Neonatology Flashcards

1
Q

What is hypoxic ischaemic encephalopathy ?

A

-> Prolonged or severe hypoxia during birth leading to ischaemic brain damage.
-> HIE can lead to permanent damage to the brain, causing cerebral palsy.

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2
Q

Give 4 causes of HIE

A

ANYTHING CAUSING ASPHYXIA

-> Maternal shock
-> Intrapartum haemorrhage
-> Prolapsed cord : causing compression of the cord during birth
-> Nuchal cord : cord is wrapped around neck of the baby

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3
Q

What is used to grade the severity of HIE?

A

-Sarnat staging

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4
Q

What are the features of mild HIE (3)

A

-Poor feeding, generally irritable and hyper-alert
-Resolves within 24 hrs
-Normal prognosis

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5
Q

What are the features of moderate HIE (4)

A

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

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6
Q

What are the features of severe HIE (4)

A

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

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7
Q

What can be done to reduce risk of severe damage from HIE

A

-> Therapeutic Hypothermia
-> Carefully cooling a baby in ICU to between 33 and 34 degrees, measruing with a rectal probe
-> Continued for 72 hrs, after which the baby is warmed over 6 hrs
-> Done to reduce inflammation and neuron loss after acute hypoxic injury

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8
Q

What 5 things are scored in apgar scores

A

-HR
-Resp effort
-Muscle tone
-Reflex irritability
-Colour

0-3 = very low
4-6 = moderate low
7-10 = baby is ok

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9
Q

Define prematurity

A

-Born before 37 weeks

<24 wks - extreme preterm
28-32 wks - very preterm
32-37 wks - moderate to later preterm

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10
Q

What is associated with prematurity ?

A

-Social deprivation
-Smoking
-Alochol
-Drugs
-Overweight or underweight mother
-Maternal co-morbidities
-Twins
-Personal or family history of prematurity

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11
Q

What 2 thing can be done to try and delay birth in evidence of prematurity ?

A

-Prophylactic vaginal progesterone
-Prophylactic cervical cerclage -> suture in cervix to hold shut

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12
Q

If preterm labour is confirmed, what can done to improve outcomes?

A

-Nifedipine to suppresses labour
-Maternal corticosteroids before 35 wks
-IV magnesium sulphate before 34 wks to protect babys brain
-Delayed cord clamping or cord milking to increase circulating blood volume and Hb in the baby

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13
Q

Give issues in early life following premature birth (10)

A

-Resp distress syndrome
-Hypothermia
-Hypoglycaemia
-Poor feeding
-Apnoea and bradycardia
-Neonatal jaundice
-Intraventricular haemorrhage
-Retinopathy of prematurity
-Necrotising enterocolitis
-Immature immune system and infection

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14
Q

Give 5 long term effects of prematurity

A

-Chronic lung disease of prematurity
-Learning and behavioural difficulties
-Susceptibility to infections
-Hearing and visual impairment
-Cerebral palsy

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15
Q

Why does respiratory distress syndrome occur in premature neonates?

A

-<32 wks there is inadequate surfactant leading to high surface tension within alveoli
-This leads to lung collapse as it is more difficult for alveoli and lungs to expand
-There is inadequate gaseous exchange, causing hypoxia, hypercapnia and resp distress

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16
Q

How is respiratory distress managed ?M (4)

A

-Intubation and ventilation
-Endotracheal surfactant
-CPAP
-Oxygen

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17
Q

What can be given to mothers with suspected or confirmed preterm labour to reduced incidence and severity of respiratory distress syndrome in the baby

A

-Antenatal steroids (e.g. dexamethasone) to increase surfactant production

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18
Q

Give 6 short term complications of respiratory distress syndrome

A

-Pneumothorax
-Infection
-Apnoea
-Intraventricular haemorrhage
-Pulmonary haemorrhage
-Necrotising enterocolitis

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19
Q

Give 3 long term complications of respiratory distress syndrome

A

-Chronic lung disease of prematurity
-Retinopathy of prematurity
-Neurological, hearing and visual impairment

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20
Q

What is necrotising enterocolitis ?

