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Paediatrics > Neonatal period > Flashcards

Neonatal period Flashcards

1
Q

Essential transitions a child makes when born

A
  1. Removal of placenta
  2. Respiratory: clearing fluids and opening alveoli
  3. Cardiovascular: reducing pulmonary vascular pressure and closure of ductus arteriosus
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2
Q

Major causes of morbidity and mortality in neonates

A

Necrotising neterocolitis

Infection

Brain injury

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3
Q

Definition of macrosomia

A

>4kg at birth (8.8lbs)

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4
Q

What is meant by neonatal mortality?

A

Deaths occurring in first 28 days following birth

UK rate = ~3 per 1000 live births

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5
Q

What is perinatal mortality?

A

Deaths up to 7 days from bith AND stillbirths

UK rate ~7-8 per thousand total births

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6
Q

What is infant mortality?

A

Deaths up to 1 year

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7
Q

Ways to help reduce PTB

A

· Continuity midwife led care

· Foetal and umbilical doppler for high risk pregnant women

· Screening for lower genital tract infections

Vitamin D supplements

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8
Q

What 4 areas does the newborn physical examination look at?

A
  1. Heart
  2. Eyes
  3. Hips
  4. Testes
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9
Q

When is the newborn blood-spot test done?

A

When baby is 5 days old

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10
Q

What does the newborn bloodspot test screen for?

A

Sickle cell disease

Cystic fibrosis

Congenital hypothyroidism

6 metabolic diseases

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11
Q

Epidemiology of sickle cell disease

A

1/2000 in the UK born with sickle cell

Screened for in newborn blood spot test to allow for early treatment

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12
Q

Epidemiology of cystic fibrosis

A

1/2500 in the UK

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13
Q

Epidemiology of congenital hypothyroidism

A

1 in 3000

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14
Q

How is gestational age calculated?

A

Age measured from the first day of the LMP before conception, expressed in complete weeks or days

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15
Q

How is corrected age calculated?

A

Chronological age minus the number of weeks born before 40weeks

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16
Q

What is spontaneous abortion/ miscarriage?

A

Conceptus born after spontaneous labour without any signs of life before 24 weeks gestation

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17
Q

Define the neonatal period

A

Birth to 28 days after birth or if baby preterm, 44 weeks post-menstrual age

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18
Q

Define preterm birth

A

Born before 37 completed weeks (8% births)

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19
Q

When is a baby considered as being born at term?

A

Between 37-42 completed weeks

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20
Q

What weight is considered low birth weight?

A

<2500g

7% births UK

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21
Q

What is very low birth weight?

A

<1500g

1.2% births

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22
Q

What is extremely low birth weight?

A

<1000g

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23
Q

When is a child said to be small for gestational age?

A

<10th centile for gestational age

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24
Q

When is a child said to be large for gestational age?

A

>90th centile for gestational age

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25
Q

How is small for gestational age classified?

A

Symmetrical or asymmetrical?

Symmetrical: all growth parameters are small, suggests foetus affected from early pregnancy

Asymmetrical: weight centile < head circumference and length, usually due to a cause late in pregnancy e.g. pre-eclampsia. Asymmetrical SGA babies are at higher risk of complications

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26
Q

Causes of small for gestational age?

A

· Small parents - most common

· Restricted foetal nutrients e.g. oxygen or glucose

· Foetal abnormality e.g. chromosomal disorders/ infection

· Maternal substance use

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27
Q

Complications of being small for gestational age

A

· Increased risk of foetal death

· May have infection

· Hypoglycaemia due to reduced glycogen stores

· Hypothermia

· Polycythaemia if chronic intrauterine hypoxia

· Necrotising enterocolitis due to bowel hypoxia

· Thrombocytopenia/ neutropenia/ coagulopathy

· Meconium aspiration - foetal hypoxia = loss of anal tone

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28
Q

Management of baby small for gestational age

A

· Manage on ward with increased midwife ratio

· Evaluate for cause

· Maintain body temp and check glucose

· Admit to neonatal unit if BW <1800g

· Discharge when baby is feeding 3-4hrly, gaining 20-30g/day and body temp is maintained, providing mum is able to care for baby

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29
Q

Prognosis of small babies

A
  • Neurodev problems more likely if SGA
  • Symmetric SGA infants often stay small
  • Barker hypothesis: suggests infants with small placenta are at risk of coronary disease, stroke, obesity and HTN later in life
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30
Q

Causes of baby being large for gestational age

A

· Most frequent cause is large parents

· Infant of mother with DM

· Hydrops fetalis

· Beckwith-Weidemann syndrome

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31
Q

Complications and management of large babies

A

Complications

  • Perinatal asphyxia, nerve palsies, shoulder dystocia, fractures
  • Hypoglycaemia

Management

  • Careful obstetric management to avoid complications
  • Examine for any signs of injury
  • Prevent hypoglycaemia
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32
Q

What are the consequences for an infant with a mother with diabetes?

A

Maternal hyperglycaemia leads to increased glucose in the foetus leads to increased insulin secretion by the foetus which leads to macrosomia, organomegaly and polycythaemia.

· This is because insulin secretion antenatally functions as growth hormone

  • Hypoglycaemia may develop due to high insulin levels leading to a lack of glucose in the blood, respiratory disease and obstetric complications are also more likely
  • Normoglycaemia occurs within 48 hours in most, however the child has a 7x increase risk of diabetes in later life and an increased risk of obesity
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33
Q

What is an APGAR score?

