Neonatology Flashcards
1
Q
Where is surfactant produced and what is its purpose?
A
Fluid produced by type II pneumocytes, reduces surface tension.
Not produced until 24-34 weeks gestation.
Keeps alveoli inflated, maximises surface area so increases compliance, reducing force needed to expand alveoli.
2
Q
What are the cardio-respiratory changes at birth?
A
Adrenaline and cortisol released in response to birth, stimulating respiratory effort.
During first breaths - alveoli expand decreasing pulmonary vascular resistance.
This causes a fall in pressure in right atrium so left atrial pressure now greater and foramen ovale closes.
Increased blood oxygenation leads to drop in PGs so ductus arterioles shuts. Ductus venosus shuts because umbilical cord has been clamped.
3
Q
What can occur in extended hypoxia?
A
Hypoxia occurs as contraction place placenta under stress, unable to carry out normal gas exchange.
Leads to anaerobic respiration, and fatal bradycardia.
Reduced consciousness, drop in respiratory effort.
Hypoxic ischaemic encephalopathy, could lead to cerebral palsy.
4
Q
What are other key issues in neonatal resus?
A
Large surface area to weight ratio, so cold easily.
Born wet, so loose heat rapidly.
Born through meconium
5
Q
What are the principles of neonatal resuscitation?
A
Warm baby; vigorous drying, heat lamp, plastic bag
APGAR score
Stimulate breathing
Inflation breaths - two cycles of five breaths
Chest compression if HR remains under 60 - 3:1
IV drugs and intubation
Possible HIE - active cooling
6
Q
What is the APGAR score?
A
Appearance:
0 blue/pale, 1 bit blue, 2 pink
Pulse:
0 absent, 1 <100, 2 >100
Grimmace:
0 none, 1 little, 2 good
Activity:
0 floppy, 1 flexed, 2 active
Respiration:
0 absent, 1 slow/irregular, 2 strong/crying
7
Q
What is the purpose of delayed cord clamping?
A
Provides time for fetal blood still in the placenta to reach the circulation of the baby - placental transfusion.
Leads to improved Hb stores, iron stores, BP and reduction in intraventricular haemorrhage and NEC.
Only negative effect is increase risk of neonatal jaundice.
If requires resuscitation, priority will be with resuscitations than cord clamping.
8
Q
What care is provided immediately after birth?
A
Skin to skin Cord clamping Keeping baby dry and warm Vitamin K Label baby Measure weight and length
9
Q
What is the purpose of Vit K injections?
A
Babies have a deficiency of Vit K when born.
IM injection given into thigh, key in clotting, prevents bleeding; intracranial, umbilical stump, GI bleeding.
10
Q
What is the Guthrie test?
A
Blood spot screen heel prick
Screening card needs 4 separate drops, screens for 9 congenital conditions
Taken on day 5 (birth is 0)
Sickle cell Cystic fibrosis Congenital hypothyroidism Phenylketonuria Medium chain acyl CoA dehydrogenase deficiency Maple syrup urine disease Isovaleric acidaemia Glutaric aciduria type 1 Homocystin
Takes 6-8 weeks to come back
11
Q
When is the NIPE completed?
A
Within first 72 hours after birth, and then repeated at 6-8 weeks by GP.
12
Q
What are some important questions to ask before NIPE?
A
Has baby passed meconium
Baby feeding ok
FH of any congenital eye, heart or hip problems?
Pregnancy details, birth, breech presentation, abnormalities on antenatal scans
13
Q
How are pre ductal and post ductal saturations measured?
A
Before the ductus arterioles closes within 1-3 days of birth.
Pre-ductal before the duct taken from right hand - receives blood from right subclavian from brachiocephalic in aorta before ductus arteriosus, and post ductal in either foot from descending aorta
14
Q
What are we looking for on general appearance in the NIPE?
A
Colour - pink is good
Tone
Cry
15
Q
What are we looking for in the head in the NIPE?
