4 - Neonatology Flashcards

1
Q

What are some cardiorespiratory changes that happen at birth?

A
  • During birth thorax is squeezed to clear fluid from the lungs. Birth, temperature change, sound and physical touch stimulate the baby to promote the first breath. A strong first breath is required to expand the previously collapsed alveoli for the first time. Adrenaline and cortisol are released to the stress of labour, stimulating respiratory effort
  • The first breaths baby takes expands alveoli, decreases pulmonary vascular resistance so fall in pressure in the right atrium. At this point the left atrial pressure is greater than the right atrial pressure, which closes foramen ovale so becomes foramen ovalis
  • Increased blood oxygenation causes a drop in circulating prostaglandins. This causes closure of the ductus arteriosus, which becomes the ligamentum arteriosum.
  • Ductus venosus stops functioning because umbilical cord is clamped and no blood flow in the umbilical veins. Closes a few days later and becomes ligamentum venosum
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2
Q

When is surfactant produced in the fetal life?

A

Between 24 and 34 weeks the type II pneumocytes start to produce surfactant

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3
Q

What is the protocol for neonatal resuscitation?

A
  1. Birth
  2. Dry and warm baby trying to stimulate breathing
  3. APGAR at 1,5 and 10 minutes
  4. If gasping or not breathing: open airway, 5 inflation breaths, give oxygen and ECG monitoring
  5. Reassess heart rate and chest movements
  6. If chest not moving optimise airway control, repeat 5 inflation breaths
  7. If no increase in heart rate at this point, re-assess for chest movement and repeat above steps if necessary
  8. If chest is moving and heart rate <60 bpm, ventilate for 30 seconds
  9. If heart rate still <60 bpm, commence chest compressions at a rate of 3:1
  10. Reassess every 30 seconds if heart rate remains <60 bpm, consider venous or osseous access and administering drugs
  11. Throughout process keep the parents updated, and keep a record
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4
Q

How can we try to stimulate baby to breathe after birth?

A
  • Dry vigorously with towel
  • Place baby’s head in neutral position
  • Check for meconium in airway and aspirate
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5
Q

What gas should you use for inflation breaths during neonatal resuscitation?

Image is important

A

For term or near term use air

For pre-term use air and oxygen

Aim for gradual rise in sats, not exceeding 95%

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6
Q

If a neonate has suspected HIE after resuscitation what can be given to them?

A

Therapeutic hypothermia

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7
Q

What are some issues to recognise in neonatal resuscitation?

A
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8
Q

What is part of the APGAR score?

A

Measure at 1,5,10 minutes giving score out of 10

  • A score of >7 is reassuring
  • A score of 4-6 requires stimulation
  • A score of <4 requires resuscitation
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9
Q

What are the benefits of delayed cord clamping and when is this done?

A

In uncompromised neonates this is done for one minute

  • Improved Hb and iron stores
  • Improved blood pressure
  • Reduction in intraventricular haemorraghe and NEC
  • Only negative is risk of neonatal jaundice so need more phototherapy
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10
Q

What care is done for the baby after birth?

A
  • Skin to skin
  • Clamp the umbilical cord
  • Dry the baby
  • Keep the baby warm with a hat and blankets
  • Vitamin K IM
  • Label the baby, measure the weight and length
  • Initiate breast feeding or bottle feeding as soon as the baby is alert
  • Newborn examination within 72 hours
  • Blood spot test
  • Newborn hearing test
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11
Q

Why are newborns given Vitamin K?

A
  • Babies have a deficiency and need it for clotting
  • Helps to prevent bleeding, particularly intracranial, umbilical stump and GI
  • Usually given IM in thigh, helps them to cry too
  • Can give oral but need 3 doses
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12
Q

What is the blood spot screening and when is it done?

A

Taken on day 5 (to day 8)

Need four drops of blood from heel to test for 9 conditions

Results take 6-8 weeks

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13
Q

What screening tests are done for newborns?

A
  • Blood spot
  • Hearing
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14
Q

What is the difference between Caput Succedaneum and Cephalohaematoma?

A

Caput Succedaneum

Fluid collecting on the scalp, outside the periosteum.

Caused by pressure to specific area of scalp during a traumatic, prolonged or instrumental delivery

Able to cross suture lines

Does not require any treatment and will resolve within a few days

Cephalohaematoma

Collection of blood between the skull and the periosteum, same cause as above

The blood is below the periosteum, therefore the lump does not cross the suture lines of the skull

Blood can discolour skin

Reesolves without treatment within a few months. There is a risk of anaemia and jaundice due to the blood that collects within the haematoma and breaks down, releasing bilirubin

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15
Q

What are some risk factors for early onset neonatal sepsis and what are common organisms causing this?

