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Block 41 > Newborn Exam > Flashcards

Newborn Exam Flashcards

1
Q

When is Newborn Exam done?

A

1st exam 72h
2nd exam 6-8w, latest 10w

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2
Q

What are you looking for in the exam?

A

Congenital HD
Developmental dysplasia of hip
Morphological abnormalities
Undescended testes

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3
Q

Important postnatal changes

A

Increased systemic vascular resistance with separation from low-resistance placental vasculature
Closure of L to R shunts (foramen ovale and DA)
Rapid lowering of pulmonary vascular resistance with onset of ventilation
Clearance of fluid away from airway pressure due to ventilation
Increased metabolic rate leading to higher glucose needs
Increased catecholamine levels to support BP

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4
Q

Foramen Ovale

A

1st postnatal breath causes pulmonary vascular resistance to decrease dramatically
Due to ventilation and increased O2 exposure
Pressure withing L atrium then increases because of distal aortic pressure and greater amount of blood returning to L atrium
L atrium pressure > R atrium pressure = flap across foramen ovale closes

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5
Q

Ductus arteriosus

A

Reversal of flow across DA with a L to R flow = greater pulmonary flow
Oxygenation of DA further leads to increased Ca channel activity/inhibition of potassium channel activity = closure

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6
Q

Surfactant

A

Surfactant secretion into foetal lungs is stimulated by labour
Alveolar stretch as a result of initiation of ventilation further increases secretion of surfactant
Surfactant lowers surface tension in lungs so can inflate at lower pressures

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7
Q

Clearance of foetal lung fluid

A

Begins before birth, increased in labour and mostly done by 2 hours old
Spontaneous labour and immediately after birth - resp epithelium changes from active fluid secretion to active fluid absorption - uses sodium transport in interstitium
Regulation of active fluid absorption is believed to be regulated by increased cortisol and thyroid hormone levels

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8
Q

Postnatal haematological changes

A

After birth, production of foetal Hb decreases and there is increase in haemoglobin B chain production
Normal adult levels of Hb achieved by 4-6m
Exposure to increased oxygenation of extrauterine environment leads to decreased erythropoeitin, leading to lower rates of erythropoeisis in neonate

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9
Q

Postnatal metabolic changes

A

Foetus has low metabolic rate

Maintain blood glucose - surge in catecholamines and glucagon levels and decrease in insulin amounts
Gluconeogenesis and glycogenolysis

Ketone bodies and lactate provide additional energy for brain

Cortisol and thyroid hormones activate sodium channel activity that drives resorption of lung fluid

Increased production and release of catecholamines renin-angiotensin and ADH - CO, plasma glucose and free fatty acids

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10
Q

Postnatal temperature regulation

A

Babies emerge covered in fluids = heavy heat loss via evaporation
Newborns not held skin-to-skin or wrapped up then hypothermia can ensue because of conduction, convection and radiant heat losses
Brown adipose tissue lipolysis triggered by noradrenaline can generate heat and peripheral vasoconstriction can minimise heat loss

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11
Q

What can you use to predict preterm birth?

A

Transvaginal USS of the cervix and measurement of foetal fibronectin
Positive foetal fibronectin from 22-37 weeks means increased risk of premature birth within 7 days

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12
Q

Maternal characteristics which increase risk of preterm birth

A
  • FHx of preterm birth
  • Lows SES
  • Low educational attainment
  • Maternal age (low or high)
  • Ethnicity (non-white race)
  • Stress
  • Depression
  • Tobacco use
  • Infections
  • Periodontal disease
  • Uterine abnormalities
  • History of cervical excisional procedures/surgery
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13
Q

Reproductive history risk factors for preterms

A
  • Prior preterm birth/ stillbirth/ pregnancy loss >16w GA
  • induced abortion
  • cervical insufficiency
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14
Q

Pregnancy risk factors for preterms

A
  • vaginal bleeding
  • assisted reprodructive technologies
  • multiple gestation
  • short cervical length
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15
Q