A
General appearance - size, shape, caput succedaneum, cephalohaematoma, injury
Circumference - occipital frontal circumference OCP
Anterior and posterior fontanelles, overlapping sutures common
Ears - skin tags, low set, asymmetry
Eyes - slight squints normal, epicanthic folds ?Down’s, purulent discharge
Check red reflex
Absent with congenital cataracts and retinoblastoma
Mouth - cleft lip, tongue tie, check suckling reflex, check palate
16
Q
What are we looking for in the shoulders and arms in the NIPE?
A
Asymmetry - clavicle fracture
Movements - Erb’s palsy
Brachial and radial pulses
Palmar creases - single crease ?Down’s
Digits - number, straight or curved - clinodactyly
Sats probe on right wrist for pre ductal reading
17
Q
What are we looking for in the chest in the NIPE?
A
Oxygen saturations Observe breathing Stridor, work of breathing Heart sounds, murmurs, rate Breath sounds, air entry
Auscultate lungs, heart
18
Q
What are we looking for in the abdomen in the NIPE?
A
Observe shape
Concave - diaphragmatic hernia with abdominal contents in the chest
Umbilical stump - look for discharge, infection, hernia
Palpate for organomegaly, hernias, masses
Inspect and palpate
19
Q
What are we looking for in the genitals in the NIPE?
A
Observe for sex, ambiguity, abnormalities
Palpate testes and scrotum, check present, descended, hernias or hydroceles
Inspect penis for hypospadias, epispadias, urination
Inspect anus to check patent
Ask about meconium
Inspect labia check not fused
Inspect clitorus, check for any vaginal discharge
20
Q
What are we looking for in the legs in the NIPE?
A
Observe legs and hips for equal movements, skin creases, tone, talipes
Barlow’s and Ortolanis
Count the toes
21
Q
What are we looking for in the back in the NIPE?
A
Inspect and palpate spine
Look for curvature
Spina bifida
Pilonidal sinus
22
Q
What reflexes are tested in the NIPE?
A
Moro - when rapidly tipped back, arms and legs extend
Suckling - finger in mouth
Rooting - tickle cheek, turns towards the stimulus
Grasp - place finger in palm
Stepping - held upright, feet touch surface to make stepping motion
23
Q
What are some common skin findings in the NIPE?
A
Haemangiomas Port wine stains Mongolian blue spot Cradle cap Desquamation Erythema toxic Milia - tiny white cysts Acne Naevus simplex - stork bite Moles Transient pustular melanosis
24
Q
What is caput succedaneum?
A
Diffuse subcutaneous fluid collection, crosses suture lines
Caused by pressure on presenting part of head during delivery, resolves in first few days
25
What is a cephalhaematoma?
Subperiosteal haemorrhage
Bound by the periosteum so does not cross sutures
More common in instrumental delivery
May cause jaundice; monitor bilirubin
26
What is a subgaleal haemorrhage?
Occurs between aponeurosis of scalp and periosteum
Forms large fluctuant collection which crosses suture lines
Rare but life threatening blood loss
27
What is craniosynostonosis?
One or more of fibrous sutures prematurely fuses
Changes growth pattern of skull
Can result in raised intracranial pressure and damage to intracranial structures
Surgical intervention needed
28
What might a tense or sunken fontanelle indicate?
Tense bulging - raised ICP e.g. hydrocephalus
| Sunken - dehydration
29
What is a cystic hygroma?
Congenital lymphatic lesion
Typically in left posterior triangle of the neck
Are benign but need surgery
30
What is caput succedaneum?
Fluid collects on the scalp, outside the periosteum
Caused by pressure to particular area of scalp - during traumatic, prolonged or instrumental delivery.
Crosses suture lines
Resolves in few days
31
What is a cephalohaematoma?
Collection of blood between skull and periosteum due to traumatic delivery
Does not cross suture lines
Risk of anaemia and jaundice
32
What is Erb's palsy?
Injury to C5/C6 in brachial plexus
Associated with shoulder dystocia, traumatic or instrumental delivery, large birth weight.
Leads to weakness of shoulder abduction, external rotation, arm flexion, finger extension - waiters tip.
Function normally returns spontaneously within a few months.