A

· Appearance, Pulse, Grimace, Activity, Respiration

· Score =<6 at 1 min indicates baby needs to be resuscitated

• APGAR score noted at 1, 5 and 10 mins

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34
Q

How is the temperature of preterm babies managed?

A

PTB babies are likelt to become cold

>28 weeks: dried, warm towel and placed under heater

<28 weeks: sandwich bag without being dried and placed under heater

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35
Q

Baby has been towel dried but isn’t breathing - management?

A

Give 5 breaths via bag mask

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36
Q

Ratio of chest compressions to breaths in newborn

A

3:1 - started after 5 rescue breaths

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37
Q

Which factors predispose to prematurity?

A

· 40% of cases are idiopathic, previous preterm birth, multiple pregnancy, maternal illness such as pre-eclampsia, chorioamnionitis and diabetes, PROM, you try malformations or cervical incompetence, dysfunctional sunder and poor maternal health

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38
Q

What problems are associated with prematurity?

A

Respiratory distress syndrome

Intraventricular haemorrhage

Retinopathy of prematurity

Necrotising enterocolitis

Impaired immune system

PDA

Jaundice: immature liver enzymes

Birth trauma

SIDS

Behavioural problems

NAI: also assoiated with higher risk of marriage breakup due to stress

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39
Q

Hypothermia in a baby

A

<36 degrees

Occurs because babies have thin skin, little fat and a large body surface area

Baby will be nursed in heated, humidified incubators with a hat to reduce heat loss

Hypothermia is associated with increased mortality

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40
Q

When do immunoglobulins cross the placenta to baby?

A

30 weeks - babies born before this are at increased risk of infection

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41
Q

Why are pre-term babies at increased risk of infection

A
  1. Before 30 weeks they won’t have any immunoglobulins from mum
  2. Thin skin
  3. Invasive device - route for infection e.g. ET tubes, central lines
  4. Antibiotics make babies more susceptible to fungal infection so some units give prophylactic anti-fingls to babies born <28 weeks
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42
Q

Why is feeding a preterm baby difficult?

A
  1. Fragile guts: vulnerable to necrotising enterocolitis
  2. Deficient suck and swallow reflex until 34 weeks
  3. When baby is able to feed, they tire quickly because they are so small

Up to 34 weeks babies receive TPN, milk is gradually introduced during this time via NG tube

Breast milk preferred as contains immunoglobulins and less risk of nectrotising enterocolitis

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43
Q

Which resp. conditions are associated with prematurity?

A
  1. Respiratory distress syndrome
  2. Transient tachypnoea of the newborn
  3. Congenital pneumonia
  4. Bronchopulmonary dysplasia
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44
Q

What is respiratory distress syndrome?

A

o Caused by lack of surfactant in the lungs causing widespread alveolar collapse

o Common in babies born before 28 weeks can also occur in term infants, especially if mother has diabetes

o Impaired surfactant synthesis and secretion leads to stiff lungs therefore increased effort to breathe

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45
Q

Clinical features of respiratory distress syndrome

A

o Signs of respiratory distress at delivery or within four hours of birth

• Tachypnoea, grunting, intercostal recession, cyanosis

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46
Q

What will a CXR show in resp. distress syndrome?

A

Ground glass apperance

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47
Q

How is respiratory distress syndrome managed?

A

o Giving steroids to the mother during the antenatal period if there is a threat of preterm delivery

o If baby has signs of respiratory distress after birth that are severe enough to require mechanical ventilation they are given exogenous surfactant via an ET tube as soon as possible and oxygen is given to maintain saturations (usually only done in babeis born <27 weeks)

o If severe baby, will need oxygenating via mechanical ventilation, if babies saturations are more than 91% mechanical ventilation is unnecessary and oxygen is given via nasal cannula or CPAP

• Complications of mechanical ventilation: pneumothorax, pulmonary haemorrhage and chronic lung disease

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48
Q

After which week is respiratory distress syndrome rare?

A

32 weeks

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49
Q

Investigation for respiratroy distress syndrome?

A

Largely clinical

CXR: ground glass

ABG: hypoxia

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50
Q

Prognosis following respiratory distress syndrome

A

• Prognosis: the majority of babies have a good recovery, mortality is 5–10% and depends on severity and gestational age.

Bronchopulmonary dysplasia may develop

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51
Q

How can respiratory distress syndrome be prevented?

A

Corticosteroids given in 2 doses 1–7 days before birth decreases the incidence and mortality by 40%, treat coexisting morbidities that can inhibit surfactant production such as hypothermia, acidosis and infection

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52
Q

What is transient tachypnoea of the newborn?

A

· Caused by a delay in clearance or absorption of lung fluid after birth, present within four hours after birth and is more common after elective caesarean section

· Chest x-ray shows streaky perihilar changes and fluid in the long horizontal fissures

· Treatment is supplemental oxygen, consider nasal CPAP and antibiotics, spontaneously resolved within 24 hours

Symptoms:

  • very fast, labored breathing of more than 60 breaths a minute.
  • grunting sounds when the baby breathes out (exhales)
  • flaring nostrils or head bobbing.
  • skin pulling in between the ribs or under the ribcage with each breath (known as retractions)
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53
Q

Congenital pneumonia

A

· Caused by aspiration of infected amniotic fluid, associated with prolonged rupture of membranes, chorioamnionitis and fetal hyperoxia

· Common positive bacteria include group B strep, E. coli and other gram-negative bacteria such as listeria and chlamydia

· Present in the first 24 hours and chest x-ray will show patchy shadowing and consolidation, give antibiotics and chest physiotherapy where appropriate, prognosis depends on severity and whether there is any associated sepsis or pulmonary hypertension of the neuron

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54
Q

What is bronchopulmonary dysplasia?