Causes of preterm labour

A
  • spontaneous preterm labour
  • intra-uterine infection
  • premature membrane ruptures
  • pre-eclampsia/pregnancy induced HTN
  • Abruption/anterpartum haemorrhage
  • abnormal amniotic fluid volume
  • severe BV
  • Previous preterm
  • Cervical incompetence
  • Gestational DM
  • high or low BMI
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16
Q

Prediction of LBW

A
  • inadequate weight gain by mother during pregnancy
  • inadequate proteins in diet
  • previous preterm/LBW
  • Anaemic mother
  • Passive smoking
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17
Q

Methods to prevent preterm birth and LBW

A
  • Limit maternal RF - smoking cessation
  • Treat BV w/ clindamycin - reduce risk of membrane rupture
  • Progesterone - short cervix
  • Cervical sutures - previous loss from weakness, short cervix or response to dilation
  • Reduction of pregnancy number
  • Bed rest
  • Tocolytic drugs (Atosiban/Ritodrine) can briefly delay labour + allow steroids to be given to reduce lung disease risk
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18
Q

What are complications of pre-term delivery and why? (think systems)

A
  • Immaturity of organ systems (lungs)
  • Temp control - heat loss is high due to high SA:V and lack of fat insulation, limited muscle activity
  • Blood and circulation - hypotension, easy bruising and bleeding
  • Resp system - narrow nasal airway, poor cough reflex, alveolar collapse due to surfactant insufficiency
  • GIT - uncoordinated suck/swallow (before 32-34w), regurg
  • Active and passive immunity limited
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19
Q

Short term disorders of preemies

A
  • Surfactant deficiency
  • Apnoeic attacks
  • PDA
  • Intracranial lesions
  • Necrotising entercolitis
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20
Q

Surfactant deficiency
Features + Mx

A
  • Immaturity of type II pneumocytes
  • Lowers surface tension in alveoli and prevents alveolar collapse
  • Worse in boys

S+S: Resp distress, tachypnoea, cyanosis, expiratory grunting

Mx: Resolves spontaneously 3-7d as endogenous surfactant produced
- glucocorticoids antenatally for 48hours
- artifical surfactant therapy (Curosurf)
- O2 + assisted ventilation

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21
Q

What does surfactant deficiency look like on xray?

A

Ground glass appearance

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22
Q

Apneoic attacks

RF

Mx

A
  • periodic respiration with some spells of very shallow breathing or complete cessation of breathing for 20s

RF = Resp distress, hypoxia, sepsis, cranial pathology

Alarms - alert staff is O2 sats reach certain point use physiological stimulation
Caffeine used to prevent apneoia as improves neurodevelopmental outcome
Vent support if severe

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23
Q

Intracranial lesions

RF

Complications

A

Intracranial haemorrhage into geminal matrix or ventricles
Ischaemia of periventricular white matter

RF: pneumothorax, asphyxia, hypovolaemia, hypotension, hypoxia

Hydrocephalus is late stage complications
Serial intracranial USS used to diagnose

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24
Q

Necrotising Enterocolitis
(what is, aetiology, S+S, Mx)

A

Necrosis of intestine - distal ileum or proximal colon
Aetiology: preterm birth, IUGR, Polycythaemia, PDA, Asphyxia, early formula milk feeding
S+S: abdo distension, vomiting, bloody stools, AXR - dilated, thick walls, static bowel loops
Mx: Large bore NG tube + parenteral nutrition, penicillin, gentamicin and metronidazole, surgical resection

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25
Q

Long term consequences of preemies

A

Retinopathy
Chronic Lung disease
Neurodevelopmental problems

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26
Q

Retinopathy of prematurity

A

Retinas are incompletely vascularised at birth
Can progress to fibrosis, retinal detachments and blindness
All infants weighing <1500g or <32w GA should have eyes screened at 6-8w
Most resolve spontaneously
Laser therapy for severe disease