33
Why might a fractured clavicle occur during birth and how does it present?
Shoulder dystocia, traumatic or instrumental delivery, large birth weight.
Noticable lack of arm movement
Asymmetry of movement in affected arm
Asymmetry of shoulders with affected shoulder lower than the normal shoulder
Pain and distress on movement of the arm
Conservative tx - immobilisation of the affected arm.
34
What common organisms can cause neonatal sepsis?
Group B strep - does not cause any problems for mother, but transferred in vagina - prophylactic antibiotics during labour
E Coli
Listeria
Klebsiella
Staph aureus
35
What are the risk factors for neonatal sepsis?
```
Vaginal GBS colonisation
GBS in previous baby
Maternal sepsis
Chorioamnionitis
Fever >38
Prematurity - less than 37 wks
Early PROM
Prolonged rupture of membranes
```
36
What are the clinical features of neonatal sepsis?
```
Non-specific
Fever
Reduced tone and activity
Poor feeding
Respiratory distress or apnoea
Vomiting
Tachycardia/bradycardia
Hypoxia
Jaundice within 24 hours
Seizures
Hypoglycaemia
```
37
What are the red flags for neonatal sepsis?
Confirmed or suspected sepsis in the mother
Signs of shock
Seizures
Term baby needing mechanical ventilation
Resp distress >4 hrs from birth
Presumed sepsis in another baby in a multiple pregnancy
38
What is the management of neonatal sepsis?
One risk factor or clinical features - monitor for 12 hrs
If two - start antibiotics
If red flag - start antibiotics
Start abx within 1 hr of decision
Blood cultures taken before abx, with baseline FBC, CRP
Perform LP if infection strongly suspected or features of meningitis
Benzylpenicillin or gentamicin
Check CRP at 24 hours
Blood cultures at 36 hours
If negative, consider stopping abx, check CRP at 5 days if still on treatment
Then consider stopping abx if clinically well, LP and BCs are negative at 5 days
39
What is it important to ask in a history to investigate neonatal sepsis?
Pregnancy:
Any concerns with growth, maternal illness, previous invasive infection
Labour and delivery:
duration of membrane rupture, fever during labour, GBS prophylaxis
Birth:
gestational age, weight, APGAR scores, any abnormalities on the NIPE
Since birth any feeding problems, passed urine and meconium, any interventions, any features of sepsis
40
What neurological features are indicative of neonatal sepsis?
Irritability, seizures, bulging fontanelle
| Consider meningitis
41
What are some of the differentials of neonatal sepsis?
```
Congenital infections: TORCH
Toxoplasmosis
Other - syphilis, varicella, HIV
Rubella
Cytomegalovirus
Herpes simplex virus
```
```
Respiratory distress syndrome
Transient tachypnoea of the newborn
Necrotising enterocolitis
Congenital pneumonia
Congenital heart disease
HDN
Metabolic diseases - galactosaemia
```
42
What specific antibiotics are required for specific symptoms in neonatal sepsis?
Flucloxacillin if late onset
Amoxicillin and cefotaxime IV if meningitis suspected
Metronidazole for NEC
Antifungal e.g. amphotericin B for fungal sepsis
Add aciclovir if HSV suspected
43
What are some of the complications of neonatal sepsis?
```
Poor cognitive development
Visual or hearing deficits
Cerebral palsy
Bronchopulmonary dysplasia
Death
```
44
What is the physiology behind jaundice?
RBCs broken down into bilirubin - unconjugated circulates bound to albumin, and some is free - can cross blood brain barrier.
UGT converts unconjugated to conjugated - cannot cross blood brain barrier, metabolised and excreted in urine and faeces.
45
What is the process of normal physiological jaundice?
Unconjugated bilirubin, presents on second or third day of life.
Due to shorter lifespan of neonatal RBCs, immature liver at birth, high concentration of beta glucuronidase which converts conjugated back to unconjugated.
46
Why are some neonates more prone to jaundice?
Preterm babies - higher bilirubin levels.