A

• Respiratory complication, occurs in babies with VLBW, diagnosed when the neonate still requires oxygen to maintain 95% saturation at a gestation age of more than 36 weeks

25% of VLBW infants (1.5kg) are diagnosed with bronchopulmonary dysplasia

• Caused by tissue inflammation

Clinical features: need for supplemental oxygen to maintain saturations of 95%, subcostal recession, fine crackles on inspiration

Diagnosis: diagnosed when the neonate requires oxygen after 36 weeks, chest x-ray not routinely carried out but may show areas of hyperinflation and areas of hypoinflation

Management: initial aim is to prevent bronchopulmonary dysplasia from occurring through considerate treatment of RDS and any ventilation should be given gently using lowest volumes and lowest oxygen concentrations, good nutrition to optimise lung growth and repair – neonates with chronic lung disease need extra calories because they use a lot of energy breathing. Babies can be discharged with equipment for home oxygen therapy if they are otherwise well

Most babies do well but are more prone to chest infections

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55
Q

What is given to babies on home oxygen due to bronchopulmonary dysplasia?

A

Palivizumab to prevent respiratory syncytial virus infection

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56
Q

2 main neurological problems associated with prematurity

A
  1. Apnoea of prematurity
  2. Intraventricular haemorrhage
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57
Q

What is apnoea of prematurity?

A

All babies born before 28 weeks will have apnoea which is defined as a pause of breathing for more than 20 seconds, apnoea in the premature baby is caused by immature respiratory drive, gastro-oesophageal reflex, infections, seizures, hypoxia

May need mechanical ventilation until mature enough to breathe for themselves

Caffeine is given to stimulate resp. centre to drive ventilation

Good prognosis: most apnoeas resolve by 34 weeks

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58
Q

What is given to stimulate resp. centre to drive ventilation in apnoea of prematurity?

A

Caffeine

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59
Q

Intraventricular haemorrhage and periventricular leukomalacia

A

· Acquired lesions of the CNS but effective preterm infants and cause long-term disability

IV haemorrhage: small vessels rupture in germinal matrix (vascular structure, lines ventricles) - germinal matrix regresses at 34 weeks so this bleeding doesn’t occur in babies 34 weeks+

Periventricular leukomalacia: results from ischaemic injury to oligodendrocytes in the developing brain, cytokines induced damage from a maternal or neonatal infection.

• Both of the above are usually asymptomatic and detected on cranial ultrasound, sudden deterioration in babies clinical state may indicate intraventricular haemorrhage

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60
Q

Diagnosis of periventricular haemorrhage and periventricular leukomalacia

A

• Intraventricular haemorrhage: cranial ultrasound, baby is born before 32 weeks will have at least three scans in the first weeks of life when the germinal matrix is most likely to bleed. Haemorrhages are graded according to severity from least to most or grade 1 – grade 4

• Periventricular leukomalacia: noticed at birth and all preterm babies will have a routine ultrasound scan of the head at 28 weeks and 36 weeks, if periventricular leukomalacia is present the ultrasound will show cysts in the brain (cysts occur because the white-matter surrounding the ventricles softens and dies which leaves fluid filled cyst), – if the ultrasound suggests leukomalacia is present and MRI is done to assess the extent

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61
Q

Management of periventricular leukomalacia and intraventricular haemorrhage

A

There is no treatment for intraventricular haemorrhage or periventricular leukomalacia therefore the aim is to prevent it occurring in the first place

If haemorrhage occurs: monitored via weekly USS, larger haemorrhages are associated with hydrocephalus because blood prevents drainage of CSF in the ventricles

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62
Q

Retinopathy of prematurity

A
  • Abnormal proliferation of blood vessels in the retina is of premature babies – begins at 34 weeks in advance is until 45 weeks
  • Incidence and severity increase with decreasing gestational age birth, risk factors are prematurity high blood oxygen saturation and prolonged oxygen therapy
  • Main concern is that it can lead to visual problems including blindness
  • Seen in 35% of VLBW infants
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63
Q

Clinical features of retinopathy of prematurity

A

• A symptomatic condition only detected through regular screening by ophthalmologists in neonates who are at high risk e.g. born before 32 weeks or weighing less than 1.5 kg

o Retinopathy is graded according to severity, severe stages include vitreous haemorrhage and retinal detachment

64
Q

Management of retinopathy of prematurity

A

• Mostly resolve spontaneously for severe stages treatment is required usually with laser therapy under general anaesthetic to prevent blood vessel proliferation

Further progression may be treated with an intravitreal injection of bevacizumab (anti VEGF)

65
Q

What is hydrops foetalis?