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27
Q

CLD of prematurity

A

Prolonged ventilation with high pressure and high concentration
Requiring supplemental O2 after 36w, corrected GA or 28 days of age whichever is later
Positive pressure ventilation causing volutrauma, oxygen toxicity and inflammation - all contribute

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28
Q

Mx of CLD

A

Assisted ventilation and CPAP
Supplemental O2 as needed
Dexamethasone - helps wean from ventilation but increase risk of neurodevelopment impairment
Strict nutrition
Prophylaxis against RSV - Plaivizumab vaccine

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29
Q

Neurodevelopmental problems

A

Very LBW infants those with gestation period under 28w are at risk of:
CP
Cognitive delay
Visual impairment
Hearing loss
Seizures
Behavioural problems
Educational difficulties

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30
Q

Types of acyanotic heart disease

A

ASD
VSD
PDA
Coarctation of aorta
Aortic stenosis
Pulmonary stenosis

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31
Q

What causes acyanotic congenital HD?

A

Lesions that allow blood to shunt from left to right side of the heart/circulation OR lesions that obstruct the flow of blood by narrowing a valve or vessel

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32
Q

What are the types of ASD?

A

Ostium primum - occurs lower in atrial septum, often associated with mitral regurg and Downs syndrome

Ostium Secondum (most common) - high in atrial septum, more common in girls, asymptomatic as left to right shunt develops slowly

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33
Q

What are causes of ASD?

A

Ostium primum - when septum primum doesn’t fuse to endocardial cushion of septum intermedium

Ostium Secondum - excessive apoptosis or resaborption of septum primum or insufficient formation of septum secondum

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34
Q

S+S of ASD

A

Abnormal RV impulse
Widely split and fixed S2
Tricuspid flow murmur - rumbling mid-diastolic murmur at left sternal edge
Pulmonary flow murmur - soft, ejection systolic murmur in pulmonary area
Sounds like an ejection systolic murmur and a fixed split of S2

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35
Q

Diagnosing an ASD (Signs on scans)

A

CXR - pulmonary plethora (increased pulmonary perfusion)
ECG - RVH with incomplete RBBB - big R wave
ECHO

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36
Q

Mx of ASD

A

Transcatheter closure of ASDs, best done between 3-5y
Prevent cardiac failure and arrhythmias later in life

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37
Q

Risk factors for VSD

A

Foetal alcohol syndrome and Down’s syndrome

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38
Q

Commonest type of CHD

A

VSD

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39
Q

Causes of VSD

A

Muscular ridge grows up from apex of heart and membranous region grows down from endocardial cushion = 2 chambers
If leaves a gap/don’t fuse = VSD

Majority caused by defect in membranous region

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40
Q

What happens in VSD?

A

Blood flows from high - low pressure so right side of heart functions normally as has lower pressure
L side of heart has higher pressure so some blood flows into RV = L to R shunt
Leads to higher O2 sats in RV and pulmonary artery
If pressure increases in R side increases (e.g Cor Pulmonale) to being more than L shunt can swap to be R to L = deoxygenated blood into systemic circulation = cyanosis

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41
Q

Eisenmenger Syndrome

A

Pressure in R side increases to being more than L shunt can swap to be R to L - deoxygenated blood in circulation = cyanosis

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42
Q

S+S of VSD

A

Pulmonary HTN - shunt means more blood volume in R side
Cyanosis - shunt swaps to R to L = Eisenmengers syndrome

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43
Q

Ductus arteriosus

A

Connects aorta to L pulmonary artery to bypass lungs and usually closes by 4th day of life
Kept open by prostaglandin E2

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44
Q

When is PDA diagnosed?