Breastfed babies - experience more marked and prolonged jaundice
Babies with significant bruising or cephalohaematoma - can occur following difficult deliveries
47
What are some pathological causes of unconjugated jaundice?
Haemolytic:
HDN, hereditary spherocytosis, G6PD def
Endocrine or metabolic causes:
Gilbert's syndrome - reduced ability to conjugate bilirubin due to reduced UGT activity
Crigler-Najjar syndrome - no UGT produce by liver, poor prognosis, severe jaundice
Congenital hypothyroidism
Galactosaemia and other inborn errors of metabolism
48
What are causes of pathological conjugated jaundice?
Biliary atresia
Neonatal hepatitis - due to CMV, hep B, rubella, HSV
Galactosaemia, or other inborn errors of metabolism
49
What is biliary atresia?
Congenital inflammatory disease of unknown cause
Leads to complete obliteration of the extra-hepatic bile ducts after birth
If not treated, can lead to liver cirrhosis and death
Presents with conjugated jaundice, pale stools, dark urine.
50
What is the management of biliary atresia?
Liver USS helpful
Percutaneous biopsy gold standard
Kasai procedure - treatment with portoenterostomy or liver transplantation
51
What are some of the risk factors for significant hyperbilirubinaemia requiring treatment?
Gestational age <38 weeks
Previous sibling with neonatal jaundice requiring phototherapy
Mother's intention to breastfeed exclusively
Visible jaundice in first 24 hours of life
52
What other important factors should be asked about in the history for neonatal jaundice?
Family history - inherited diseases, previous sibling
Pregnancy history - congenital infections, diabetes, maternal drugs e.g. sulphonamides
Labour and delivery history - birth trauma
Feeding history - breast-feeding, formula history, intake - poor intake, infrequent stooling increases enterohepatic circulation of bilirubin
53
What are signs of definite pathological jaundice?
Jaundice in the first 24 hours of life, and conjugated jaundice
54
What is seen on clinical examination in neonatal jaundice?
Naked, examined in bright light
Most obvious in sclerae and gums, skin can be pressed revealing jaundice in blanched skin
Look for signs of unwell
Inspect nappy for stools and urine - pale chalky stools, dark urine
55
What are the investigations for neonatal jaundice?
Transcutaneous bilirubinometry - bedside test evaluates light absorption through skin over forehead
Serum bilirubin - babies jaundiced within 24 hrs, gestational age <35, or monitoring bilirubin after starting treatment
56
What investigations are needed for babies who require treatment for jaundice?
Blood packed cell volume - assess degree of anaemia
Blood group of mother and baby - incompatibility, HDN
Direct antiglobulin test aka Coomb's - HDN, if negative hereditary spherocytosis
FBC and blood film
G6PD level
Blood, urine, CSF if any signs of infection
Liver ultrasound or percutaneous biopsy - biliary atresia
Genetic testing - Gilbert's or Crigler Najjar
Urinary reducing substances - galactosaemia
57
What is the management of neonatal jaundice?
Phototherapy - placed under blue green light, converts neurotoxic unconjugated bilirubin to isomer called lumirubin which can be excreted
Exchange transfusion - swap blood with donor blood
For high levels of bilirubin
58
What are the complications of neonatal jaundice?
Bilirubin encephalopathy - kernicterus
Unconjugated bilirubin can cross the blood-brain barrier, accumulates in nuclei, basal ganglia, hippocampus, cerebellum; is neurotoxic.
59
How does kernicterus present?
Lethargy
Hypotonia
Poor suck reflex
```
Then progresses to hypertonia
Opisthotonos - spasm of muscles causing back arching
Fever
Seizures
High pitched cry
```
Early damage can be reversible but if prolonged;
cerebral palsy
sensorineural hearing loss
cognitive impairment
60
What is HIE?
Hypoxic ischaemic encephalopathy
| Hypoxia during birth
61
When can HIE be suspected?
```
Perinatal or intrapartum hypoxia
Acidosis pH < 7 on umbilical artery blood gas
Poor APGAR scores
Features of mild, mod or severe HIE
Evidence of multi organ failure
```
62
What are the causes of HIE?