A
  • This is the abnormal accumulation of fluid in the skin and body compartment, results from the rate of production of interstitial fluid exceeding the rate of absorption
  • Characterised in the foetus by gross generalised oedema, ascites and plural and pericardial effusion
66
Q

Causes of hydrops foetalis

A

Causes

• Occurs as a result of underlying disease which results in increased capillary hydrostatic pressure, decreased colloid osmotic pressure, lymphatic obstruction and capillary leakage

Associated complications

• Intrauterine or perinatal death, obstetric complications such as shoulder dystocia, PTB, pulmonary hypoplasia due to plural effusion, perinatal asphyxia

67
Q

Management of hydrops foetalis

A

Disorders treatable antenatally

o Intrauterine blood transfusion for haemolytic disease, antiarrhythmic drugs to treat foetal supraventricular tachycardia, laser ablation of foetal muscles in twin – twin transfusion syndrome

Birth planning

o Organise expert help, prepare for full resuscitation including ventilation, paracentesis or pleural effusion drainage

Neonatal management

o Resuscitation

o Support of management as appropriate

68
Q

Immune vs non-immune hydrops

A

Immune hydrops occurs when the mother’s immune system attacks and destroys the baby’s red blood cells due to incompatible maternal and fetal blood types. This form of hydrops is uncommon today because of medication available to prevent the condition

Up to 90% of all cases of hydrops today are non-immune hydrops

69
Q

Prognosis of hydrops foetalis

A
  • For foetuses or infants with non-– immune hydrops the survival rates are around 50%, higher survival rate in those with SVT, chylothorax and parvovirus infection and lower survival rate in those with chromosomal abnormalities
  • Survival rates with immune hydrops is >80%
70
Q

What is vitamin K also known as?

A

Phytomenadione

71
Q

When do babies have their hearing tested?

A

Within first 4 weeks via otoacoustic emission, then if any uncertainty regarding result automatic auditory brainstem response is carried out

72
Q

What is necrotising enterocolitis?

A

Serious, acute inflammatory bowel condition that occurs in the second or third week of life in premature babies – the most common GI emergency in the inmates, associated with high morbidity and mortality

Affects 1-3/1000

73
Q

Epidemiology of necrotising enterocolitis

A
  • Most common neonatal surgical emergency affects 1-3/1000
  • Affects 5-10% VLBW
  • 6x less likely to occur in preterm infants fed breast milk
  • In 90% cases sporadic and affects preterms
74
Q

Whic areas of bowel are most commonly affected by necrotising enterocolitis?

A

Distal terminal ileum and proximal colon most freq. affected

Can be diffuse - associated with multi organ failure

75
Q

Causes of necrotising enterocolitis

A

Specific cause is unknown but it is associated with prematurity, hypoxia, infection and formula milk

Commonly affects preterm babies but can affect babies born at any gestation

Rarely occurs before milk feeding begins

Predisposing factors:

  • Prematuirty
  • IUGR
  • Hypoxia
  • Polycythaemia
  • Exchange transfusion
  • Hyperosmolar milk feeds
76
Q

Pathophysiology of necrotising enterocolitis

A

Severe intestinal necrosis is due to exaggerated immune response within immature bowel >> inflammation and tissue injury >> bowel tissue dies due to a lack of bloodflow

77
Q

Presentation of necrotising enterocolitis

A

Most commonly in 2nd week after birth

Early

  • Non-specific illness
  • Vomiting/ bilius aspirate
  • Poor feed tolerance
  • Abdo distension

Late

  • Abdo tenderness
  • Blood, mucous, tissue in stool
  • Bowel perforation
  • Shock
  • DIC, multi organ failure
  • AXR – intestinal distension
  • Pneumonitis intestinalis (gas in bowel wall) - highly suggestive NEC
  • Hepatic portal venous gas
  • Sign of intestinal perforation
78
Q

Which methos of imaging used to support diagnosis of necrotising enterocolitis?

A

AXR - will show unusually dilated bowel

79
Q

How is necrotising enterocolitis diagnosed?

A

Based on clinical features because there is no test that is confirmatory, AXR can support the diagnosis because it will show an unusually dilated bowel

  • Abdominal x-ray may also show new pneumatosis intestinalis which is gas in the wall of the bowel and this is pathognomonic for necrotising enterocolitis – occurs as micro organisms produce gas in the bowel wall.
  • In severe cases perforation can occur in which case abdominal x-ray will show free air in abdomen
80
Q

Management of necrotising enterocolitis

A
  • Prophylaxis: antenatal steroids and breast milk are protective
  • Investigations: FBC, U&E, creatinine, coag screen, albumin, blood gas, cultures, AXR, group and cross match
  • Stop milk feeds for 10-14 days and insert gastric tube on free drainage
  • Categorised according to Bell staging
  • IV antibiotics for 10-14 days
  • Indications for surgery: perforation, deterioration despite treatment, obstruction
  • If localised: resection of bowel with primary repair
  • If extensive: 2 stage repair, second stage with intestinal reanastamoses later
81
Q

Prognosis of necrotising enterocolitis

A
  • Babies can develop short bowel syndrome which is significant malabsorption caused by extensive resection of the small intestine
  • In babies with the LBW necrotising enterocolitis increases mortality by 20–40%
82
Q

Antenatal management of prematurity

A

Predisposing factors - birth should be planned in a centre capable of caring for preterm infants

If in a centre unable to care for preterm baby, cosnider giving tocolysis to delay until transfer occurred

Give IM corticosteroids 2 doses, 12-24hrs apart if baby <34 weeks

83
Q

Post natal management of prematurity

A

Most preterm infants require stabilisation and support - senior paediatrician should be present if baby <28 weeks

Delayed cord clamping for 1 minute if baby is stable

Resp support where required

Consider intubation and ET surfactant if baby born <27 weeks

Broad spec antibiotics if any infection

Aim for miimal handling with appropriate levels of noise and cycled lighting

>> Important to offer support to parents <<

84
Q

What is the EPICure study?