Pathophysiology of PDA

Complications of PDA

A

If doesn’t close 1 day after life

After birth, R side of heart functions normally as is lower pressure area so blood flows to lungs as normal
L side = higher pressure, blood flows high - low, some is shunted back to lower pressure side - back to lungs
No deoxygenated blood travels round systemic circulation = acyanotic

Increased RV can lead to pulmonary HTN pressure in R > L so then shunts to L and then deoxygenated blood travels systemically = Eisenmengers

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45
Q

RF for PDA

A

Preterm infants
Down’s syndrome
High altitudes
Maternal rubella

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46
Q

S+S of PDA

A

Asymptomatic
Bounding pulses - wide pulse pressure
Murmur - continuous machinery

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47
Q

What do you seen on scan with a PDA?

A

Similar on ECG and CXR to VSD
Large PDA - increased pulmonary markings are seen
Shown on ECHO
Ductal shunt confirmed by US

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48
Q

Mx of PDA

A

Indomethacin = NSAID inhibits protaglandin E so can shut
If large, may be closed at 1-3 months
Closed in cardiac catheter lab at 1y

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49
Q

Coarctation of aorta

A

Obstructive lesion caused by narrowing or constriction in a portion of aorta
Preductal or postductal
Forces heart to pump harder to get blood through aorta and circulation

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50
Q

Preductal coarctation of aorta
(definition. presentation, mx)

A

Abnormal circulation often diagnosed antenatally

Present as a sick neonate with absent femoral pulses
Whilst DA is open - RV can maintain adequate CO to systemic circulation

Prostaglandin infusion given to maintain ductal patency
Transfer to cardiac centre for surgery

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51
Q

Postductal coarctation of aorta
(s+s, mx)

A

normally asymptomatic

leg pains or headaches
HTN in arm, weak or absent femoral pulses
Ejection click (bicuspid valve) and ejection systolic murmur

Balloon dilatation
Resection of coarcted segment with end-end anastamosis

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52
Q

Mx of aortic stenosis

A

Sustained, strenuous exercise avoided in moderate to severe aortic stenosis
Surgery: depends on severity and site - balloon or surgical valvotomy
Aortic valve replacement for neonates and infants with significant stenosis

53
Q

S+S of aortic stenosis

A

mild or moderate stenosis presents with asymptomatic murmur and a thrill
Severe stenosis can present with HF in infant or with chest pain on exertion and syncope in older children

54
Q

S+S of Pulmonary stenosis

A

Most cases are mild and asymptomatic
Widely split S2 with a soft pulmonary component
Systolic ejection click and/or murmur - upper left sternal border

55
Q

Mx of pulmonary stenosis

A

Transvenous balloon dilatation
Pulmonary valvotomy

56
Q

Cyanotic heart disease

A

Tetralogy of Fallot
Transposition of great arteries

57
Q

Pathophysiological mechanisms for cyanosis in CHD

A
  1. Increased pulmonary blood flow with shunting of deoxygenated blood from right to left (systemic circulation) = ToF
  2. Abnormal mixing of systemic and pulmonary venous return, associated with increased pulmonary blood flow
    = transposition of great arteries
58
Q

What are the four parts of ToF

A
  1. Stenosis - narrowing of valve or infundibulum - harder for deoxygenated blood to get to pulmonary circulation
  2. = RVH so can contract harder and push blood past stenosis = boot shaped heart
  3. Large VSD - RV outflow obstruction can block blood flow so much that RV pressure is really high so deoxygenated blood goes R to L
  4. Overriding aorta - deoxygenated blood shunted from R to L flow to LV and out of body
59
Q

what affects severity of tetralogy of fallot?

A

How much obstruction there is
Less obstruction = shunt is L to R so oxygenated blood circulates through lungs again
More obstruction = R to L shunt and deoxygenated blood to systemic circulation

60
Q

Symptoms

A

Present cyanosis in first 1-2m of life
Hypoxic spells
‘Tet spells’ when there is an increased O2 demand so heart pumps more blood and leads to sudden drop in O2 sats due to faulty circulation
Squatting on exercise - helps as kinks femoral arteries - increases vascular resistance in peripherals and then in systemic circulation - increased LV pressure = L to R shunt temporarily reverses so blood travels to lungs and reduced cyanosis

