neonatology Flashcards

1
Q

what is the purpose of a screenign porgram

A

good treatment

reasonable test for it

acceptable test

cost effective

can be detected early

common conditions

sensitive/specific

wilsons criteria

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2
Q

screening tests in pregnancy

A

blood tests

scans - dating 12 weeks, normal scan 20 weeks - 11 conditions can be identified

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3
Q

screening for trisomies

A

first trimester - combined - serum HCG and PAPP-A
combined with nuchal translucency
crown rump length

second trimester - qaurdruple test - oestradiol, HCG, AFP, inhibin A

higher than 1 in 150 is HIGH RISK

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4
Q

chorionic villous sampling v amniocentesis

A

done earlier

amniocentesis - risk of infection, miscarriage

FISH for chromosome

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5
Q

20 week scan what conditions

A
anencephaly
open spina bifida
cleft lip
diaphragmatic hernia
gastroschisis
exomphalos
serious cardiac abnormalities
bilateral renal agenesis
lethal skeletal dysplasia
Edwards' syndrome, or T18
Patau's syndrome, or T13
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6
Q

bilateral renal genesis

A

oligohydraminos

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7
Q

NIPE

A

newboen infant physical examination

hips
heart
eyes
testes

feel femoral -> coarction

midwife does it
NIPE smart portal

KPIs key performance indicators - are we delivering what we are supposed to

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8
Q

why we look at eyes in nIP

A

congenital cataracts

retinoblastoma prognosis POOR
immediate nucleation of eye with adverse chemo

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9
Q

tests for hips called

A

Barlow test
Ortolani test

clicks - US
FH and first degree relative - dislocated hip in newborn

pavlik harness

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10
Q

heart NIPE

A

murmurs and pulse

transposition

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11
Q

newborn blood spot

A

day 5

TFTs as thyroxine spikes on birth

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12
Q

newborn blood spot

A

day 5
TFTs as thyroxine spikes on birth

who might miss it
if their on neonatal units
families moving around a lot

metabolic disorders
Phenylketonuria - brain dev, MCADD, maple syrup, IVA, glutaric aciduria, homocystinuria
congenital hypothyroisism
CF - RIP

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13
Q

hearing tests

A

everyone gets it

otoacoustic emissions
AEBR

Ix if positive
cochlear implant

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14
Q

causes of preterm delivery

A
idiopathic
intauterine stretch
- multiples gestation
- polyhydraminos
- uterine abnormality
endocrine maturation
- premature onset of labour
intrauterine bleeding
- abruption
- antepartum haemorrhage
intrauterine infection
- chorioamnioitis
- bacterial vaginosis
- preterm PROM
fetus
- IUGR
- congenital malformations
maternal medical conditins
- pre-eclampsia, HTN
chronic medical conditions
UTIs
cervical weakness
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15
Q

RFs or preterm delivery

A
  • previous preterm infant, - a short inter-pregnancy interval (<6 months)
  • maternal age (<20 or >35 years)
  • obesity
  • ethnicity (e.g. higher in Black mothers)
  • multiple births
  • maternal infection
  • smoking
  • substance misuse
  • maternal psychological/social stress
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16
Q

define prematurity

classification

A

birth before 37 weeks

Under 28 weeks: extreme preterm
28 – 32 weeks: very preterm
32 – 37 weeks: moderate to late preterm

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17
Q

Management to hold baby in for longer

A
  • > Prophylactic vaginal progesterone: putting a progesterone suppository in the vagina to discourage labour
  • > Prophylactic cervical cerclage: putting a suture in the cervix to hold it closed
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18
Q

what can be done with preterm delivery to improve outcomes

A
  • Tocolysis with nifedipine: nifedipine is a calcium channel blocker that suppresses labour
  • Maternal corticosteroids: can be offered before 35 weeks gestation to reduce neonatal morbidity and mortality
  • IV Magnesium sulphate: can be offered before 34 weeks gestation and helps protect the baby’s brain
  • Delayed cord clamping or cord milking: can increase the circulating blood volume and haemoglobin in the baby
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19
Q

premauture babies problems in early life

A
Respiratory distress syndrome
Hypothermia
Hypoglycaemia
Poor feeding
Apnoea and bradycardia
Neonatal jaundice
Intraventricular haemorrhage IVH - small grade 1 upto 4 which are large - damage into brain tissue
white matter damage periventricular leuko-malacia
Retinopathy of prematurity
Necrotising enterocolitis
Immature immune system and infection
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20
Q

long term effects of premature babies

A

Chronic lung disease of prematurity (CLDP)
Learning and behavioural difficulties
Susceptibility to infections, particularly respiratory tract infections
Hearing and visual impairment
Cerebral palsy

