP results are more than 10.

104
Q

Pathophysiology of neonatal jaundice

A

There is a high concentration of red blood cells in the fetus and neonate.

These red blood cells are more fragile than normal red blood cells.

The fetus and neonate also have less developed liver function.

Fetal red blood cells break down more rapidly than normal red blood cells, releasing lots of bilirubin.

Normally this bilirubin is excreted via the placenta, however at birth the foetus no longer has access to a placenta to excrete bilirubin.

This leads to a normal rise in bilirubin shortly after birth, causing a mild yellowing of skin and sclera from 2 – 7 days of age.

This usually resolves completely by 10 days. Most babies remain otherwise healthy and well.

105
Q

When is neonatal jaundice normal and how long does it take to resolve?

A

This leads to a normal rise in bilirubin shortly after birth, causing a mild yellowing of skin and sclera from 2 – 7 days of age.

This usually resolves completely by 10 days.

Most babies remain otherwise healthy and well.

106
Q

Causes of neonatal jaundice - increased bilirubin production

A

Haemolytic disease of the newborn

ABO incompatibility

Haemorrhage

Intraventricular haemorrhage

Cephalo-haematoma

Polycythaemia

Sepsis and disseminated
intravascular coagulation

G6PD deficiency

107
Q

Neonatal jaundice causes - decreased clearance of bilirubin

A

Prematurity

Breast milk jaundice

Neonatal cholestasis

Extrahepatic biliary atresia

Endocrine disorders (hypothyroid and hypopituitary)

Gilbert syndrome

108
Q

Jaundice in the first 24 hours of life

A

Jaundice in the first 24 hours of life is pathological. This needs urgent investigations and management. Neonatal sepsis is a common cause. Babies with jaundice within 24 hours of birth need treatment for sepsis if they have any other clinical features or risk factors.

109
Q

Why do bilirubin levels need to be carefully monitored in the neonate?

A

In premature babies, the process of physiological jaundice is exaggerated due to the immature liver.

This increases the risk of complications, particularly kernicterus.

Kernicterus is brain damage due to high bilirubin levels.

Bilirubin levels need to be carefully monitored in premature babies, as they may require treatment.

110
Q

Why are breastfed babies more likely to be jaundiced?

A

Components of breast milk inhibit the ability of the liver to process the bilirubin.

Breastfed babies are more likely to become dehydrated if not feeding adequately.

Inadequate breastfeeding may lead to slow passage of stools, increasing absorption of bilirubin in the intestines.

Breastfeeding should still be encouraged, as the benefits of breastfeeding outweigh the risks of breast milk jaundice.

Mothers may need extra support and advice to ensure adequate breastfeeding.

111
Q

How can haemolytic disease of the newborn occur?

A

Haemolytic disease of the newborn is a cause of haemolysis (red blood cells breaking down) and jaundice in the neonate. It is caused by incompatibility between the rhesus antigens on the surface of the red blood cells of the mother and fetus. The rhesus antigens on the red blood cells vary between individual. This is different to the ABO blood group system.

When a woman that is rhesus D negative (does not have the rhesus D antigen) becomes pregnant, we have to consider the possibility that her child will be rhesus D positive (has the rhesus D antigen).

It is likely at some point in the pregnancy the blood from the baby will find a way into her bloodstream.

When this happens, the baby’s red blood cells display the rhesus D antigen.

The mother’s immune system will recognise this rhesus D antigen as foreign and produce antibodies to the rhesus D antigen.

The mother has then become sensitised to rhesus D antigens.

Usually, this sensitisation process does not cause problems during the first pregnancy (unless the sensitisation happens early on, such as during antepartum haemorrhage).

During subsequent pregnancies, the mother’s anti-D antibodies can cross the placenta into the fetus.

If that fetus is rhesus positive, these antibodies attach themselves to the red blood cells of the fetus and causes the immune system of the fetus to attack their own red blood cells.

This leads to haemolysis, causing anaemia and high bilirubin levels.

112
Q

After how long is considered prolonged neonatal jaundice?