A

-Disorder affecting premature neonates where part of the bowel becomes necrotic
-Death of bowel tissue can lead to perforation -> peritonitis -> shock

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21
Q

Give 5 risk factors for necrotising enterocolitis

A

-Very low birth weight or very premature
-Formula feeds
-Respiratory distress and assisted ventilation
-Sepsis
-Patient ductus arteriosus and other congenital heart disease

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22
Q

How can necrotising enterocolitis present ?

A

-Intolerance to feeds
-Vomiting, usually green bile
-Generally unwell
-Distended, tender abdomen
-Absent bowel sounds
-Blood in stool

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23
Q

What is the investigation of choice for diagnosing necrotising enterocolitis ?

A

-Abdo X-ray
-Done front on in supine position

24
Q

What will an abdo x-ray show in necrotising enterocolitis ?

A

-Dilated loops of bowel
-Bowel wall oedema
-Gas in the bowel wall

25
Q

What will be seen on bloods in necrotising enterocolitis ?

A

-FBC : thrombocytopenia and neutropenia
-CRP : raised
-Capillary blood gas -> metabolic acidosis
-Blood culture for sepsis

26
Q

How is necrotising enterocolitis managed ?

A

-Total parenteral nutrition (TPN) and antibiotics to stabilise
-Nasogastric tube to drain fluid and gas from stomach and intestines
- Laparotomy if perforation

27
Q

Give 8 complications of necrotising enterocolitis

A

-Perforation and peritonitis
-Sepsis
-Death
-Strictures
-Abscess formation
-Recurrence
-Long term stoma
-Short bowel syndrome after surgery

28
Q

What are breastfed babies more likely to develop jaundice ?

A

-Components of breast milk inhibit the ability of the liver to process bilirubin
-Breastfed babies are more likely to become dehydrated if not feeding adequately.
-Inadequate breastfeeding = slow passage of stools, increasing absorption of bilirubin in the intestines

29
Q

Explain haemolytic disease of the newborn

A

-Mum = rhesus D negative
-Baby = rhesus D positive
-Mother recognises the rhesus antigen as foreign and produces antibodies
-Second baby = anti-D antibodies cross the placenta
-If the second baby is rhesus D positive = haemolysis = anaemia and high bilirubin levels

30
Q

Give the 6 steps of neonatal resus

A
  1. Warm the baby by getting them dry
  2. Caclulat APGAR score
30
Q

Give the 5 steps of neonatal resus

A
  1. Warm the baby by getting them dry
  2. Calculate APGAR score
  3. Stimulate breathing : head in neutral position, dry vigourously.
  4. Inflation breathes : 2 cycles of 5 breathes lasting 3 seconds each.If no response, 30 secs of ventilation breathes
  5. Chest compressions if HR remains below 60 bpm -> 3:1 ratio with ventilation breaths
31
Q

What 5 organisms commonly cause neonatal jaundice ?

A

-GBS -> common
-E.coli
-Listeria
-Klebsiella
-Staph aureus

32
Q

What are the clinical features of neonatal sepsis (10)

A

-fever
-Reduced tone and activity
-Poor feeding
-Resp distress or apnoea
-Vomiting
-Tachy or bradycardia
-Hypoxia
-Jaundice within 24 hrs
-Seizures
-Hypoglycaemia

33
Q

Give 6 RF for neonatal sepsis

A

-Vaginal GBS
-GBS in previous baby
-Maternal sepsis
-Prematurity (<37 wks)
-Early rupture of membrane
-Prolonged rupture of membranes (PROM)

34
Q

What are the two 1st line medications for neonatal sepsis ?