61
Q

Signs of ToF

A

Cyanosis with or without clubbing
Loud and single S2
Loud ejection systolic murmur

62
Q

Investigations for ToF

A

ECG: RAD and RVH, but normal at birth
CXR: ‘boot shaped’ heart caused by RVH and concavity on left border
ECHO

63
Q

What is transposition of great arteries

A

Aorta rises anteriorly from RV
PA arises posteriorly from LV
Blood goes from LV to Pulmomary artery to lungs and back to LA = never deoxygenated
Blood goes from RV to aorta and round systemic circulation = never oxygenated
Transposition of great arteries where parallel circuits are completely separated is incompatible with life

64
Q

What increases survival with TGA?

A

Defects that allow mixing of 2 circulation systems co-exist = ASD, VSD or foramen ovale = some oxygenated blood to tissues = more likely to survive

65
Q

Levo-TGA

A

“Congenitally corrected TGA”
Aorta to the L of PA
Ventricles and valves swap meaning circulatory loops still work as normal
LV and mitral valve built for higher pressure is swapped and now RV has higher pressure for systemic circulation - after years can lead to RVH and HF

66
Q

RF for TGA

A

Maternal RF:
Rubella
DM
Poor nutrition
Consumes alcohol
is >40y/o

67
Q

S+S for TGA

A

severe cyanosis within 1st day of life
Spontaneous closure of DA reduces mixing of systemic and pulmonary circulations
Arterial hypoxaemia is profound and unresponsive O2 inhalation
RV is high pressure - RVH
LV - low pressure can lead to atrophy = big changes in structure = HF
S2 single and loud
VS is intact = no murmur

68
Q

How do neural tube defects occur?
How to prevent them?

A
  • Failure of fusion of neural plate in first 38 days after conception
  • Folic acid supplements should ideally be taken preconception
  • All pregnant women are advised to take folic acid supplements in 1st trimester as a way of reducing neural tube defects
69
Q

3 main types of neural tube defects

A
  1. Spina Bifida occulta
  2. Meningocele
  3. Myelomeningocele
70
Q

What is spina bifida?

A
  • neural tube formed from ectoderm
  • skin that usually comes over spinal cord to cover don’t fuse leaving an opening in back
  • Dorsal vertebral arch fails to fuse or are absent
  • may be an overlying skin lesion such as a tuft of hair or a small dermal sinus
71
Q

Causes of spina bifida and RF

A
  • unknown
    RF: folate deficiency (vit B9), obesity, poorly controlled DM, meds that interfere with folate production
72
Q

Diagnosis of spina bifida

A

Prenatal
Increased AFP - neural tube not closed leaks from CSF leaks into bloodstream (not specific can be raised in other conditions)
Other blood tests: HCG, Inhibin A, Estriol
Amniocentesis - serious cases

73
Q

Mx

A

Prenatal surgery - close myelomeningocele, can be dangerous
Postnatal surgery - within days of birth, minimise risk of meningitis

74
Q

Meningocele

A

Uncommon (5%)
Only meninges, not spinal nerves, slip through gaps
Smooth, intact, skin-covered cystic swelling is filled with CSF
Spinal cord itself not damaged = no neurological deficit or hydrocephalus
Excision and closure of defect is undertaken after 3m

75
Q

Myelomeningocele

A

Accounts for 90% of overt spina bifida - worst type
Cord and meninges protrude out of a hole in spine - held together by sack of skin
Severe cases no skin - nerve exposed = open spina bifida
Causes neurological deficits - motor and sensory loss in lower limbs and/or neuropathic bladder and bowel
Often scolisosis and associated hydrocephalus due to Arnold-Chiari II malformation
Mx = prenatal surgery = close myelomeningocele, can be dangerous

76
Q

What is Arnold-Chiari II malformation?