(Early onset up to 72 hours, Late onset after 72 hours)

A

Can come from chorioamnionitis, birth canal or external environment

Risk Factors

  • Vaginal GBS colonisation
  • GBS sepsis in a previous baby
  • Maternal sepsis, chorioamnionitis or fever > 38ºC
  • Prematurity (less than 37 weeks)
  • Premature rupture of membrane
  • Prolonged rupture of membranes (PROM)

Common Organisms

  • Group B streptococcus (GBS)
  • Escherichia coli (e. coli)
  • Listeria
  • Klebsiella
  • Staphylococcus aureus
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16
Q

How is GBS prevented from causing neonatal sepsis?

A

Give intrapartum IV benzylpenicillin

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17
Q

How may neonatal sepsis present? (inc red flags)

A
  • Fever
  • Reduced tone and activity
  • Poor feeding
  • Respiratory distress or apnoea
  • Vomiting
  • Tachycardia or bradycardia
  • Hypoxia
  • Jaundice within 24 hours
  • Seizures
  • Hypoglycaemia
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18
Q

When should you start treatment for suspected neonatal sepsis?

A
  • If there is one risk factor or clinical feature, monitor observations and clinical condition for at least 12 hours
  • If there are two or more risk factors or clinical feature of neonatal sepsis start antibiotics
  • Antibiotics should be started if there is a single red flag
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19
Q

What is the initial management of neonatal sepsis?

A
  • Take baseline FBC and CRP
  • Blood cultures before antibiotics
  • Antibiotics given within 1 hour
  • Lumbar puncture if infection strongly suspected or features of meningitis (e.g. seizures)
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20
Q

What antibiotics are used for neonatal sepsis?

A

Early Onset

  • IV Benzylpenicillin and IV Gentamicin
  • If Gram -ve add in Cefotaxime IV and remove the Benzylpenicillin

Late Onset

  • IV Flucloxacillin and IV Gentamicin

Meningitis

  • IV Amoxicillin and IV Cefotaxime
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21
Q

What is the ongoing management of neonatal sepsis once antibiotics have been initiated?

A

ANTIBIOTIC TREATMENT IS 7 DAYS MAX (stop if well and negative culture, continue if positive)

  • Check CRP again at 24 hours and check blood culture results at 36 hours:
  • Consider stopping antibiotics if baby is clinically well, blood cultures are negative 36 hours after taking them and both CRP results are less than 10
  • Check the CRP again at 5 days if they are still on treatment:
  • Consider stopping antibiotics if the baby is clinically well, the lumbar puncture and blood cultures are negative and the CRP has returned to normal at 5 days
  • Consider performing a lumbar puncture if any of the CRP results are more than 10
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22
Q

How long is neonatal sepsis treated for?

A

7 days if culture positive

If meningitis 14-21 days

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23
Q

What is the incidence of HIE and when do we suspect HIE may have occurred?

A

2 to 5 in 1000 births

  • Events that could lead to hypoxia during the perinatal or intrapartum period
  • Acidosis (pH < 7) on the umbilical artery blood gas
  • Poor Apgar scores
  • Features of mild, moderate or severe HIE
  • Evidence of multi organ failure.
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24
Q

What are some causes of HIE?

A

Primary neuronal death from ischaemia and then secondary reperfusion injury

  • Maternal shock
  • Intrapartum haemorrhage e.g placental abruption
  • Twin to twin transfusion syndrome
  • Sepsis
  • Prolapsed cord, causing compression of the cord during birth
  • Nuchal cord, where the cord is wrapped around the neck of the baby
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25
Q

How is HIE graded?

A

Sarnat Staging

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26
Q

How can HIE be investigated?

A

EEG monitoring

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27
Q

How is HIE managed?

A
  • Respiratory support
  • Anticonvulasant therapy
  • Fluid balance, electrolyte monitoring and inotropes
  • Therapeutic Hypothermia for secondary reperfusion injury
  • Follow up by paediatrician to check for learning disability
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28
Q

How is therapeutic hypothermia carried out for HIE management?