A
  • IV Benzylpenicillin and gentamycin
35
Q

What are the 5 increased bilirubin production causes of jaundice in neonates

A
  1. Haemolytic disease of newborn
  2. ABO incompatibility
  3. Polycythaemia
  4. G6PD deficiency
  5. Sepsis and DIC
36
Q

what is a common cause of jaundice in the 1st 24 hrs of life

A

Neonatal sepsis

37
Q

what are 6 decreased bilirubin clearance causes of neonatal jaundice

A
  1. Prematurity
  2. Breast milk jaundice
  3. Neonatal cholestasis
  4. Gilberts
  5. Biliary atresia
  6. Endocrine disorders (hypothyroid, hypopituitary)
38
Q

how is neonatal jaundice managed

A

-Phototherapy -> converts unconjugated bilirubin to isomers which can be excreted in bile and urine

39
Q

what is physiological jaundice

A

-Neonate = high conc of fragile RBCs & less developed liver function
-These RBCs break down rapidly
-There is a normal rise in bilirubin shortly after birth with mild yellowing of sclera

40
Q

What is kernicterus ?

A

-Brain damage due to excess bilirubin in neonate as bilirubin can cross BBB
-Can cause cerebral palsy, learning difficulties and deafness

41
Q

-Traumatic, prolonged or instrumental delivery (e.g.ventouse)
-Soft, puffy occipital swelling that crosses suture lines
-No treatment needed, will resolve in a few days

A

Caput seccedaneum : fluid collecting on the scalp OUTSIDE the periosteum and caused by pressure

42
Q

-Traumatic, prolonged, instrumental delivery.
-Lump on the skull, that DOES NOT CROSS suture lines
-Discolouration of the skin in the affected area

A

-Cephalohaematoma : collection of blood between skull and periosteum. As it is BELOW the periosteum it does not cross suture lines

43
Q

Normal vaginal delivery
Convulsion within 48 hrs
No head trauma or swellings

A

Intra-ventricular haemorrhage -> in premature neonates can occur spontaneously

44
Q

what causes an erb’s palsy

A
  • Injury to C5/C6 during birth
  • Is associated with shoulder dystocia, traumatic or instrumental delivery and large birth weight
45
Q

How does Erb’s palsy present

A
  • Internally rotated shoulder
  • Elbow extended
  • Flexed wrist facing backwards (pronated)
  • Lack of movement in affected arm

‘waiters tip”

46
Q

what is gastroschisis and its managed

A
  • Congenital defect in the anterior abdo wall LATERAL to the umbilical cord.
  • Management : vaginal delivery, take newborn to theatre within 4 hrs
47
Q

what is exomphalos (omphalocoele) and its management

A
  • Abdominal contents protrude through abdo wall but are covered by amniotic sac
  • C section to protect the sac from rupture with staged repair
48
Q

Oesophageal atresia : associations, presentation

A
  • Associations : tracheo-oesophageal fistula, polyhydramnios
  • Presents : chocking and cyanotic spells following aspiration
49
Q

RF for meconium aspiration (5)

A
  • Post term delivery
  • Maternal HTN
  • Pre eclmapsia
  • Chorioamnionitis
  • Smoking or substance use
50
Q

How is neonatal hypoglycaemia managed if asymptomatic

A
  • Encourage normal feeding
  • Monitor blood glucose
51
Q

How is neonatal hypoglycaemia managed if symptomatic / very low blood glucose

A
  • Admit
  • IV 10% dextrose
52
Q

Most common causes of neonatal sepsis

A

GBS
E.coli

53
Q

Give 4 RF for GBS infection

A
  • Prematurity
  • Prolonged rupture of membranes
  • Previous sibling with GBS
  • Maternal pyrexia (e.g. secondary to chorioamnionitis)
54
Q

Where does HSV typically affected in encephalitis

A

Temporal lobes

55
Q

What can increase the risk of cleft lip and palate

A
  • Maternal antiepileptic use