A

Look at likely outcomes of infants born <26 weeks in UK

0.5% babies born <22-23 weeks survive without disability

9% babies born at 24 weeks survive without disability

20% babies born at 25 weeks survive without disability

Typical disabilities associated with birth <26 weeks: cerebral palsy, blindness, hearing loss, epilepsy, cognitive impairment and behavioural disorders

85
Q

How many babies does meconium aspiration syndrome affect?

A

1-5/1000 live births

Usually affects term infants - rarely occurs <34 weeks

86
Q

Do all babies with meconium stained liqour suffer with meconium aspiration syndrome?

A

No, 5%

87
Q

Why does meconium aspiration occur?

A

Hypoxia >> gasping and meconium passage in utero >> aspiration

88
Q

Complications of meconium aspiration?

A

Aspiration inhibits surfactant production, obstructs the resp. tract and induces pneumonitis

Baby does not cry at birth so adaptation of birth do not fully occur

89
Q

How does meconium aspiration present?

A

Resp. distress shortly after birth, CXR will show generalsied lung overinflation + patchy collapse and consolidation

90
Q

How is meconium aspiration synrome prevented?

A

If meconium staining is apparent - expedite delivery to prevent further hypoxia and gasping, suck meconium from larynx

91
Q

Management of meconium aspiration syndrome

A

Supplemental oxygen

Give surfactant if needed

Give antibiotics

92
Q

Prognosis following meconium aspiration syndrome

A

Mortality <5%, survivors do well but increased risk of asthma

If ECMO required increased risk of neuro dysfunction

93
Q

Epidemiology of neonatal jaundice

A

Very common

Affects 60% term babies and 80% preterm babies in the first week

94
Q

Jaundice during which time after birth is always pathological?

A

Baby with jaundice in 1st 24hrs - never normal!

95
Q

Why are high serum levels of unconjugated bilirubin suh a problem?

A

Unconjugated bilirubin can cross the BBB and accumulate in the basal ganglia >> kernicterus

Unconjugated bilirubin is neurotoxic and can cause deafness, cerebral palsy, seizures

96
Q

How is neonatal jaundice diagnosed?

A

Appearance is not a measure of severity

Total serum concentration of unconjugated and conjugated bilirubin must be measured ideally within 6hrs

Transcutaneous bilirubinometer can be used in babies >35 weeks but the serum test is more accurate

97
Q

Management of neonatal jaundice

A

Depends on whether the case is conjugated or unconjugated bilirubin

Unconjugated: baby placed under phototherapy unit to speed up bilirubin metabolism, regular bloods to check levels are decreasing - if extremely high and increasing there is a risk of brain damage so exchange transfusion may be needed (babies blood replaced with donor blood)

Conjugated: advice is to investigate the cause and treat based on the cause, abdominal USS to rule out biliary atresia (surgical emergency)

98
Q

What is physiological jaundice?

A

Most common cause of jaundce in neonates

Affects 60% term and 80% preterm infants

Due to low levels of UDPGT (poor conjugation in the liver) and accelerated haemolysis

Levels of unconjugated bilirubin peak around day 5 and return to normal within 2 weeks

99
Q

Management of elevated serum bilirubin

A

· Treat underlying cause, start blue light phototherapy (converts bilirubin to water soluble form that can be excreted in the urine), measure serum levels frequently, ensure adequate hydration, cover the babies eyes to avoid damage

· Intravenous Ig may be needed if the baby has Rhesus haemolytic disease or ABO haemolytic disease

· If baby show signs of jaundice within the first 24 hours assume that it’s pathological and begin treatment

100
Q

What might cause prolonged jaundice – defined as jaundice remaining more than 14 days in a term infant and more than 21 days in a preterm infant?

A
  • Breastfeeding, enclosed bleeding, haemolysis, hypothyroidism, hepatic enzyme disorders such as Crigler Najjar
  • If a baby is jaundiced and also passing pale, clay-like stalls and dark urine think obstruction e.g. biliary atresia
  • biliary atresia
  • hypothyroidism
  • galactosaemia
  • urinary tract infection
  • breast milk jaundice
  • congenital infections e.g. CMV, toxoplasmosis
101
Q

Causes of jaundice in the first 24 hrs

A

· rhesus haemolytic disease

· ABO haemolytic disease

· hereditary spherocytosis

· glucose-6-phosphodehydrogenase

Jaundice in the neonate in the first 2-14 days is common (up to 40%) and usually physiological. It is more commonly seen in breastfed babies

102
Q

How is prolonged jaundce investigated?

A
  • conjugated vs unconjugated bilirubin: the most important test as a raised conjugated bilirubin could indicate biliary atresia which requires urgent surgical intervention
  • direct antiglobulin test (Coombs’ test)
  • TFTs
  • FBC and blood film
  • urine for MC&S and reducing sugars
  • U&Es and LFTs
103
Q

What is the direct Coombs test?