Anything that leads to asphyxia e.g.
maternal shock
intrapartum haemorrhage
prolapsed cord - causing compression during birth
nuchal cord - cord wrapped around neck of the baby
63
What is the Sarnat staging?
Staging for HIE grades
Mild - poor feeding, generally irritability, hyper alert, resolves within 24 hours, normal prognosis
Mod - poor feeding, lethargic, hypotonic, seizures, can take weeks to resolve, up to 40% develop cerebral palsy
Severe - reduced consciousness, apnoeas, flaccid, reduced or absent reflexes, 50% mortality
64
What is the management of HIE?
```
Supportive care
Acid base balance
Treatment of seizures
Optimal ventilation
Therapeutic hypothermia
```
65
What occurs in therapeutic hypothermia?
Actively cooling core temperature to 33-34
Continued for 72 hours, then warmed to normal over 6 hours
Reduces inflammation and neurone loss after injury
Reduces risk of cerebral palsy, developmental delay, learning disability, blindness, death
66
What is the definition of prematurity?
Extreme - under 28 weeks
Very preterm - 28-32 weeks
Mod-late - 32-37 weeks
67
What is associated with prematurity?
```
Social deprivation
Alcohol, smoking, drugs
Overweight or underweight mother
Maternal co-morbidities
Twins
Personal or FH of prematurity
```
68
What management can be given before birth for likely premature birth?
For a history of preterm birth or cervical length less than 25mm before 24 weeks:
Prophylactic vaginal progesterone to discourage labour
Prophylactic cervical cerclage
Tocolysis with nifedipine
Maternal corticosteroids
IV mag sulphate
Delayed cord clamping or cord milking
69
What is the pathophysiology of respiratory distress syndrome?
Inadequate surfactant leads to high surface tension
| Leads to atelectasis - lung collapse, inadequate gas exchange, results in hypoxia, hypercapnia and resp distress.
70
What is the management of respiratory distress syndrome?
Antenatal steroids e.g. dexamethasone given to mothers with suspected or confirmed preterm birth to increase surfactant.
Intubation, ventilation
Endotracheal surfactant - delivered via endotracheal tube
CPAP
Supplementary oxygen
71
What are the short term complications of RDS?
```
Pneumothorax
Infection
Apnoea
Intraventricular haemorrhage
Pulmonary haemorrhage
Necrotising haemorrhage
```
72
What are the long term complications of RDS?
Chronic lung disease of prematurity
Retinopathy of prematurity
Neurological, hearing and visual impairment
73
What is retinopathy of prematurity?
Affects preterm and LBW babies, typically before 32 weeks gestation.
Abnormal development of blood vessels in retina can lead to scarring, retinal detachment, blindness.
74
What is the pathophysiology of retinopathy of prematurity?
Retinal blood vessel development is from 16 weeks to 37-40 weeks.
Vessel formation stimulated by hypoxia, normal condition in the retina during pregnancy.
Pre-term babies exposed to higher oxygen conc, plus supplementary oxygen
When this is then removed - can continue growth but responds with neovascularisation and scar tissue.
Abnormal blood vessels regress, retina left without blood supply, may cause retinal detachment.
75
What screening is advised for ROP?
Babies born before 32 weeks or under 1.5kg should be screened by ophthalmologist:
30-31 weeks gestational age, in babies born before 27 weeks
4-5 weeks if born after 27 wks
Happens at least every 2 weeks, can cease once retinal vessels enter zone 3.
76
What is the treatment for ROP?
Target areas of retina to stop new blood vessels developing
Transpupillary laser photocoagulation to halt and reverse neorevascularisation
Cryotherapy
Injections of intraviteral VEGF inhibitors
Surgery for retinal detachment
77
What is apnoea of prematurity?
Apnoea common in premature neonates, decreases with increased gestational age
Breathing stops spontaneously for more than 20 seconds or shorter periods with oxygen desats and bradycardia
78
What is the cause of apnoea?
```
Due to immaturity of the ANS
Usually sign of developing illness e.g.