A

More than 14 days in full term babies

More than 21 days in premature babies

113
Q

Prolonged jaundice should prompt further investigation to look for an underlying cause, such as what?

A

Biliary atresia
Hypothyroidism
G6PD deficiency

114
Q

Investigating neonatal jaundice

A

Full blood count and blood film for polycythaemia or anaemia

Conjugated bilirubin: elevated levels indicate a hepatobiliary cause

Blood type testing of mother and baby for ABO or rhesus incompatibility

Direct Coombs Test (direct antiglobulin test) for haemolysis

Thyroid function, particularly for hypothyroid

Blood and urine cultures if infection is suspected. Suspected sepsis needs treatment with antibiotics.

Glucose-6-phosphate-dehydrogenase (G6PD) levels for G6PD deficiency

115
Q

How is it decided what treatment is required for neonatal jaundice?

A

In jaundiced neonates, total bilirubin levels are monitored and plotted on treatment threshold charts.

These charts are specific for the gestational age of the baby at birth.

The age of the baby is plotted on the x-axis and the total bilirubin level on the y-axis.

If the total bilirubin reaches the threshold on the chart, they need to be commenced on treatment to lower their bilirubin level.

116
Q

Management to lower bilrubin level in neonatal jaundice?

A

Phototherapy is usually adequate to correct neonatal jaundice.

Extremely high levels may require an exchange transfusion.
Exchange transfusions involve removing blood from the neonate and replacing it with donor blood.

117
Q

How is phototherapy used to treat high bilirubin in the neonate

A

Phototherapy converts unconjugated bilirubin into isomers that can be excreted in the bile and urine without requiring conjugation in the liver.

Phototherapy involves removing clothing down to the nappy to expose the skin and eye patches to protect the eyes.

Blue light is the best at breaking down bilirubin. A light-box shines blue light on the baby’s skin. Little or no UV light is used.

Double phototherapy involves two light-boxes.

Bilirubin is closely monitored during treatment.

Once phototherapy is complete, a rebound bilirubin should be measured 12 – 18 hours after stopping to ensure the levels do not rise about the treatment threshold again.

118
Q

What is Kernicterus?

A

Kernicterus is a type of brain damage caused by excessive bilirubin levels.

It is the main reason we treat neonatal jaundice to keep bilirubin levels below certain thresholds.

Bilirubin can cross the blood-brain barrier. Excessive bilirubin causes direct damage to the central nervous system. Kernicterus presents with a less responsive, floppy, drowsy baby with poor feeding.

The damage to the nervous system is permeant, causing cerebral palsy, learning disability and deafness. Kernicterus is now rare due to effective treatment of jaundice.

119
Q

When does respiratory distress syndrome occur and why?

A

Respiratory distress syndrome affects premature neonates, born before the lungs start producing adequate surfactant. Respiratory distress syndrome commonly occurs below 32 weeks.

120
Q

Appearance of respiratory distress syndrome on CXR

A

Chest xray shows a “ground-glass” appearance.

121
Q

Neonatal RDS pathophysiology

A

Inadequate surfactant leads to high surface tension within alveoli.

This leads to atelectasis (lung collapse), as it is more difficult for the alveoli and the lungs to expand.

This leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia (high CO2) and respiratory distress.

122
Q

Management of RDS

A

Antenatal steroids (i.e. dexamethasone) given to mothers with suspected or confirmed preterm labour increases the production of surfactant and reduces the incidence and severity of respiratory distress syndrome in the baby.

Premature neonates may need:

Intubation and ventilation to fully assist breathing if the respiratory distress is severe

Endotracheal surfactant, which is artificial surfactant delivered into the lungs via an endotracheal tube

Continuous positive airway pressure (CPAP) via a nasal mask to help keep the lungs inflated whilst breathing

Supplementary oxygen to maintain oxygen saturations between 91 and 95% in preterm neonates

Support with breathing is gradually stepped down as the baby develops and is able to maintain their breathing, until they can support themselves in air.