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21
Q

examination of premature baby

A

dubowitz/balllard examination estimate neonatal maturity

external physical and neuromuscular features to determine a score. This is then used to give an estimate of a 2 week window of gestation.

Physical features assessed include skin, lanugo (thin, soft hairs), and eye, ear and genital formation.

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22
Q

Ix for premature babies

A
blood gas - metabolic state
FBC - high risk of infection/anaemia
U&Es
blood culture
CRP
direct coombs test.direct antiglobuline test

chest xray if resp distressed
abdo xray - risk of necrotising enteroclitis

cranial US scan <32 weeks as they are at high risk of ntraventricular haemorrhage or ischaemic periventricular white matter damage

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23
Q

why do we administer steroids in premature babies

A

reduce the risk of death, intraventricular haemorrhage, respiratory distress

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24
Q

guidelines to start resuscitation

A

Less than 23 weeks then resuscitation should not be performed

Between 23 and 23+6 weeks then there may be a decision not to start resuscitation in the best interests of the baby, especially if parents have expressed this wish.

Between 24 and 24+6 weeks, resuscitation should be commenced unless the baby is thought to be severely compromised. Response to initial measures should be considered before the decision is made to commence intensive care.

After 25 weeks, it is appropriate to resuscitate and start intensive care.

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25
Q

what is physiological jaundice

A

mild yellowing of skin and sclera from 2 – 7 days of age. This usually resolves completely by 10 days

increased destruction of RBCs as the foetal HB is broken down. THis releases bilirubin into the blood and the immature liver is unable to conjugate and excrete it rapidly enough

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26
Q

causes of neonatal jaundice

A

increased production of bilirubin

Haemolytic disease of the newborn
rhesus and ABO incompatibility
Haemorrhage
Intraventricular haemorrhage
Cephalo-haematoma
Polycythaemia
Sepsis and disseminated intravascular coagulation
G6PD deficiency
decreased clearance of bilirubin
Prematurity
Breast milk jaundice
Neonatal cholestasis
Extrahepatic biliary atresia
hypothyroid and hypopituitary
Gilbert syndrome
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27
Q

what is breast milk jaundice

A

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

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28
Q

haemolytic disease of the newborn

A

cause of haemolysis (red blood cells breaking down) and jaundice in the neonate. It is caused by incompatibility between the rhesus antigens on the surface of the red blood cells of the mother and fetus.

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29
Q

what is sensitisation to rhesus D

A

When a woman that is rhesus D negative (does not have the rhesus D antigen) becomes pregnant, we have to consider the possibility that her child will be rhesus D positive (has the rhesus D antigen). It is likely at some point in the pregnancy the blood from the baby will find a way into her bloodstream. When this happens, the baby’s red blood cells display the rhesus D antigen. The mother’s immune system will recognise this rhesus D antigen as foreign and produce antibodies to the rhesus D antigen. The mother has then become sensitised to rhesus D antigens.

If that fetus is rhesus positive, these antibodies attach themselves to the red blood cells of the fetus and causes the immune system of the fetus to attack their own red blood cells. This leads to haemolysis, causing anaemia and high bilirubin levels. This leads to a condition called haemolytic disease of the newborn.

