neonatal Flashcards

1
Q

when is surfactant produced

A

betweeen 24 and 34 weeks gestation

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2
Q

why is there a fall in pulmonary vascular resistance when a baby takes its first breath and how does this lead to closure of the foramen ovale.

A

the first breath expands the alveoli - decreasing pulmonary vascular resistance

which causes a fall in RA pressure and at this point the LA pressure is greater (squashing the atrial septum and causing closure of the foramen ovale)

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3
Q

why does the ductus arteriolus close after birth

A

prostaglandins are required to keep it open

increased 02 causes a drop in circulating prostaglandins

causing closure

becomes the ligamentum arteriosum

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4
Q

why does the ductus venous stop functioning after birth

A

the umbilical cord is clamped and there is no blood flow in the umbilical veins

structurally closes a few days later and becomes the ligamentum venosum

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5
Q

when are inflation breathes given

A

when the neonate is grasping or not breathing adequtely despite stimulation

  1. two x (5 inflation breaths lasting 3 seconds)
  2. heart rate low - 30 seconds of ventilation breaths
  3. chest compressions co-ordinated with ventilation breaths
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6
Q

resus procedure in neonates

A
  1. warm the baby
  2. APGAR score (0-10 , higher is better)
  3. stimulate breathing (place head in neutral position, drying with towel)
  4. check for meconium/obstruction
  5. inflation breaths
  6. chest compressions 3:1
  7. severe - therapeutic hypothermia
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7
Q

when are chest compressions used in neonate

A

HR < 60 despite resuscitation and inflation breaths

3:1 ratio with ventilation breaths

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8
Q

why might it be good to delay clamping to umbilical cord in neonates

A

allows more time for blood to enter the circulation of the babies - improve Hb, iron stores and blood pressure is reduced in intraventicular haemorrhage and necrosting enterocolitis

  • negative - increased neonatal jaundice - requiring phototheraphy
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9
Q

what vitamin is given after birth

A

vitamin K

babies are born deficient in vitamin K - important part of blood clotting

via IM injection in thigh (also helps stimulate cry) - explands the lungs

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10
Q

when is blood spot screening carried out

A

day 5

  • heel prick
  • screens for 9 conditions (CF, sickle cell, congenital hypothyroidism, phenylketonuria ….

come back in 6-8 weeks

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11
Q

when is newborn examination carried out

  • is a screening tool
A

72 hours after birth - (trainined midwife or doctor)

repeated 6-8 weeks by GP

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12
Q

where is the ductus arteriosus located?

A

arch of the aorta - and connects the pulmonary artery

stops functioning 1-3 days after birth

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13
Q

what to do if clinky/clunky sounds in hips of neonate

A

USS

to rule out development dysplasia of the hip

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14
Q

erbs palsy is a result of injury to what nerves

A

C5/C6 nerves

-> internally rotated shoulder
-> extended elbow
-> flexed wrist

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15
Q

what is caput succedaneum

A

traumatic birth
-> odema collects on scalp (outside the periosteum)
-> is able to cross sutures and usually mild or no discolouration of skin
- resolves in few days

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16
Q

what is cephalohaematoma

A

blood collects underneath the perisoteum but not within the skull

result of traumatic birth

blood does not cross * suture lines

blood can cause discolouration

usually resolves without treatment - might be anaemia and juandice due to blood that collects and breaks down

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17
Q

most common cause of neonatal sepsis

A

GBS***

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18
Q

risk factors for neonatal sepsis

A

GBS in mother

GBS previous baby

chorioamnionitis or fever > 38

prematurity < 37

early PROM or prolonged ROM

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19
Q

antibitoics used in sepsis in neonates

A

benzylpenicillin/gentamycin

***cefotraxime (lower risk)

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20
Q

what is hypoxic ishcaemic encephalopathy

A

lack of oxygen during birth - there is a lack of blood flow to tissues which affects the brain

ischaemic brain damge

(cerebral palsy/death)

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21
Q

potential causes of HIE (hypoxic ischaemic encephalopathy)

A

anything that leads to reduced oxygen to brain
-APH
- prolasped cord
- maternal shock
- nuchal cord (wrapped around neck)

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22
Q

symptoms of HIE

A
  • poor feeding, irritability, hyper alert (mild)
  • poor feeding, lethargic, hpotonic and seizures (cerebral palsy) - moderate
  • reduced consciousness, apnoeas, flaccid , reduced or absent reflexes (high mortality and death)
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23
Q

what is therapeutic hypothermia

A

babies who are near or at term can benefit if they have HIE

  • cooling baby - to 33 - 44C for 72 hours

to reduce inflammation and neurone loss after acute hypoxic injury

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24
Q

the main cause of neontal jaundice

A

physiological (mild from Day 2 - 7)

resolves day 10

  • high concentration of fragile RBC
  • less developed liver function

lots of RBC broken down/but liver is not conjugated faster

more dramatic in neontates -> immature liver

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25
Q

what is kernicterus

A

brain damage due to high levels o biliruben in the blood

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26
Q

why are breast fed babies more likely to become jaundice

A

components of breast milk inhibit the ability of liver to process biliruben

more likely to become dehyrated if not feeding adequetely - (slow passage of stools, increasing absorption of bilirubin in the intestines)

27
Q

what is haemoltyic disease of the newborn

A

causes haemolysis - increased biliruben in the blood

caused by incomptibility (rhesus antigens on mother verus foetus)

rhesus antigens - > rhesus D antigen

rhesus D negative (do not have the D antigen) -> will attack rhesus D positive (have D antigen on RBC)

28
Q

what is prolonged jaundice

A

> 14 days in full term
21 days in preterm

-> prompt further investigation (look for biliary atresia , hypothyroidism, G6PD deficiency)