123
Q

Neonatal RDS - short term complications

A

Pneumothorax
Infection
Apnoea
Intraventricular haemorrhage
Pulmonary haemorrhage
Necrotising enterocolitis

124
Q

Neonatal RDS - long term complications

A

Chronic lung disease of prematurity
Retinopathy of prematurity occurs more often and more severely in neonates with RDS
Neurological, hearing and visual impairment

125
Q

What is hypoxic ischaemic encephalopathy (HIE)

A

Hypoxic ischaemic encephalopathy (HIE) occurs in neonates as a result of hypoxia during birth.

Hypoxia is a lack of oxygen, ischaemia refers to a restriction in blood flow to the brain and encephalopathy refers to malfunctioning of the brain.

Some hypoxia is normal during birth, however prolonged or severe hypoxia leads to ischaemic brain damage.

HIE can lead to permanent damage to the brain, causing cerebral palsy.

Severe HIE can result in death.

126
Q

When should HIE be suspected in neonates?

A

When there are events that could lead to hypoxia during the perinatal or intrapartum period, acidosis (pH < 7) on the umbilical artery blood gas, poor Apgar scores, features of mild, moderate or severe HIE or evidence of multi organ failure.

127
Q

Causes of HIE

A

Anything that leads to asphyxia (deprivation of oxygen) to the brain can cause HIE. For example:

Maternal shock

Intrapartum haemorrhage

Prolapsed cord, causing compression of the cord during birth

Nuchal cord, where the cord is wrapped around the neck of the baby

128
Q

Mild HIE

A

Poor feeding, generally irritability and hyper-alert

Resolves within 24 hours

Normal prognosis

129
Q

Moderate HIE

A

Poor feeding, lethargic, hypotonic and seizures

Can take weeks to resolve

Up to 40% develop cerebral palsy

130
Q

Severe HIE

A

Reduced consciousness, apnoeas, flaccid and reduced or absent reflexes

Up to 50% mortality

Up to 90% develop cerebral palsy

131
Q

Management of HIE

A

Management will be coordinated by specialists in neonatology, on the neonatal unit.

This involves supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures.

Therapeutic hypothermia is an option in certain circumstances to help protect the brain from hypoxic injury.

Children will need to be followed up by a paediatrician and the multidisciplinary team to assess their development and support any lasting disability.

132
Q

Role of therapeutic HIE in

A

Babies near or at term considered to have HIE can benefit from therapeutic hypothermia.

Therapeutic hypothermia involves actively cooling the core temperature of the baby according to a strict protocol.

The baby is transferred to neonatal ICU and actively cooled using cooling blankets and a cooling hat.

The temperature is carefully monitored with a target of between 33 and 34°C, measured using a rectal probe.

This is continued for 72 hours, after which the baby is gradually warmed to a normal temperature over 6 hours.

The intention of therapeutic hypothermia is to reduce the inflammation and neurone loss after the acute hypoxic injury. It reduces the risk of cerebral palsy, developmental delay, learning disability, blindness and death.

133
Q

What is surface tension?

A

Surface tension is the attraction of the molecules in a liquid to each other, pulling them together and minimising surface area.

134
Q

What are alveoli and what forces act on them?

A

Alveoli are the small sacs where gas collects and diffuses into the blood during inhalation.

These are lined with fluid. The molecules of this fluid pull together due to surface tension, in turn pulling the walls of the alveoli towards each-other, attempting to collapse the space in the alveoli.

135
Q

Role of surfactant

A

It contains proteins and fats. It sits on top of the water in the lungs. It has a hydrophilic side, that faces the water, and a hydrophobic side, that faces the air. The surfactant reduces the surface tension of the fluid in the lungs, essentially providing a barrier that reduces the water molecules tendency to pull towards each other.

The result is that surfactant keeps the alveoli inflated and maximises the surface area of the alveoli. This reduces the force needed to expand the alveoli and therefore the lungs during inspiration. This is known as compliance. Therefore, surfactant increases lung compliance.