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30
Q

what is prolonged jaundice

A

More than 14 days in full term babies
More than 21 days in premature babies

Structural – Biliary atresia / choledochal cyst / Alagille’s syndrome
Infective – CMV / EBV / Hep-B / Bacterial / Toxoplasmosis
Metabolic – Galactosaemia / Alpha-1-antitrypsin deficiency / Storage disease
Genetic – CF / Trisomy 21 / Trisomy 18
Neoplastic – Hepatoblastoma / Neuroblastoma
Toxic – Drug induced
Endocrine – Hypothyroidism / Panhypopituitarism
Vascular – Budd-Chiari / Congestive heart failure

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31
Q

Ix for jaundice in neonates

A
  • FBC +Blood film for polycythaemia or anaemia
  • Total serum bilirubin/LFTs
  • Blood type testing of mother and baby for ABO or rhesus incompatibility
  • coagulation study - deranged indicates poor liver function
  • Paternal blood group and rhesus status
  • Peripheral blood smear - misshapen blood cells could indicate RBC disorder
  • Reticulocyte count - for presence of haemolysis
  • Direct Coombs Test (direct antiglobulin test) for haemolysis
  • Thyroid function, particularly for hypothyroid
  • Blood and urine cultures if infection is suspected.
  • G6PD levels ->deficiency
  • Galactosaemia screen
  • TORCH fro infection
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32
Q

Mx of jaundiced neonates

A

observe for 24 hours

total bilirubin levels are monitored and plotted on treatment threshold charts. These charts are specific for the gestational age of the baby at birth. The age of the baby is plotted on the x-axis and the total bilirubin level on the y-axis. If the total bilirubin reaches the threshold on the chart, they need to be commenced on treatment to lower their bilirubin level.

  • > Phototherapy is usually adequate to correct neonatal jaundice. Extremely high levels may require an exchange
  • > transfusion. Exchange transfusions involve removing blood from the neonate and replacing it with donor blood.
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33
Q

how does phototherapy work

A

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

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

considerations

  • distance of light of baby
  • eye protection
  • remove clothes off baby except nappy
  • temperature
  • bilirubin levels
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34
Q

what is kernicterus

A

type of brain damage caused by excessive bilirubin levels. It is the main reason we treat neonatal jaundice to keep bilirubin levels below certain thresholds.

Bilirubin can cross the blood-brain barrier. Excessive bilirubin causes direct damage to the central nervous system. Kernicterus presents with a less responsive, floppy, drowsy baby with poor feeding. The damage to the nervous system is permeant, causing cerebral palsy, learning disability and deafness

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35
Q

what is hypoxic ischaemic encepholapthy

when to suspect it

A

hypoxia during birth.

hypoxia during the perinatal or intrapartum period, acidosis (pH < 7) on the umbilical artery blood gas, poor Apgar scores, features of mild, moderate or severe HIE (see below) or evidence of multi organ failure.

36
Q

causes of HIE

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord, causing compression of the cord during birth
  • Nuchal cord, where the cord is wrapped around the neck of the baby
37
Q

staging in HIE

A

sarnat staging

Mild

Poor feeding, generally irritability and hyper-alert
Resolves within 24 hours
Normal prognosis

Moderate
Poor feeding, lethargic, hypotonic and seizures
Can take weeks to resolve
Up to 40% develop cerebral palsy

Severe
Reduced consciousness, apnoeas, flaccid and reduced or absent reflexes
Up to 50% mortality
Up to 90% develop cerebral palsy

38
Q

Mx of HIE

A

oordinated by specialists in neonatology, on the neonatal unit. This involves supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures. Therapeutic hypothermia is an option in certain circumstances to help protect the brain from hypoxic injury.

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

39
Q

what is therapeutic hypothermia

A

involves actively cooling the core temperature of the baby according to a strict protocol. The baby is transferred to neonatal ICU and actively cooled using cooling blankets and a cooling hat. The temperature is carefully monitored with a target of between 33 and 34°C, measured using a rectal probe. This is continued for 72 hours, after which the baby is gradually warmed to a normal temperature over 6 hours.

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

40
Q

qs parents ask

A

development milestones
extension of
independent as adults or not

41
Q

viability of baby

A

24 weeks

42
Q

cerebral palsy deine

A

long term neuro underdevelopment

lower gestation = greater risk of cerebal palsy

43
Q

respiratory neonatal long term outcomes

A

rehospitalisation rate increased
CLD or BPD may require home oxygen - chronic lung disease at 36 weeks gestation if u need oxygen til 36 weeks
- wheezing more common with CLD
- FORD
- GI disorders esp necrotising enterocolitis

increased risk of COPD at later stages

44
Q

what affects risks of development issues

A

all children at less than 30 weeks at 2 years

45
Q

downs syndrome causes

A

robertsonian translocation

abnormal division

46
Q

features of downs

A

Palpebral fissure (up slanting), Round face
Occipital + nasal flattening, Brushfield spots (pigmented spots on iris)/Brachycephaly
Low-set small ears
Epicanthic folds
Mouth open + protruding tongue
Strabismus (squint)/Sandal gap deformity/Single palmar (Simian) crease