A
  • Babies near or at term
  • Baby transferred to neonatal ICU and actively cooled using cooling blankets and a cooling hat
  • Target of between 33 and 34°C, measured using a rectal probe.
  • Continued for 72 hours then warmed back up over 6 hours

Reduces the inflammation and neurone loss after the acute hypoxic injury. It reduces the risk of cerebral palsy, developmental delay, learning disability, blindness and death

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29
Q

What is the prognosis with HIE?

A

Assess extent of damage with MRI

  • Chronic neurological disability e.g cerebral palsy
  • Epilepsy
  • Learning disabilities
  • Blindness
  • Delayed motor skills and speech
  • ⅓ are fatal
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30
Q

What is neonatal jaundice and the epidemiology of this?

A

Jaundice (high bilirubin) that occurs in the first month of life, more common in preterm

May be physiological or pathological

  • Term ( ≥ 37 weeks gestation): affects 60% of newborns
  • Preterm (< 37 weeks gestations): affects 80% of newborns
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31
Q

What are some risk factors for newborn jaundice?

A
  • Preterm <37 weeks
  • Ethnicity: Asian, European, or native American
  • Male
  • Cephalohaematoma
  • Maternal factors: diabetes mellitus, >25 years old, exclusive breastfeeding
  • Other: previous sibling needing phototherapy for neonatal jaundice
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32
Q

What is physiological neonatal jaundice?

A
  • More common in breast fed babies
  • Neonate has high concentration of RBC and less developed liver function
  • Neonate RBCs break down more rapidly than normal releasing lots of bilirubin. Normally this bilirubin is excreted via the placenta, however at birth the foetus no longer has access to a placenta to excrete bilirubin

Mild yellowing of skin and sclera at 2-7 days, resolves by 10 days

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33
Q

What are some pathological causes of newborn jaundice?

A

Any jaundice that occurs before 24 hours, needs urgent investigations

ALWAYS CONSIDER SEPSIS

Increased production of bilirubin:

  • Haemolytic disease of the newborn
  • Sepsis
  • ABO incompatibility
  • Haemorrhage
  • Intraventricular haemorrhage
  • Cephalo-haematoma
  • Polycythaemia
  • G6PD deficiency

Decreased clearance of bilirubin:

  • Prematurity
  • Breast milk jaundice
  • Neonatal cholestasis
  • Extrahepatic biliary atresia
  • Endocrine disorders (hypothyroid and hypopituitary)
  • Gilbert syndrome
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34
Q

Why do the following babies often develop jaundice:

  • Pre-term
  • Breast feed
  • Haemolytic Disease of Newborn
A

Preterm: Immature liver function

Breast fed: Components of breast milk inhibit ability of liver to conjugate bilirubin. Also may be dehydrated so constipated so absorb more from intestines

HDN: haemolysis due to rhesus antibodies on rhesus positive antigens

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35
Q

What is prolonged jaundice?

A

When physiological jaundice occurs for longer than expected:

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

Should prompt further investigation e.g biliary atresia, hypothyroidism and G6PD deficiency.

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36
Q

What is Kernicterus?

A
  • Unconjugated bilirubin is potentially toxic to neural tissue in newborns and able to cross the blood-brain barrier
  • Yellow staining of cerebral tissue, particularly in the deep grey matter of the brain due to bilirubin deposition
  • Short term: less responsive, floppy, drowsy baby with poor feeding.
  • Long term: cerebral palsy, learning disability and deafness
37
Q

What are the clinical features of neonatal jaundice?

A
  • Yellowing of skin: check in bright natural light, harder in dark skin
  • Irritable baby
  • Poor feeding
38
Q

How is jaundice diagnosed in the neonate after clinically noticing the yellowing of skin, sclera or mucous membranes?

A
  • Gestational age < 35 weeks or < 24 hours old: serum bilirubin measurement
  • Gestational age > 35 weeks and > 24 hours old: transcutaneous bilirubinometer measurement. If level > 250 umol/L proceed to serum bilirubin measurement.
39
Q

What investigations are done for neonatal jaundice?

A

Routine screen:

  • Serum bilirubin
  • Blood packed cell volume
  • Blood group (mother and baby)
  • Direct Coombs Test

If clinically indicated:

  • Full blood count
  • Blood film
  • LFTs
  • G6PD levels
  • Cultures: work up for sepsis
  • CRP
40
Q

How is prolonged jaundice investigated?