Additionally, as an alveolus expands, the surfactant becomes more thinly spread and therefore the surface tension increases, making it more difficult to expand that alveolus further. This stops one alveolus expanding massively whilst another alveolus only expands a little. Therefore, surfactant promotes equal expansion of all alveoli during inspiration.

136
Q

Which cells produce surfactant and when do they mature?

A

Surfactant is a fluid produced by type II alveolar cells.

Type II alveolar cells become mature enough to start producing surfactant between 24 and 34 weeks gestation. Therefore, pre-term babies have problems associated with reduced pulmonary surfactant.

137
Q

Cardio-Respiratory Changes at Birth

A

During birth the thorax is squeezed as the body passes through the vagina, helping to clear fluid from the lungs.

Adrenalin and cortisol are released in response to the stress of labour, stimulating respiratory effort.

The first breaths the baby takes expands the alveoli, decreasing the pulmonary vascular resistance.

The decrease in pulmonary vascular resistance causes a fall in pressure in the right atrium.

At this point the left atrial pressure is greater than the right atrial pressure, which squashes the atrial septum and causes functional closure of the foramen ovale.

The foramen ovale then structurally closes and becomes the fossa ovalis.

Prostaglandins are required to keep the ductus arteriosus open.

Increased blood oxygenation causes a drop in circulating prostaglandins.

This causes closure of the ductus arteriosus, which becomes the ligamentum arteriosum.

Immediately after birth the ductus venosus stops functioning because the umbilical cord is clamped and there is no blood flow in the umbilical veins.

The ductus venosus structurally closes a few days later and becomes the ligamentum venosum.

138
Q

The newborn examination is used as a screening tool to pick up abnormalities in the newborn baby, when is it performed and by whom?

A

The examination is performed within the first 72 hours after birth. It is repeated at 6 – 8 weeks by their GP.

The initial check can be performed by a trained midwife or paediatric doctor. For home births the GP may visit to perform the baby check.

139
Q

What can you ask the parents when examining the newborn?

A

Has the baby passed meconium?
Is the baby feeding ok?
Is there a family history of congenital heart, eye or hips problems?

140
Q

Pre ductal vs post ductal sats

A

Babies should have their pre-ductal and post-ductal oxygen saturations checked.

This measures the oxygen level before and after the ductus arteriosus.

Normal saturations are 96% or above.

There should not be more than a 2% difference between the pre-ductal and post-ductal saturations.

Abnormal saturations require further investigation and potentially admission to the neonatal unit.

141
Q

What is the ductus arteriosis?

A

The ductus arteriosus is located along the arch of the aorta and connects the aorta with the pulmonary artery.

142
Q

At what point does the ductus arteriosis close?

A

It normally stops functioning within 1 – 3 days of birth.

143
Q

What is the function of the ductus arteriosus?

A

It allows blood from the deoxygenated right sided circulation before the lungs to mix with the oxygenated left sided circulation after the lungs.

144
Q

Certain congenital heart conditions are duct-dependent, what does this mean and how can they be picked up?

A

They rely on the mixing of blood across the ductus arteriosus.

When the ductus arteriosus closes there can be a rapid deterioration in symptoms.

These duct-dependent conditions may be picked up by measuring the difference in pre-ductal and post-ductal saturations.

145
Q

Where a pre ductal and post ductal saturations measured?

A

Pre-ductal saturations are measured in the baby’s right hand.

The right hand receives blood from the right subclavian artery, a branch of the brachiocephalic artery, which branches from the aorta before the ductus arteriosus.

Post-ductal saturations are measured in either foot. The feet receive blood traveling from the descending aorta, which occurs after the ductus arteriosus.

146
Q

Newborn examination: steps

A

General appearance

Head

Shoulders and arms

Chest

Abdomen

Genitals

Legs

Back

Reflexes

Note any skin findings

147
Q

What to note about general appearance when examining the newborn?

A

Colour (pink is good)
Tone
Cry

148
Q

What to note about the head when examining the newborn?