47
Q

hearing tests

A

automated otoacoustic emission

automate auditory brainstem response

48
Q

hearing tests

A

first 4-5 weeks of life

automated otoacoustic emission
abnormal reasons
your baby was unsettled when the test was done
there was background noise
your baby has fluid or a temporary blockage in their ear

abnormal
automate auditory brainstem response

abnormal
hearing specialist

49
Q

causes of hearing loss

A

glue ear – a build-up of fluid in the middle ear, which is common in young children
infections that develop in the womb or at birth, such as rubella or cytomegalovirus, which can cause progressive hearing loss
inherited conditions, such as otosclerosis, which stop the ears or nerves from working properly
damage to the cochlear or auditory nerves (which transmit hearing signals to the brain); this could be caused by a severe head injury, exposure to loud noise or head surgery, for example
being starved of oxygen at birth (birth asphyxia)
illnesses such as meningitis and encephalitis (which both involve swelling in the brain)

50
Q

turners

A
web neck
short stature
wide spaced nipples
underdeveloped ovaries -> amenorrhoea
infertility
bicuspid valve
coarction of aorta
acute otitis media

monosomy - one normal sex chromosome

51
Q

problems with breastfeeding

A
mastitis
ductal candida
cracked 
breast engorgement
baby not latching
52
Q

problems with breastfeeding

A
mastitis
ductal candida
cracked nipples
breast engorgement
baby not latching
blocked duct
attachment issues
53
Q

infant feeding problems

A

colic
GORD
Gastroenteritis
lactose intolerance

54
Q

RFs of phototherapy

A
minimise the separation of mum and baby
loose stools
dehydration 
retinal damage
bronze baby syndrome
55
Q

when do we not use phototherapy

A

conjugated bilirubin as it does not lead to kernicterus

56
Q

kernicterus clinical features

A

accumulates in CNS grey matter
irreversible neurological damage - bilirubin neurotoxic

early signs
- severe jaundice
hypotonia
poor sucking and feeding
- absent startle reflex
- high pitched cry
- bulging fontanelles
neurological features
sensory hearing loss
intellectual disability
speech difficulties
seizures
movement disorder
muscle rigidity
57
Q

Sudden infant death syndrome

A
cosleeping
low birth weight
smoking
tangles
breathing obstruction
58
Q

What can I do to help prevent SIDS?

A

always place your baby on their back to sleep
place your baby in the “feet to foot” position – with their feet touching the end of the cot, Moses basket, or pram
keep your baby’s head uncovered – their blanket should be tucked in no higher than their shoulders
let your baby sleep in a cot or Moses basket in the same room as you for the first 6 months
use a mattress that’s firm, flat, waterproof and in good condition
breastfeed your baby,

59
Q

neonatal hypoglycaemia define

A

<2.6mmol/L
it is common within the first 24 hours

<1 VERY LOW so administer IV 10% dextrose infusion

60
Q

persistent/severe hypoglycaemia caused by

A
preterm birth (< 37 weeks)
maternal diabetes mellitus
IUGR
hypothermia
neonatal sepsis
inborn errors of metabolism
nesidioblastosis
Beckwith-Wiedemann syndrome
61
Q

features of neonatal hypoglycaemia

A
may be asymptomatic
autonomic (hypoglycaemia → changes in neural sympathetic discharge)
- 'jitteriness'
- irritable
- tachypnoea
- pallor
neuroglycopenic
- poor - feeding/sucking
- weak cry
- drowsy
- hypotonia
- seizures
other features may include
- apnoea
- hypothermia
62
Q