A

accumulation of CSF in brain, often associated with scoliosis and hydrocephalus

77
Q

Spina Bifida

A

Most common and most mild
Not picked up antenatally as only tiny amounts protrude
asymptomatic - pick up later in life
May have a mole or hair at site of lesion

78
Q

Rarer neural tube defects

A
  1. Encephalocele: extrusion of brain and meninges through a midline skull defect
  2. Anencephaly: cranium and brain fail to develop (detected on antenatal USS and termination of pregnancy is offered)
79
Q

Trisomy

A

3 rather than 2 copies of a specific chromosome are present in cells of individual
Occur due to mitotic error called non-dysjunction in gamete of mother or father

80
Q

Down’s syndrome

A
  • Trisomy 21
  • Risk increases with maternal age, increasingly steeply over 35
81
Q

S+S of Down’s syndromes

A

Round face
Flat nasal bridge
Small ears
Protruding tongue
Single palmar crease
Flat occiput
Gap between first and second toes
Small stature
Cardiac deficits
Increased risk of leukaemia, hypothyroidism, resp. infections, alzheimers disease

82
Q

Diagnosis of Down’s syndrome

A

Often suspected at birth - due to characteristic facial appearance
Rapid chromosomal analysis is performed via FISH, but may not exclude mosaicism
Complete karyotype is performed to confirm initial result

83
Q

Complications of Down’s sydnrome

A

AVSD
Colonic atresia
Duodenal atresia
Increased risk of AML

84
Q

Mx

A

Parents need info about implications of diagnosis and assistance available from professionals and self-help groups
Genetic counselling for recurrence risks required
Cardiology review and ECHO should be arranged shortly after birth due to associations with cardiac defects
Life expectancy in Down’s syndrome has increased - living situation and employment in adulthood may need additional support
Screening for diseases associated with Down’s syndrome should be performed throughout life (e.g hypothyroidism and coeliac disease)

85
Q

Edwards syndrome

A

Trisomy 18
Most babies die in infancy

86
Q

S+S of Edwards syndrome

A

Phenotype: microcephaly and micrognathia with cleft lip/palate, ocular abnormalities (palpebral fissures, hypertelorism and ptosis)
Hands are often clenched with overlapping fingers
Club foot and absent radii may also feature
Systemic abnormalities include congenital cardiac malformations, renal disease, exopthalmos, atresia and developmental delay

87
Q

Patau syndrome

A

Trisomy 13
Small proportion survive to adulthood
Those with mosaicism have a better prognosis, but most die in early childhood

88
Q

S+S of Patau syndrome

A

Polydactyl, low set ears, talipes, cutis aplasia and cleft palate
Problems with CNS (low IQ, microcephaly and holoprosencephaly)
Micropthalmia and other eye problems
Abnormal genitalia
Renal malformation
Cardiac malformation

89
Q

Turner syndrome

A

Female only has 1 X chromosome
45 XO
Incidence does not increase with maternal age

90
Q

S+S of turner syndrome

A

Short stature
Primary amenorrhoea
Intelligence is normal but may be specific learning difficulties
Dysmorphic features: lymphoedema of hands and feet at birth, neck webbing, widely spaced nipples (shield shaped chest), wide carrying angle (cubitus valgus)
Gonadal dysgenesis
CHD (coarctation of aorta)
Renal anomalies

91
Q

Diagnosis of turner syndrome

A

Antenatally by USS
Presence of puffy hands and feet or cardiac abnormality
During childhood because of short stature
Adolescence because of primary amenorrhoea and lack of pubertal development
Confirmed by karyotype

92
Q

Mx of Turners syndrome

A

Therapy with growth hormone improves final height
Oestrogen therapy at appropriate age (11) to produce matruation od secondary sexual characteristics
End of puberty progestogen is added to maintain uterine health and allow monthly withdrawal bleeds
Although pregnancy can occur, most are infertile, can be achieved with IVF
Treatments may be necessary for other abnormalities

93
Q

Klinefelter syndrome

A

Presence of one or more extra X chromosome in males
Most common karyotype is 47 XXY, can also be 48XXXY or 49XXXXY