A

The direct Coombs test is used to test for autoimmune hemolytic anemia—that is, a condition where the immune system breaks down red blood cells, leading to anemia. The direct Coombs test is used to detect antibodies or complement proteins attached to the surface of red blood cells

104
Q

Consequences of congenital rubella infection

A

Eyes: cataracts

Heart: PDA

Ears: sensorineural deafness

Congenital heart disease, sensorineural hearing loss, IUGR, hepatosplenomegaly, cataracts

105
Q

Pathophysiology of congenital rubella infection

A
  • Pregnant women with confirmed rubella who are at a gestational age 20 weeks or less should be referred urgently to an obstetrician for risk-assessment and counselling.
  • After 20 weeks gestational age there is no documented risk of congenital rubella syndrome.
106
Q

Consequences of congenital CMV infection

A

One of the TORCH infections

Most common long term problem is hearing loss

IUGR, hepatosplenomegaly, jaundice, thrombocytopenia, microcephaly, intracranial calcification and sensorineural hearing loss

107
Q

Consequences of toxoplasmosis infection

A

🐈 🐈 🐈 🐈nOne of the TORCH infections

Toxoplasmosis - parasite

Congenital infection = jaundice, hepatosplenomegaly, IUGR, chorioretinitis, sensorineural hearing loss

108
Q

Congenital chicken pox infection

A

Congenital varicella syndrome

Mother infected during first 20 weeks of pregnancy puts child at risk

Consequences: skin lesions, eye defects, IUGR, limb abnormalities

109
Q

Women has come into contact with chicken pox while pregnant - what is done?

A

If the pregnant woman is not immune to VZV and she has had a significant exposure, she should be
offered varicella-zoster immunoglobulin (VZIG) as soon as possible. VZIG is effective when given
up to 10 days after contact (in the case of continuous exposures, this is defined as 10 days from the appearance of the rash in the index case).

VZIG has no therapeutic benefit once chickenpox has developed and should therefore not be used in pregnant women who have developed a chickenpox rash.

110
Q

What are TORCH infections?

A

The causative organisms of congenital infection:

T: toxoplasmosis

O: other - listeria, parvovirus, syphillis

R: rubella

C: CMV

H: herpes simplex

111
Q

Consequence of congenital parvovirus infection

A

Severe anaemia leading to hydrops fetalis

Fetal demise and miscarriage in approximately 10% of cases (Risk is highest in the first and second trimesters.)

Most intrauterine infections do not result in fetal developmental defects

112
Q

Most common risk factors for perinatal neonatal sepsis

A

Maternal group B strep, PROM, maternal urinary tract infection, maternal chorioamnionitis

113
Q

How do babies with group B strep infection present?

A

Present at birth or within the first 12 hours with respiratory distress, apnoea, lethargy, poor feeding, irritability and sometimes seizures

Most babies who develop GBS infection become unwell in the first week of life (which is known as early- onset GBS infection), usually within 12–24 hours of birth

Late-onset GBS infection can affect baby up until they are 3 months old

114
Q

Management of group B strep infection in baby

A
  • High dose IV antibiotics and symptomatic management where appropriate e.g. fluids, mother is known to be colonised with GBS can be given intrapartum penicillin to prevent neonatal infection
  • 5–15% mortality due to GBS infection in developed countries
115
Q

Consequence of maternal diabetes on the foetus

A

Macrosomia, hypoglycaemia, resp distress due to lack of surfactant, congenital heart disease, sacral agenesis, microcolon

116
Q

Consequence of maternal SLE on foetus

A

Complete heart block, Ro antibodies cross placenta and damage foetal cardiac conduction

117
Q

Congenital diaphragmatic hernia

A
  • Bowel spleen and liver herniate through diaphragm into thorax - hernia results from defect in diaphragm during antenatal development
  • One in 3000 live births with boys twice as likely to be affected
  • Mainly due to defect in posterolateral segment of diaphragm and most commonly on left side
  • Lungs are underdeveloped because there is less space
118
Q

Clinical features of congenital diaphragmatic hernia

A

o Diagnosed on antenatal scan in 60–80% of cases with the remainder diagnosed at birth, baby will have severe respiratory distress and a scaphoid or concave abdomen with no breath sounds audible on the affected side

· If the defect is on the left hand side the heart may be pushed to the right and therefore heart sounds will be displaced towards the right

119
Q

How is congenital diaphragmatic hernia diagnosed?

A

o Antenatal scan at 18–21 weeks showing bowel in thorax otherwise diagnosis is made at birth following chest x-ray where loops of bowel will be visible in the hemithorax

120
Q

Management of congenital diphragmatic hernia

A

o Newborns require immediate installation and ventilation, large NG tube is placed into the stomach to allow air to escape and prevent it from further dilating and compressing the lungs

o Surgery is carried out to repair the defect but this is delayed until the respiratory status is stable

121
Q

When are cleft lip and palate usually closed?

A

Lip: 4 months

Palate: 1 year

122
Q

What is craniosynostosis?

A

· Some of the sutures of the skull prematurely fuse, this should normally only occur at 18–24 months when the brain needs its full size

· Fusion of one or two suture lines causes an abnormal headshake to form, it is unusual for this to cause restricted Brain growth

· The type of craniosynostosis depends on which suture lines are fused

123
Q

Management of craniosyntosis?

A

Treatment not always needed

Surgery offered if it will affect brain growth or affect self esteem, if child has pressure headaches or if the defect is afecting face and causing brathing difficulty

124
Q

What is plagiocephaly?

A

AKA flat head syndrome

This produces the same misshapen had as in craniosynostosis however it is not caused by premature suture fusion it is caused by external pressure for example lying on one side of the head preferentially – investigations are not needed and parents are advised to vary babies position

125
Q

Deos the NHS recommend use of helmets and bands to re-shape head?