A

General appearance: size, shape, dysmorphology, caput succedaneum, cephalohaematoma and any facial injury

Head circumference: known as the occipital frontal circumference (OCP)

Anterior and posterior fontanelles
Sutures: overlapping sutures are common and usually resolve as the baby grows

Ears: skin tags, low set ears and asymmetry

Eyes: slight squints are normal, epicanthic folds can indicate Down’s, purulent discharge could indicate infection

Red reflex using an ophthalmoscope: check for symmetry. It is often more pale in darker skinned babies. It is absent with congenital cataracts and retinoblastoma.

Mouth: cleft lip or tongue tie
Put your little finger in their mouth to check the suckling reflect and feel the palate all the way back, checking for a cleft palate.

149
Q

What to note about the arms and shoulders when examining the newborn?

A

Shoulder symmetry: check for a clavicle fracture

Arm movements: check for an Erbs palsy

Brachial pulses

Radial pulses

Palmar creases: a single palmar crease is associated with Down’s, but can be normal

Digits: check the number of digits and if the fingers are straight or curved (clinodactyly)

Use a sats probe on the right wrist for a pre-ductal reading

150
Q

What to note about the chest when examining the newborn?

A

Oxygen saturations in the right wrist and a feet: 95% and above is normal

Observe breathing: look for respiration distress, symmetry and listen for stridor

Heart sounds: listen for murmurs, heart sounds, heart rate and identify which side the heart is on heart

Breath sounds: listen for symmetry, good air entry and added sounds

151
Q

What to note about the abdomen when examining the newborn?

A

Observe the shape: a concave abdomen may indicate diaphragmatic hernia with abdominal contents in the chest

Umbilical stump: look for discharge, infection and a periumbilical hernia

Palpate for organomegaly, hernias or masses

152
Q

What to note about the genitals when examining the newborn?

A

Observe for the sex, ambiguity and any obvious abnormalities

Palpate testes and scrotum: check both are present and descended, check for hernias or hydroceles

Inspect the penis for hypospadias, epispadias and urination

Inspect the anus to check if it is patent

Ask about meconium and whether the baby has opened the bowel

153
Q

What to note about the legs when examining the newborn?

A

Observe the legs and hips for equal movements, skin creases, tone and talipes

Barlows and Ortolani manoeuvres: check for clunking, clicking and dislocation of the hips

Count the toes

154
Q

What to note about the back when examining the newborn?

A

Inspect and palpate the spine: look for curvature, spina bifida and a pilonidal sinus

155
Q

What reflexes are tested when examining the newborn?

A

Moro reflex: when rapidly tipped backwards the arms and legs will extend

Suckling reflex: placing a finger in the mouth will prompt them to suck

Rooting reflex: tickling the cheek will cause them to turn towards the stimulus

Grasp reflex: placing a finger in the palm will cause them to grasp

Stepping reflex: when held upright and the feet touch a surface they will make a stepping motion

156
Q

What skin findings to note when examining the newborn?

A

Haemangiomas
Port wine stains
Mongolian blue spot
Cradle cap
Desquamation
Erythema toxicum
Milia
Acne
Naevus simplex (“stork bite”)
Moles
Transient pustular melanosis

157
Q

Common foot/leg issue arising in examination of the newborn?

A

Talipes, also known as clubfoot, is where the ankles are in a supinated position, rolled inwards.

It can be positional or structural.

158
Q

Positional vs structural talipes?

A

Positional talipes is where the muscles are slightly tight around the ankle but the bones are unaffected. The foot can still be moved into the normal position. This requires referral to a physiotherapist for some simple exercises and will resolve with time.

Structural talipes involves the bones of the foot and ankle and requires referral to an orthopaedic surgeon.

159
Q

If undescended testes are found on newborn examination what should be done?

A

Undescended testes require monitoring and referral to a urologist.

160
Q

Significance of skin findings on examination of the newborn?

A

Skin findings generally do not require any action. Many will fade with time.

Haemangiomas near the eyes, mouth or affecting the airway may require referral for treatment with beta blockers (i.e. propranolol). Otherwise they can be monitored and usually resolve with time.