94
Q

S+S of Klinefelter syndrome

A

Tall stature with long legs
Small testes
Weaker muscles
Wider hips
Reduced libido
Shyness
Infertility
Gynaecomastia
Learning difficulties

95
Q

Mx of Klinefelter syndrome

A

Manage features of condition
Testosterone injection improve many symptoms
Advanced IVF techniques have potential to allow fertility
Breast reduction surgery for cosmetic purposes
SALT
OT
Physio
Educational support

96
Q

Prognosis

A

Life expectancy is close to normal
Slight increased risk of:
Breast ca, osteoporosis, DM, anxiety and depression

97
Q

What is a cleft lip?

A

Congenital condition where there is a split or open section of upper lip
Opening can occur at any point along top lip and can extend as high as nose
can occur with cleft palate or on its own

98
Q

What is a cleft palate?

A

Defect is in the hard or soft palate at roof of the mouth and nasal cavity
Leaves an opening between mouth and nasal cavity
Can occur with cleft lip or on its own

99
Q

What is the epidemiology for cleft lip/palate?

A

35% cleft lip alone
25% cleft lip and palate
40% cleft palate alone

100
Q

Aetiology of cleft lip/palate

A

Unclear
Polygenic
Teratogenic drugs e.g anticonvulsants and methotrexate
Relative increases risk, but inheritance patterns are random

101
Q

How is diagnosis made of cleft lip/palate?

A

18-20 week scan
Isolated cleft palates hard to diagnose antenatally

102
Q

Mx of cleft lip/palate

A

MDT: priority to ensure baby can eat and drink
Surgical repair of cleft palate at 6-12m
Cleft lip early (1st week of life) or late (3m)

103
Q

Complications of cleft lip/palate

A

Problems feeding, swallowing and speech
Psycho-social implications - affect bonding between mother and child
Can be more prone to hearing problems, ear infections and glue ear

104
Q

What is club foot/talipes?

A

Fixed abnormal ankle position that presents at birth
Occurs spontaneously or be associated with other syndromes
Usually identified at birth or during newborn exam

105
Q

Talipes equinovarus

A

ankle in plantar flexion and supination

106
Q

Talipes calcaneovalgus

A

ankle in dorsiflexion and pronation

107
Q

Ponseti method

A

Treats talipes without surgery
Usually very successful, started almost immediately after birth
Foot manipulated towards a normal position and cast applied to hold in position
Achilles tenotomy performed to release achilles tendon
After treatment with cast, a brace is used to hold foot in correct position when not walking until child if 4 years old

108
Q

Positional Talipes

A

Common condition where resting position of ankle is in plantar flexion and supination - but not fixed in position and there is no structural boney issue in ankle
Muscle are slightly tight around ankle but bones are unaffected
Foot can be moved into normal position
Referral to physio for simple exercises to help foot return to a normal postion
Resolves with time

109
Q

Physiological jaundice

A

Common
Appears after 24 hours
Peaks around 3-4d
Resolves by 14d
Progresses in cephalic-caudal direction

110
Q

Causes of physiological jaundice

A

Combination of increased RBC breakdown and immature hepatic enzymes causes unconjugated hyperbilirubinaemia
Exacerbated by dehydration which can occur if establishment of feeding is delayed
May indicate underlying disease

111
Q

Causes of high serum unconjugated bilirubin

A

Exaggerated physiological jaundice (preterm, bruising)
Sepsis
Haemolytic disorders
Hepatic disease

112
Q

What are the dangers of high serum unconjugated bilirubin?