A

No, no clear evidence to support use, uncomfortable for baby, can irritate skin, expensive

126
Q

What is brachycephaly?

A

The back of the head becomes flattened, causing the head to widen, and occasionally the forehead bulges out

127
Q

Causes of neonatal hypoglycaemia

A

Increased demand for glucose with decreased supply available caused by prematurity, IUGR, hypothermia, infection, hypoxic ischaemic encephalopathy

Hyperinsulinism caused by maternal DM, Beckwith-Wiedemann syndrome and transient neonatal hyperinsulinism

Babies born to mothers who have been taking beta-blockers are also at risk of hypoglycaemia

128
Q

Which medication taken by mothers might cause hypoglycaemia in the foetus

A

Beta blockers

129
Q

Management of hypoglycaemia in neonate

A

Aim is to prevent this occurring but

Babies who have hypoglycaemia are fed soon after birth and at regular intervals to prevent hypoglycaemia

Blood glucose is measured for 24 hours and prompt treatment is given if it falls too low

  • Dextrose gel massaged into babies cheek or if persisting hypoglycaemia then give IV dextrose
130
Q

What is the purpose of the neonatal examination?

A
  • Provide reassurance for the mother
  • Health education and explaining common variations
  • Detecting asymptomatic problems such as congenital heart disease and DDH
  • Screening for rare but serious conditions
131
Q

Initial part of neonatal examination

A
  • Ask if there are any concerns or problems
  • Check patient’s notes for relevant details of maternal medical history, family history, antenatal and obstetric history and social history
  • Ask if baby is feeling and whether they have passed meconium and urine
  • When baby is quiet note the general posture and movement, skin colour, listen to heart and lungs, examine eyes for size and strabismus and examine eyes for bilateral red reflexes to exclude cataract or retinoblastoma
132
Q

Head to to newborn examination

A
  1. Cranium: measure (normal = 33-37cm term), skull shape, fontanelle tension and size
  2. Face: any dysmorphism, insepct for cleft palate
  3. Ears: size, shape, position
  4. Neck: inspect, palpate clavicles
  5. Chest: shape, symmetry, nipples, resp. rate (normal = 40-60), palpate apex beat
  6. Abdomen: umbilical stump, inguinal hernias, masses, liver, spleen, kidneys, bladder
  7. Genital: inspect, ensure testes have descended, position of meatus
  8. Femoral pulses
  9. Anus: position and patency
  10. Spine : defrmity, hair patch, pigmentation
  11. Limbs: palmar creases, movements, digits, hips DDH
  12. CNS
  13. Check urine and meconium have been passed
133
Q

Outline weight loss after birth

A

· Up to 10% weight loss in well term infants is common over the first week of life

  • Failure to lose weight may suggest fluid retention or overload
  • Infants with more than 10% weight loss require further assessment of feeding as there is a risk of hypernatraemic dehydration

o Check U&E if weight loss is more than 12%

o Support mother with breastfeeding and breast expressing/top up feeds

134
Q

What are the key physiological and metabolic adaptive processes that allow transition from intra-uterine support after birth?

A

Birth: umbilical cord clamped > loss of oxygen delivery

Babies first cry opens up lungs, enables oxygenation from the babies lungs

Oxygen inhalation leads to pulmonary artery vasodilation >> decrased arterial resistance and increased pulmonary blood flow

Systemic vascular resistance increases due to low resistance placental circulation

Ductus arteriosus constricts

Foramen ovale closes as pulmonary venous return to the left atrium increases

The above changes become permanent over 2-3 weeks

135
Q

Outline foetal circulation

A
  1. Blood is oxygenated in the placenta
  2. Highly oxygenated and nutrient-enriched blood returns to the fetus from the placenta via the left umbilical vein.
  3. Some blood enters liver sinusoids; most of the blood bypasses the sinusoids by passing through the ductus venosus and enters the inferior vena cava (IVC)
  4. From the IVC, blood enters the right atrium, where most of the blood bypasses the right ventricle through the foramen ovale to enter the left atrium.
  5. From the left atrium, blood enters the left ventricle and is delivered to fetal tissues via the aorta.
  6. Poorly oxygenated and nutrient-poor fetal blood is sent back to the placenta via right and left umbilical arteries.
  7. Some blood in the right atrium enters the right ventricle; blood in the right ventricle enters the pulmonary trunk, but most of the blood bypasses the lungs through the ductus arteriosus
136
Q

How is venous access estabished in a newborn?

A

Umbilical vein - the walls of the vessel come together but it remains patent for a few days

Large central venous catheter can be used as a routs for IV access

137
Q

What is persistent pulmonary HTN of the newborn?

A

Failure of pulmonary vascular resistance to fall after birth - this decreases pulmonary blood flow

Affecs 1/1000 - 1/1500

Rarely a primary condition, usually due to underlying serious illness

138
Q

Causes of persistent pulmonary HTN

A

Meconium aspiration

Infections: pneumonia, group B strep

Diaphragmatic hernia

Lung hypoplasia

Cause is not always found

139
Q

Presentation of persistent pulmonary hypertension

A
  • Hypoxia, discrepancy between pre-and post doctoral arterial oxygen saturations, mild breathlessness, acidosis and hypotension
  • Loud single second heart sound
  • Echocardiogram will show increased pulmonary arterial pressure, large right to left shunt at the level of the foramen ovale and ductus arteriosus
140
Q

Management of persistent pulmonary HTN

A
  • Treat underlying cause, optimise obs, inhaled nitric oxide will result in selective pulmonary vasodilation ECMO if severe
  • 10–30% mortality
141
Q

When dos the ductus arteriouss normally close after birth?