A
  • Assess for features of obstructive jaundice (i.e. pale stools, dark urine)
  • Conjugated bilirubin levels as if raised then hepatobilliary cause
  • LFTs
  • Full blood count
  • Urine culture
  • Metabolic screen
  • TFTs for hypothyroidism
41
Q

How is neonatal jaundice treated?
What is the aim of treatment?

A
  • Treatment threshold table for newborns > 38 weeks gestation or treatment threshold graphs for preterm newborns
  • Phototherapy or Exchange transfusion

Refer to gastro if profound conjugated hyperbillirubinaemia as could mean biliary atresia

  • Treatment is to prevent irreversible Kernicterus
42
Q

What is phototherapy and red cell exchange?

(count in hours on chart)

A

Phototherapy

  • Blue-green light in the range of 460-490 nm, converts unconjugated bilirubin into water soluble molecules isomers that can be excreted without conjugation by liver
  • Regular assessment of bilirubin levels every 6 hours

Red cell exchange

Removal of the newborns blood and simultaneously replacing it with a compatible donor. This leads to a dramatic reduction in bilirubin levels.

Done for extremely high levels

43
Q

What monitoring should be done after phototherapy?

A

Rebound bilirubin should be measured 12 – 18 hours after stopping to ensure the levels do not rise about the treatment threshold again

Explain little to no UV light is used

44
Q

What is Crigler Najjar syndrome?

A
  • Mutations within the UGT1A1 gene, which encodes glucuronosyltransferase
  • They cause an unconjugated hyperbilirubinaemia
  • Similar to Gilbert’s but more severe as it leads to a profound reduction or absence of the enzyme activity,
45
Q

What is low birth weight?

A

Less than 2500g

Very low if <1500g

Extremely low if <1000g

SGA if below 10th centile for age

46
Q

How is prematurity classified?

A

Before 37 weeks gestation

The WHO classify prematurity as:

  • Under 28 weeks: extreme preterm
  • 28 – 32 weeks: very preterm
  • 32 – 37 weeks: moderate to late preterm
47
Q

What are some risk factors for prematurity?

A

Number one cause of neonatal death and big cause of death in under 5’s

Risks

  • Social deprivation
  • Smoking
  • Alcohol
  • Drugs
  • Overweight or underweight mother
  • Maternal co-morbidities
  • Twins
  • Personal or family history of prematurity
48
Q

If a baby is born with no scans and mother does not know the date of LMP, how can we estimate gestational age?

A

Dubowitz Score

Combination of 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, eye, ear and genital formation. Neuromuscular assessment looks at areas such as posture and arm recoil.

49
Q

If women have a previous preterm birth, what measures can try to reduce this for the next pregnancy?

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
50
Q

If a woman goes into premature labour, what management should be put into place to improve the outcomes for the neonate?

A
  • Tocolysis with nifedipine: suppress labour
  • Maternal corticosteroids: can be offered before 35 weeks gestation
  • IV Magnesium sulphate: before 34 weeks gestation to protect baby’s brain
  • Delayed cord clamping or cord milking: can increase the circulating blood volume and haemoglobin in the baby
51
Q

Can you do resuscitation in pre-term babies?

A
  • Less than 23 weeks: 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
  • After 25 weeks, it is appropriate to resuscitate and start intensive care.
52
Q

What are some issues in early life for premature babies?

A
  • Respiratory distress syndrome
  • Hypothermia
  • Hypoglycaemia
  • Poor feeding
  • Apnoea and bradycardia
  • Neonatal jaundice
  • Intraventricular haemorrhage
  • Retinopathy of prematurity
  • Necrotising enterocolitis (NEC)
  • Immature immune system and infections
53
Q

What are some long term effects of prematurity?

A
  • ROP
  • Chronic lung disease of prematurity
  • Cerebral palsy
  • Developmental delay
54
Q

What is apnea?

A

Breathing stops spontaneously for more than 20 seconds, or shorter periods with oxygen desaturation or bradycardia

Happens to all babies before 28 weeks gestation but can also happen at any gestational age

55
Q

Why does apnea occur in neonates and what are some of the causes?

A

Due to immaturity of autonomic nervous system, more so in preterm babies

Apnoea are often a sign of developing illness, such as:

  • Infection
  • Anaemia
  • Airway obstruction (may be positional)
  • CNS pathology e.g seizures or haemorraghe
  • GORD
  • Neonatal abstinence syndrome
56
Q

How is apnea of prematurity managed?

A
  • Apnea monitors that alarm when happening
  • Tactile stimulation to prompt baby to move
  • IV caffeine if recurrent episodes
  • Baby will eventually grow out of them
57
Q

What is the pathophysiology of retinopathy of prematurity?