Port wine stains are pink patches of skin, often on the face, caused by abnormalities affecting the capillaries. They don’t fade with time and typically turn a darker red or purple colour. Rarely they can be related to a condition called Sturge-Weber syndrome, where there can be visual impairment, learning difficulties, headaches, epilepsy and glaucoma.

161
Q

What should be done if clicky or clunky hips are found o/e of the newborn

A

Clicky or clunky hips require referral for a hip ultrasound to rule out developmental dysplasia of the hips.

162
Q

What type of murmurs may be normal in a new born and what might cause them?

A

Soft systolic murmurs of grade 2 or less in otherwise healthy well neonates may be monitored, as these often resolve after 24 – 48 hours.

This may be caused by a patent foramen ovale that closes shortly after birth.

Any suspicion of heart failure or congenital heart disease requires referral to cardiology for an ECG and echocardiogram.

If they are unwell, they require admission to the neonatal unit and immediate management.

163
Q

What to do after examining the newborn?

A

Discuss any abnormalities with a senior

Action any abnormalities (e.g. ultrasound request for clicks hips)

Document the examination findings on the newborn and infant physical examination (NIPE) computer system and in the baby’s red book

Explain, reassure and answer any questions with the parents

Arrange referrals and followup if required

164
Q

Meconium aspiration syndrome preaentatiin

A

respirstory distress

greenish-tinged skin

intercostal recession

poor cry

165
Q

Compressions to rescue breaths neonatal ressuciation

A

3:1 is the recommended ratio of chest compressions to ventilation breaths for neonatal resuscitation.

166
Q

For how long can it take for a neonate to achieve normal sats

A

10 minuites

167
Q

Taking history when parents present with an infant

A

Birth complications: hypoxia, breech, should dystocia
Gestation: premature (37 weeks) or late (42 weeks)
Birth weight
Growth and weight percentiles
Growth rate
Milestones +/- regression
Vaccinations
Screening tests + results
Examinations + results
Any hospital stays?
Any problems at or around birth e.g. jaundice, sepsis, stays on NICU, ARDs
Known or family history of genetic syndromes
Multiple births?

168
Q

When should the APGAR score be assessed?

A

1 and 5 mins following birth

169
Q

For a child born in the United Kingdom, at what age would their hearing first be formally assessed?

A

Newborn - otoacoustic emission

170
Q

Shaken baby syndrome encompasses the triad of what features?

A

Retinal haemorrhages, subdural haematoma, and encephalopathy.

171
Q

Bilious vomiting on the first day is likely due to what?

A

intestinal atresia

172
Q

Early onset neonatal sepsis - time frame and pathogens

A

48-72 hrs

Groub B strep (40%)
E. Coli (20%)

173
Q

Late onset neonatal sepsis - time frame and pathogens

A

After 72 hrs

Coagulase negative staph (majority)
Enterococcus
Staph aureus
Klebsiella

174
Q

Congenital infection

A

Infection aquired in-utero - haematogenous or transplacental

175
Q

Neonatal infection

A

Infection acquired during or after delivery (ascending infection from vaginal pathogens or enviromental source)

176
Q

Why is GBS not screened for in mothers

A

Carriage is variable, up to 35% of women are colonized

Not all colonized women will come back positive

The density of infant colonization determines the risk of early-onset invasive disease

Only a small number of colonized babies will develop invasive disease, however they will present in the early hours of life

177
Q

Risks for infection in the neonate

A

Prelabour +/- prolonged (>18 hours) rupture of membranes

Prematurity, preterm birth following spontaneous labour before 37 weeks gestation

Maternal infection (during labour e.g. chorioamnionitis, GBS colonisation) - intrapartum fever higher than 38 degrees if there is a suspected or confirmed bacteria; infection

Suspected or confirmed infection in another baby in the case multiple pregnancy

Low birth weight

Invasive procedures (iv catheters, intubation)

Maternal GBS colonisation

Apnoea

Signs of shock

Need for CPR or mechanical ventilation

Seizures