A

1-3 days after birth in term infants

Common in preterm infants

142
Q

How does a patent ductus arteriosus present?

A
  • Small: asymptomatic
  • Large: poor growth, difficulty feeding, resp. difficulty, machinery murmur at the left upper sternal edge radiating to the back, heart failure
  • CXR: cardiomegaly, PDA and degree of shunt
  • Echo: confirms PDA and degree of shunt
143
Q

Complications associated with a patent ductus arteriosus

A
  • Poor growth, HF, pulmonary haemorrhage, pulmonary dysplasia
144
Q

Management of a patent ductus arteriosus

A

o Wide variation in practice with some units treating many cases and other units treating none

o If asymptomatic: observe, most close spontaneously

o Symptomatic: restrict fluids, optimise oxygenation, treat any heart failure with furosemide, consider pharmacological closure with indomethacin or ibuprofen – note that indomethacin is contraindicated if baby has severe jaundice, necrotising enterocolitis, thrombocytopenia or renal failure

o Surgery may be necessary if medical management fails to control symptoms or if there is prolonged failure to close

145
Q

Breast feeding rates in the UK

A

Breastfeeding rates in the UK are poor with only 20–25% exclusively breastfeeding at six weeks and only 15% at three months

146
Q

Why is it not advised to give cow’s milk <12 months?

A

Contains too much protein, sodium and potassium for the immature kidneys to process

147
Q

Up to what age does WHO recommedn breast feeding?

A

6 months

148
Q

Normal volume requirement of formula milk?

A

150ml/kg/day

149
Q

Advantages and disadvantages of formula milk

A

Advantages

  • Allows for paternal involvement and allows for the milk intake to be determined
  • Formula milk contains more vitamin K and breastmilk although all newborn children receive vitamin K injections meaning mothers can breastfeed without concern that baby is deficient in vitamin K

Disadvantages

  • Constipation, oral thrush, milk bezoars (accumulation of undigested milk/ mucous)
  • Iron deficiency can also occur because cows milk is low in iron and the iron this is present is more difficult to absorb than that in breastmilk
150
Q

Contra-indications to breast feeding

A
  • Positive maternal HIV status, certain maternal medications such as amiodarone, herpes zoster on the breast, infantile galactosaemia or phenylketonuria, primary lactose intolerance
151
Q

What is the ‘healthy start’ programme?

A

Governemtn scheme for those with low income or on benefits

Gives vouchers for healthy food and formula milk

152
Q

What is the APGAR score?

A

The Apgar score is used to assess the health of a newborn baby

0-3 = very low

4-6 = moderate

7-10 = good state

Score

Pulse

Respiratory effort

Colour

Muscle tone

Reflex irritability

2

> 100

Strong, crying

Pink

Active movement

Cries on stimulation/sneezes, coughs

1

< 100

Weak, irregular

Body pink, extremities blue

Limb flexion

Grimace

0

Absent

Nil

Blue all over

Flaccid

Nil

153
Q

What do the centiles on growth charts show?

A
  • Optimum range of weights and heights
  • Describes the percentage expected to be below that line
  • 50% below 50th centile
  • 91% below the 91st
  • 1 in 250 below the 0.4th
  • 50% of children should be between 25-75th centile
154
Q

Centile terminology

A
  • If the point is exactly on the centile line or within 1/4 space of the centile line the child is described as being on the centile
  • If not, they should be described as being between centile x and y
  • A centile space is the distance between two centile lines, two measurements can be described as a centile space apart if they are both midway between centiles
  • Falls or rises should be expressed as multiples of centile spaces e.g. a fall through 21/2 centile spaces
155
Q

Discuss SUDI

A
  • Unexpected and initially unexplained death of a previously well child under the age of one year
  • Cause of death may be determined following investigation however if it remains unexplained it is defined as sudden infant death syndrome also known as cot death
  • Causes include infection, metabolic conditions and trauma
  • The risk of cot death is highest during the first four months of life and babies who were born prematurely or born at a low-birth-weight are at greater risk
  • Investigations
    • Main aims are to investigate the cause of death and support the family. Death must be referred to the coroner and a post-mortem is carried out. Police are informed and will question the family and representatives from agencies then attend an information sharing meeting to consider any concerns about the family and share any concerns regarding death caused by non-accidental injury
  • Outline strategies to avoid sudden infant death syndrome
    • Do not smoke in the same room as the baby, avoid bed sharing after drinking alcohol or taking drugs, avoid sleeping with the baby on a couch, consider breastfeeding, offer the baby a dummy while they are falling asleep
    • Do not use pillows or duvets within the cot, always place the baby on their back to sleep, ensure that the babies feet are at the bottom of the cot and took the babies blanket below their shoulders to avoid covering their head
  • Families who have experienced sudden unexplained death of an infant needs support during bereavement and will need help with preventative measures if they go on to have another baby – these two areas of support can be integrated in a service known as the care of next infant program
    • Parents are also provided with an apnoea monitor and resource training for any subsequent babies, their subsequent baby will also be weighed weekly

Paediatrics (19 decks)

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