A

Neurotoxic
Kernicterus (deafness, athetoid CP, seizures)

113
Q

Pathological Jaundice

A

Onset of jaundice within first 24 hours of life is always pathological
Recognise severe neonatal unconjugated hyperbilirubinaemia to avoid encephalopathy or kernicterus (brain damage due to deposition of bilirubin in basal ganglia)

114
Q

Causes of pathological jaundice (<24h)

A

Haemolysis
Haemolytic disease of newborn - rhesus or ABO incompatibility
ABO more common
Intrinsic red defects - spherocytosis, G6PD deficiency or pyruvate kinase deficiency
Infection: CMV

115
Q

Causes of prolonged jaundice (>2w)

A

Usually ‘breast milk jaundice’ - cause unknown usually resolves by 12w of age
Infection: UTI
Congenital hypothyroidism
Enclosed bleeding (cephalohaematoma)
Prematurity
Haemolysis
Sepsis
Hepatic enzyme disorders

116
Q

Investigations for pathological jaundice

A

Measure of total and unconjugated bilirubin
FBC
U&Es
LFTs
Blood group (mother and baby)
Direct antiglobulin test
Urine culture
Thyroid function

117
Q

Causes of conjugated hyperbilirubinaemia

A

Sepsis
TPN
Biliary tract obstruction (e.g biliary atresia/choledochal cyst)
Viral hepatits
TORCH infections
Alpha-1 anti-trypsin deficiency
CF
Galactosaemia

118
Q

Investigations for conjugated hyperbilirubinaemia

A

As for unconjugated hyperbilirubinaemia
Radiology
Enzyme testing
Viral serology
Liver biopsy
Histology

119
Q

Mx of neonatal jaundice

A

Phototherapy - blue light converts bilirubin in skin and superficial capillaries into harmless, water-soluble metabolites which are excreted in urine and bowel
Eyes are covered to prevent discomfort and additional fluids are given to counteract increased fluid losses

Exchange transfusion - if bilirubin rises to levels considered dangerous despite phototherapy
Rapidly reduce level of circulating bilirubin
Done via umbilical artery and vein catheters
In immune mediated haemolysis give Ig is recommended as it may avoid need for exchange transfusion

120
Q

How much nutrition do neonates need?

A

115kcal/kg/day

121
Q

Why are infants and children vulnerable to undernutrition?

A

Low stores of fat and protein
Nutritional demands of growth
Brain growth
Acute illness or surgery - catecholamine secretion is increased, causing metabolic rate and energy requirement to increase nutritional demands
- post surgery catecholamines secretion is increased causing metabolic rate and energy requirement to increase

122
Q

Long term outcome of early nutritional deficiency

A

Linear growth of populations - closely related to mean height of populations
Diseases in adult life - increased incidence of CHD, stroke, non-insulin dependent diabetes and HTN

123
Q

Sudden infant death syndrome

A

Sudden and unexplained death of a child under age of 1, apparently occurring during sleep
Cause of death remains unexplained after through investigation including a complete autopsy and review of circumstances of death
All other possible causes of death must be excluded first

124
Q

Sudden and unexpected infant death (SUID)

A

Terms used to describe all infant deaths, regardless of cause
80% of SUID cases are due to SIDS
The rest have clear cause such as infection, inherited disorders

125
Q

What campaigns have reduced SIDS?

A

‘back to sleep’ and ‘reduce the risks’

126
Q

What is the triple risk model for SIDS?

A

3 factors occur simultaneously
1. Underlying vulnerability (LBW or prematurity)
2. Critical development period (usually 1-3m of age)
3.Exogenous stressor (e.g sleeping more)

127
Q

Risk factors for SIDS

A

Immature cardioresp control systems
failure to be roused from sleeo
Maternal RF: maternal smoking, alcohol and substance abuse, age <20 at first pregnancy, poverty or low SES, being single
Preterm birth
Late or no antenatal care
LBW
Placental abnormalaties
Sleep position - prone sleeping
Co-sleeping
Bedding

128
Q

Protective factors for SIDS

A

Breast feedings
Dummies?
Room sharing

129
Q

Guidance for parents

A

Can not be entirely prevented but risk can be reduced
Place baby to sleep in supine position
Allow baby to sleep in parental room
Avoid parental smoking

Block 41 (4 decks)

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