Infection
Anaemia
Airway obstruction
CNS pathology e.g. seizures or haemorrhage
GORD
Neonatal abstinence syndrome
```
79
What is the management of apnoea of prematurity?
Apnoea monitors
Tactile stimulation
Intravenous caffeine
80
What is NEC?
Necrotising enterocolitis
Part of the bowel becomes necrotic
Death of bowel tissue can lead to bowel perforation, peritonitis and shock
81
What are some of the risk factors for NEC?
```
Very low birth weight or very premature
Formula feeds - less common in babies fed by breast milk
RDS, assisted ventilation
Sepsis
Patient ductus arteriosus
Other congenital heart disease
```
82
What is the presentation of NEC?
```
Intolerance to feeds
Vomiting, green bile
Generally unwell
Distended tender abdomen
Absent bowel sounds
Blood in stool
```
If perforation, there will be signs of peritonitis and shock, baby will be severely unwell
83
What are the investigations for NEC?
```
FBC - thrombocytopenia, neutropenia
CRP - inflammation
Cap blood gas
Blood culture
Abdominal x-ray - supine
```
84
What are the x-ray findings in NEC?
Dilated loops of bowel
Bowel wall oedema - thickened bowel walls
Pneumatosis intestinalis - gas in bowel wall
Pneumoperitoneum - free gas in peritoneal cavity, indicates perforation
Gas in portal veins
85
What is the management of NEC?
```
NBM, IV fluids
Total parenteral nutrition
Antibiotics
NG tube to drain fluid and gas
Surgical emergency
```
86
What are the complications of NEC?
```
Perforation and peritonitis
Sepsis
Death
Strictures
Abscess formation
Recurrence
Long term stoma
Short bowel syndrome after surgery
```
87
What is neonatal abstinence syndrome?
Withdrawal symptoms that happens in neonates of mothers that used substances in pregnancy
88
What are substances that can cause neonatal abstinence syndrome?
```
Opiates
Methadone
Benzodiazepines
Cocaine
Amphetamines
Nicotine or cannabis
Alcohol
SSRI antidepressants
```
89
What are the signs and symptoms of neonatal abstinence syndrome?
```
CNS:
Irritability
Increased tone
Unsettled
High pitched cry
Tremors
Seizures
```
Vasomotor and resp:
Yawning, sweating
Unstable temp, pyrexia
Tachypnoea
Metabolic and GI:
Poor feeding, regurg
Hypoglycaemia
Loose stoles
90
What is the management of NAS?
NAS chart for at least 3 days/48 hrs for SSRIs
Urine sample to test for substances
Oral morphine sulphate for opiate withdrawal
Oral phenobarbitone for non-opiate withdrawal
Test for Hep B,C HIV
Safeguarding, safety net
Support
91
What is seen in metal alcohol syndrome?
```
Microcephaly
Thin upper lip
Smooth flat philtrum
Short palpebral fissure - short horizontal distance from one side to other
Learning disability
Behavioural difficulties
Hearing and vision problems
Cerebral palsy
```
92
What are the features of congenital rubella syndrome?
Due to maternal infection with rubella, highest risk in first 3 months
Congenital cataracts
Congenital heart disease - PDA and pulmonary stenosis
Learning disability
Hearing loss
93
What is seen in congenital varicella syndrome?
Can cause pneumonitis, hepatitis and encephalitis in the mother
Fetal varicella syndrome
Severe neonatal varicella infection if mum infected around delivery
If mum not immune requires IV varicella immunoglobulins with 10 days of exposure
Congenital varicella:
Fetal growth restriction
Microcephaly, hydrocephalus, learning disabilities
Scars, significant skin changes on dermatomes
Limb hypoplasia - underdeveloped
Cataracts and inflammation
94
What is seen in congenital CMV?
```
Fetal growth restriction
Microcephaly
Hearing loss
Vision loss
Learning disability
Seizures
```
95
What is the triad of congenital toxoplasmosis?
Intracranial calcification
Hydrocephalus
Chorioretinitis
96
What are the risk factors for SIDS?