Mx of neonatal hypoglycaemia

A
asymptomatic
encourage normal feeding (breast or bottle)
monitor blood glucose
symptomatic or very low blood glucose
admit to the neonatal unit
intravenous infusion of 10% dextrose
63
Q

neonatal resuscitation

A

Birth: Dry the baby, remove any wet towels and cover and start the clock or note the time.
Within 30 seconds: Assess tone, breathing and heart rate.
Within 60 seconds: If gasping or not breathing - open the airway and give 5 inflation breaths
Re-assess: If no increase in heart rate look for chest movement
If chest not moving: Recheck head position, consider 2-person airway control and other airway manoeuvres, repeat inflation breaths and look for a response.
If no increase in heart rate look for chest movement
When the chest is moving: If heart rate is not detectable or slow (< 60 min-1) - start chest compressions with 3 compressions to each breath.
Reassess heart rate every 30 seconds. If heart rate is not detectable or slow (<60 beats per minute) consider venous access and drugs

64
Q

NEC is ass with

A

Perinatal asphyxia.
Polycythaemia.
Respiratory distress.
Congenital anomalies (myelomeningocele, congenital heart disease).
Cow’s milk protein-induced enterocolitis and glucose-6-phosphate dehydrogenase deficiency have been mooted as possible pathophysiological mechanisms.

65
Q

history and examination of NEC

A

first two weeks of life

  • Abdominal distension with increasing gastric aspirates.
  • Visible intestinal loops.
  • Altered stool pattern.
    Bloody mucoid stool and bilious vomiting.
  • Decreased bowel sounds with erythema of the abdomen.
    Palpable abdominal mass or ascites.
    Associated features are bradycardia, lethargy, shock, apnoea, respiratory distress, temperature instability.
66
Q

RFS of NEC

A

prematuring low birth weight

67
Q

DD of NEC

A
Sepsis.
Haemolytic disease of the newborn.
Swallowed maternal blood.
Volvulus/malrotation.
Intussusception.
Pseudomembranous colitis.
Stress ulcer.

abdominal xray
dilated bowel loops
bowel oedema
poneumoatosis intestinalis - intramural gas
portal venous gas
rigler’s sign air inside and outside of bowel
football signs - outline falciform ligaments
pneumoperitoneum perforation

68
Q

Mx of NEC

A

Nil by mouth to rest the bowel.
Nasogastric or orogastric tube to decompress the bowel with low intermittent orogastric suction.
Intravenous (IV) fluids, total parenteral nutrition (TPN) and IV antibiotics for 10-14 days:
Ampicillin/gentamicin or cefotaxime.
Plus metronidazole or clindamycin.

perforation - laparotomy

69
Q

complications of NEC

A
Perforation.
Acquired short bowel syndrome (following surgery).
Stoma-related complications.[18]
DIC.
Sepsis and shock.
Intestinal strictures (~30%).
Enterocolic fistulae.
Abscess formation.
Recurrent NEC (rare)
70
Q

TOF onset daignosis is 12 days worse during feeding

A

TOF in mum can cause polyhydraminos

71
Q

Sx TOF

A
Frothy, white bubbles in the mouth
Coughing or choking when feeding
Vomiting
Blue color of the skin (cyanosis), especially when the baby is feeding
Difficulty breathing
Very round, full abdomen
72
Q

Sx TOF

A
Frothy, white bubbles in the mouth
Coughing or choking when feeding
Vomiting
Blue color of the skin (cyanosis), especially when the baby is feeding
Difficulty breathing
Very round, full abdomen
73
Q

Ix of TOF

A

NG tube curls up on xray
air
Demonstration of the nasogastric tube curled in the proximal oesophagus in a child where the passage of the tube has been unsuccessful is usually sufficient for diagnosis. The proximal oesophageal stump may be distended with air (types A and C ).
The presence of air in the stomach and bowel in the setting of oesophageal atresia implies that there is a distal fistula.
Often the lungs demonstrate areas of consolidation/atelectasis due to recurrent aspiration.