A

Usually afters before 32 weeks and low birth weight babies

  • Retinal blood vessel development is stimulated by hypoxia and finishes around 37-40 weeks
  • When the retina is exposed to higher oxygen concentrations in a preterm baby, particularly with supplementary oxygen during medical care, the stimulant for normal blood vessel development is removed
  • When the hypoxic environment recurs, the retina responds by producing excessive blood vessels (neovascularisation), as well as scar tissue. These abnormal blood vessels may regress and leave the retina without a blood supply. The scar tissue may cause retinal detachment
58
Q

How is retinopathy of prematurity assessed?

A

Retina has 3 zones

  • Zone 1: optic nerve and the macula
  • Zone 2 : edge of zone 1 to the ora serrata, the pigmented border between the retina and ciliary body
  • Zone 3: outside the ora serrata

Stage 1 (slightly abnormal vessel growth) to stage 5 (complete retinal detachment).

59
Q

Which babies need to be screened for retinopathy by an ophthalmologist?

A

Babies born before 32 weeks or under 1.5kg

Start screening at:

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

Screening should happen at least every 2 weeks and can cease once the retinal vessels enter zone 3. Look for plus disease

60
Q

How is retinopathy of prematurity treated?

A
  • Target areas of retina to stop blood vessels growing
  • First line: transpupillary laser photocoagulation to halt and reverse neovascularisation
  • Other options: cryotherapy, intravitreal VEGF inhibitors, surgery for retinal detachment
61
Q

What are some differentials for respiratory distress in the newborn?

A
  • Transient tachypnea of the newborn (excess lung fluid)
  • Respiratory distress syndrome
  • Meconium aspiration
  • Sepsis
  • Tracheooesophageal fistula
62
Q

What is the aetiology of respiratory distress syndrome of the newborn?

A

Inadequate surfactant leads to high surface tension within alveoli. This leads to atelectasis (lung collapse), as it is more difficult for the alveoli and the lungs to expands

Results in hypoxia, hypercapnia and respiratory distress

63
Q

What are the signs of respiratory distress syndrome of the newborn?

A
  • Increased work of breathing shortly after birth (1st 4h)
  • Tachypnoea (>60/min)
  • Grunting
  • Nasal flaring
  • Intercostal recession
  • Cyanosis
64
Q

What investigation can help to diagnose respiratory distress syndrome and what does it show?

A

CXR

Ground glass appearance and air bronchograms

65
Q

How is RDS prevented?

A
  • IM Dexamethasone in women of risk of preterm labour from 23-35 weeks
66
Q

How its RDS managed?

A
  • Intubation and ventilation to fully assist breathing if severe
  • Endotracheal surfactant delivered into the lungs via endotracheal tube
  • Continuous positive airway pressure (CPAP) via a nasal mask to help keep the lungs inflated whilst breathing
  • Supplementary oxygen to maintain between 91 and 95% (not too high to prevent retinopathy and bronchopulmonary dysplasia)

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

67
Q

What are some short term complications of RDS?

A
  • Pneumothorax
  • Infection
  • Apnoea
  • Intraventricular haemorrhage
  • Pulmonary haemorrhage
  • Necrotising enterocolitis
68
Q

What are some long-term complications of RDS?

A
  • Chronic lung disease of prematurity
  • Retinopathy of prematurity
  • Neurological, hearing and visual impairment
69
Q

What is chronic lung disease of prematurity?

A

Bronchopulmonary Dysplasia

Persistent hypoxia and difficult ventilator weaning at 36 weeks’ postmenstrual age. Usually due to oxygen toxicity

Early issues: Feeding problems. O2 desaturation during feeds, severe RSV bronchiolitis, GORD

Late issues: cerebral palsy, asthma and exercise limitation

70
Q

How is Meconium Aspiration Syndrome managed?

A

Usually occurs in utero and causes meconium stained liqour

Surfactant, ventilation, inhaled nitric oxide, and antibiotics may be required

71
Q

What is necrotising enterocolitis?

A

Disorder affecting premature babies where part of the bowel becomes necrotic

Life threatening emergency as death of the bowel tissue can lead to bowel perforation which leads to peritonitis and shock

72
Q

What are some risk factors for developing NEC?