Prematurity
Low birth weight
Smoking during pregnancy
Male baby
97
What can be done to minimise the risk of SIDS?
```
Put baby on back when not directly supervised
Keep head uncovered
Place feet at foot of bed
Keep cot clear of toys
Maintain comfortable room temp
Avoid smoking
Avoid handling baby after smoking
Avoid co-sleeping, avoid alcohol, drugs, smoking, sleeping tablets, deep sleepers
```
98
Why are preterm infants so vulnerable to hypothermia?
Large surface area relative to their mass
Greater heat loss than heat generation
Skin is thin and heat permeable, transepidermal water loss
Little sub cut fat for insulation
Often nursed naked, cannot conserve heat by curling up or generate by shivering
99
What are common problems in preterm infants following discharge?
Poor growth
Pneumonia, wheezing, asthma
Bronchiolitis from RSV - respiratory syncytial virus
Bronchopulmonary dysplasia
GORD
Complex nutritional and GI disorders following NEC or GI surgery
Inguinal hernias
100
What is the most likely cause of jaundice starting <24 hrs of age?
Haemolytic disorders - rhesus or ABO incompatibility, G6PD deficiency, spherocytosis
101
What are the causes of jaundice at 24 hrs - 2 weeks of age?
```
Physiological jaundice
Breast milk jaundice
Infection e.g. UTI
Haemolysis
Bruising
Polycythaemia
```
102
What are the causes of jaundice at >2 weeks?
Unconjugated - physiological, breast milk, infection, hypothyroid, haemolytic anaemia
Conjugated - >25umol/L
Bile duct obstruction, neonatal hepatitis
103
What is meconium aspiration?
Passed in preterm infants in response to fatal hypoxia
| Asphyxiated so start to gasp and aspirate meconium before delivery - results in obstruction and pneumonitis
104
What is seen in a CXR in an infant with respiratory distress syndrome?
Bilateral pneumothoraces
105
What is PPH?
Persistent pulmonary hypertension of the newborn
Associated with birth asphyxia, meconium aspiration, sepsis or RDS
High pulmonary vascular resistance - right to left shunt
Cyanosis
ECHO ensures does not have heart disease
Require mechanical ventilation
106
What are causes of neonatal seizures?
```
Hypoxic ischaemic encephalopathy
Cerebral infarction
Septicaemia
Metabolic - hypo/hyper
Intracranial haemorrhage
Cerebral malformations
Drug withdrawal
Congenital infection
Kernicterus
```
107
What is the cause of cleft lip?
Failure of fusion of the frontonasal and maxillary processes
108
What is the cause of cleft palate?
Failure of fusion of the palatine processes and the nasal septum
109
What is oesophageal atresia?
Usually associated with tracheo-oesophageal fistula
Associated with polyhydramnios
If suspected, insert feeding tube and check with x-ray
110
What can be the causes of small bowel obstruction?
```
Atresia or stenosis of duodenum, seen in Down's
Atresia or stenosis of jejunum or ileum
Malrotation with volvulus
Meconium ileus
Meconium plug
```
111
What are the causes of large bowel obstruction?
Hirschsprung disease - absence of myenteric plexus - will not pass meconium within 48 hrs of birth
Rectal atresia
Bile stained vomiting is from intestinal obstruction until proved otherwise
112
What is exomphalos?
Abdominal contents protrude through the umbilical ring, with a transparent sac formed by amniotic membrane and peritoneum
113
What is gastroschisis?
Bowel protrudes through defect in anterior abdominal wall
Adjacent to umbilicus
No covering sac
Greater risk of dehydration and protein loss
114
What is the management of a sudden unexpected death of an infant?
Initiate resuscitation unless inappropriate
Care of parents
Baby pronounced dead - detailed clinical exam, aspiration, blood toxicology, chromosomes if dysmorphic, blood culture, LP, urine
Break bad news, parents offered to see and hold baby
Home visit within 24 hours
Post mortem
115
What is the management of cleft lip and cleft palate?
Cleft lip repaired earlier than cleft palate
From first week of life to 3 months
Cleft palate usually between 6-12 months of age