74
Q

Mx

A
ripogle drain out oesophagus
anti
laparoscopic
thoracotomy
ICU
discharge once feeding and gaining weight
75
Q

what is neonatal sepsis

causes

RFs

A

affects within 28 days of life
EOS - <72 hrs of birth
LOS between 7-28 days of life

causes
group b strep
Ecoli

LOS - coagulase-negative staphylococcal species such as Staphylococcus epidermidis, Gram-negative bacteria such as Pseudomonas aeruginosa, Klebsiella and Enterobacter, and fungal species

Staphylococcus aureus
Enterococcus
Listeria monocytogenes
Viruses including herpes simplex and enterovirus

  • Mother who has had a previous baby with GBS infection, who has current GBS colonisation from prenatal screening, current bacteruria, intrapartum temperature ≥38ºC, membrane rupture ≥18 hours, or current infection throughout pregnancy
  • Premature (<37 weeks): approximately 85% of neonatal sepsis cases are in premature neonates
  • Low birth weight (<2.5kg)
  • Evidence of maternal chorioamnionitis
76
Q

CFs of neonatal sepsis

A
1. Respiratory distress (85%)
Grunting
Nasal flaring
Use of accessory respiratory muscles
Tachypnoea
  1. Tachycardia
  2. Apnoea
  3. Apparent change in mental status/lethargy
  4. Jaundice
  5. Seizures: if cause of sepsis is meningitis
  6. Poor/reduced feeding
  7. Abdominal distention
  8. Vomiting
  9. Temperature
77
Q

Ix of neonatal sepsis

A

blood culture - 2 if possible

  • FBC - abnormal neutrophils
  • CRP
  • Blood gases - metabolci acidosis
  • urine microscopy culture and sensitivity - raised leukocytes, positive culture, haematuria, proteinuria
  • LP -> MAYBE

Mx
<1m gentamicin + amoxicillin + cefotaxime
1-3m amoxicillin + ceftriaxone
3m ceftriaxone

  • CRP should be re measure 18-24hrs after presentation
  • antibiotics can be ceased at 48 hours in neonates who have CRP of <10 mg/L and a negative blood culture at presentation and at 48 hours

Other important management factors to consider include:

  • Maintaining adequate oxygenation status
  • Maintaining normal fluid and electrolyte status: severely ill neonates may require volume and/or vasopressor support. Body weight needs to be measured daily for accurate assessment of fluid status
  • Prevention and/or management of hypoglycaemia
  • Prevention and/or management of metabolic acidosis
78
Q

what is haemorrhagic disease of the newborn

A

deficient in vit k

Vit K orally or IM

RFs

  • breast milk
  • maternal use of antiepileptics
79
Q

NRDS

A

Other risk factors for SDLD include

  • male sex
  • diabetic mothers
  • Caesarean section
  • second born of premature twins

tachypnoea, intercostal recession, expiratory grunting and cyanosis

ground-glass’ appearance with an indistinct heart border

Management
1. prevention during pregnancy: maternal corticosteroids to induce fetal lung maturation
2. CPAP
oxygen
assisted ventilation
exogenous surfactant given via endotracheal tube

80
Q

what is TTN

A

commonest cause of respiratory distress in the newborn period. It is caused by delayed resorption of fluid in the lungs

Csection

Ix Chest x-ray may show hyperinflation of the lungs and fluid in the horizontal fissure

Supplementary oxygen may be required to maintain oxygen saturations. Transient tachypnoea of the newborn usually settles within 1-2 days

81
Q

congenital cystic adenomatoid malformation of the lung

A

A rare
benign lung lesion made up of abnormal lung tissue arising from an error in lung
development that does not function properly but continues to grow. Also called
congenital pulmonary airway malformation. CCAMs develop antenatally and would
usually thus be visible on antenatal scans. They vary in size and are either solid or cystic

82
Q

O/E of a jaundice baby

A

General: is the child alert? A high pitched cry could indicate he is unwell. Any rashes?

Face: any signs of dysmorphia?

Head: size may be affected by congenital infections. Trauma such as cephalohaematoma can lead to jaundice

Abdominal: hepatomegaly? Splenomegaly?

83
Q

RFs of jaundice

A
American-Indian descent 
Maternal diabetes
Decreased gestational age
Family history of neonatal jaundice
Breastfeeding
84
Q

when do we not do transcutaneous bilirubinometer

A

early onset jaundice <24 hours
gestational age <35 weeks
if encephalopathy is suspected

85
Q

biliary atresia

A

idiopathic destructive inflammatory process. The fibrotic remains can be seen at the porta hepatis.

Mx
kapasi portoenterostomy