A
  • Very low birth weight or very premature
  • Formula feeds (breast milk is protective)
  • Respiratory distress and assisted ventilation
  • Sepsis
  • Patient ductus arteriosus and other congenital heart disease
73
Q

How may NEC present?

A
  • Vomiting, particularly with green bile aspirate
  • Fresh blood in stools
  • Intolerance to feeds
  • Generally unwell
  • Distended, tender abdomen
  • Absent bowel sounds
74
Q

What investigations are done if NEC is suspected?

A

Blood tests:

  • FBC for thrombocytopenia and neutropenia
  • CRP
  • Capillary blood gas will show a metabolic acidosis
  • Blood culture for sepsis

Abdominal xray is the investigation of choice. This is done supine

75
Q

What may an AXR show in NEC?

A
  • Pneumatosis intestinalis is gas in the bowel wall and is a sign of NEC
  • Pneumoperitoneum is free gas in the peritoneal cavity and indicates perforation
  • Dilated loops of bowel
  • Bowel wall oedema (thickened bowel walls)
  • Gas in the portal veins
76
Q

How is NEC managed?

A
  • Make nil by mouth
  • IV fluids and total parenteral nutrition (TPN)
  • Triple antibiotics
  • NG tube to drain fluid and gas from stomach
  • Barrier nurse

NEC is a surgical emergency and requires immediate referral to the neonatal surgical team. Some recover medically, some need surgery to remove dead bowel and have temporary stoma

77
Q

What is the prognosis and complications with NEC?

A

Fatal in 20% of cases

  • Perforation and peritonitis
  • Sepsis
  • Strictures
  • Abscess formation
  • Recurrence
  • Long term stoma
  • Short bowel syndrome after surgery
78
Q

What are some signs of neonatal abstinence syndrome?

A
79
Q

How is neonatal abstinence syndrome managed?

A

Monitoring on a NAS chart for at least 3 days (48 hours for SSRI antidepressants) to monitor for withdrawal symptoms

Medical treatment options for moderate to severe symptoms are:

  • Oral morphine sulphate for opiate withdrawal
  • Oral phenobarbitone for non-opiate withdrawal
80
Q

How may fetal alcohol syndrome present?

A
  • Microcephaly
  • Thin upper lip
  • Smooth flat philtrum
  • Short palpebral fissure
  • Learning disability
  • Behavioural difficulties
  • Hearing and vision problems
  • Cerebral palsy
81
Q

What are some conditions that can cause issues with feeding?

A
  • Cleft pallate
  • Tracheooesophageal fistula
  • Prematurity (poor suckle)
  • Jaundice
  • Neonatal abstinence syndrome
82
Q

What is SIDS and some risk factors for this?

A

Sudden unexplained death in an infant, “cot death”. Usually occurs in first 6 months

All babies need autopsy!!!

Risk Factors

  • Prematurity
  • Low birth weight
  • Smoking during pregnancy
  • Male baby
83
Q

How can we minimise the risk of SIDS?

A
  • Put baby on back when not directly supervised
  • Keep their head uncovered
  • Place feet at the foot of the bed to prevent sliding down and under the blanket
  • Keep cot clear of lots of toys and blankets
  • Maintain a comfortable room temperature (16 – 20 ºC)
  • Avoid smoking
  • Avoid co-sleeping, particularly on a sofa or chair
  • If co-sleeping avoid alcohol, drugs, smoking, sleeping tablets or deep sleepers
84
Q

What support is given to families after a death due to SIDS?

A
  • Lullaby Trust charity for bereavement supports
  • Care of Next Infant Team (CONI): extra support and home visits, resuscitation training and access to equipment such as movement monitors that alarm if the baby stops breathing for a prolonged period
85
Q

What are the main causes of neonatal death?

A

RESPIRATORY DISTRESS OF NEWBORN

  • Infections (36%, which includes sepsis/pneumonia, tetanus and diarrhoea)
  • Pre-term (28%)
  • Birth asphyxia
86
Q

How is ROP prevented?

A
  • Keep oxygen sats of premature baby between 88-92%
87
Q

How does surfactant deficiency appear on CXR in premature babies?

A

Ground glass appearance

88
Q

What is the definition of chronic lung disease of prematurity and what medication do these babies qualify for?

A

Oxygen dependent over the age of 37 weeks gestation corrected

Given Palivizumab against RSV once a month for 4 months in first year of life to prevent against bronchiolitis

89
Q

When is ROP screened for and how?
(see picture)

A

Need laser therapy for neovascularisation

Risk factors: prematurity and low birth weight