29
Q

why treat neonatal jaundice

A

phototheraphy (blue light*/exchange transfusions

-> precent kernicterus (present with less responsive, floppy, drowsy baby with poor feeding)

-> cerebral palsy, deafness and CNS damage

30
Q

features of necrotising enterocolitis (symptoms)

A
  • pre-term neonates**

bilous vomit
bloody stools
absent bowel sounds

31
Q

test findings on imaging for necrotising enterocolitis

A

bloods - metabolic acidosis due to systemic compromise

Abdominal XR
- dilated asymmetrical loops of the bowel
- bowel wall oedema
- thumbprinting
- pneumonitis intestinalis - GAS in the bowel

32
Q

prematurity is birth before

A

< 37 weeks

33
Q

prophylactic treatment for mothers who have a history of preterm birth or USS showing cervical length of 25mm or less before 24 weeks gestations?

A
  • prophylactic vaginal progesterone (supositary)
  • prophylactic cervical clerage (suture)
34
Q

treatment when preterm labour is suspected or confirmed

A
  1. tocolysis - nifedipine (CCB)
  2. maternal corticosteroids - before 35 weeks
  3. IV magnesium sulphate (before 34 weeks - protect brain)

4 delayed cord clamping or cord milking - increase blood volume and haemoglobulin

35
Q

what is apnea of prematury

A

breathing stops for more than 20 seconds (spontaneous)

or shorter periods with oxygen desaturation and bradycardia

common in premature neonate

term - usually underlying pathology

36
Q

causes of apnea in neonates

A

immaturity of autonomic nervous system - that controls RR and HR

37
Q

management of apnea of prematurity

A

apnea monitoring

tactile stimulation - prompt to start breathing

IV caffiene*** to prevent apnoea and bradycardia if having recurrent episodes

settle as baby grows and develops

38
Q

what is retinopathy of prematurity

A

preterm and low birth weight babies < 32 weeks

abnormal development of blood vessels in the retina can lead to scarring, retinal dettachment and blindness

retinal blood vessel development comple 37-40 weeks

39
Q

why does reintopathy occur in premature babies

A

blood vessel grow is stimulated by hypoxia in utero

when born - supplmenetal oxygen -> neovascularisation (abnormal blood vessels then regress and leave the retina without a blood supply)

screened in babies in premature babies < 32 weeks

40
Q

when does RDS usually occur

A

in babies born before 32 weeks gestation

41
Q

CXR of babies with RDS

A

ground glass appearance

42
Q

complications of RDS in babies (ST)

A

atelectasis (lung collaspe)

inadequte gas exchange - hypoxia

pneumothorax

apnoea

intraventricular haemorrhage

necrotising enterocolitis

43
Q

long term complications of RDS

A

chronic lung disease of prematurity

retinopathy of prematurity

neurological , hearing and visual impairments

44
Q

management of RDS in neonates

A

antenatal - dexamethasone

intubation/ventilation - if severe

endotracheal surfactant (delivered via endotracheal tube)

CPAP

supplementary 02 - (maintain 92-95)

45
Q

what is broncho-pulmonary dysplasia

A

chronic lung disease (CLD) of prematurity - when

  • infant requires oxygen theraphy beyond 36 weeks
  • changes on XR
46
Q

how to prevent chronic lung disease of prematurity

A

corticosteroids - betamethasone at signs of premature labour

CPAP rather than intubation/ventilation

use caffiene to stimulate respiratory effort

not over oxygenating with supplementory oxygen (aim 92-95%)

47
Q

what are children bronchopulmonary dysplasia (chronic lung disease of prematurity) given to reduce risks of infection

A

palivizumab injections (given monthly in babies with chronic lung disease to prevent RSV)

monoclonal antibody

48
Q

what is necrotising enterocolitis

A

affects PREMATURE neonates

part of the bowel becomes necrotic

life threathening emergency

death of bowel tissue - can lead to bowel perforation

perforation -> peritonitis and shock

49
Q

risk factors for necrotising enterocolitis

A

low birth weight
prematurity
RDS and assisted ventilation
sepsis
PDA/congenital heart disease

50
Q

presentation of necrotising enterocolitis

A

intolerance to feeds
vomiting - green bile
distended , tender bowel
blood in stools

peritonitis and shock -> severely unwell

51
Q

what will capillary blood gas show in necrotising enterocolitis

A

metabolic acidosis

52
Q

what will abdominal XR show in necrotising enterocolitis

A

taken in supine position +/- lateral side

  • dilated bowel loops
  • bowel wall oedema (thickened bowel walls)
    - pneumatosis intestinalis - gas in bowel wall
  • pneumoperitoneum -> free gas in the peritoneal cavity and indicates perforation
  • gas in portal veins
53
Q

inital management of necrotising enterocolitis while waiting on surgery

A
  • nil by mouth
  • IV fluids
  • total parenteral nutrition
  • antibiotics

surgery -> stoma

54
Q

characteristics of fetal alcohol syndrome

A

(preterm, small for date, miscarriage)

  • small head (mirocephaly)
  • thin upper lip
  • smooth flat philtrum (groove between nose and upper lip)
  • short palpable fissure (distance from one side of eye to other)
  • hearing /vision
55
Q

features of congenital rubella syndrome

A

congenital catarcts

PDA and pulmonary stenosis

Hearing loss

56
Q

if in doubt mother has previously had the chicken pox

A

check IgG levels for VZV

positive - immune

if not - vaccine before or after pregnancy

57
Q

what to do if mother is not immune of chicken pox - what is the prophylactic treatment

A

IV varicella immunoglobulins (within 10 days of exposure)

58
Q

what to do if chicken pox starts in pregnancy (Treatment)

A

oral acyclovir - if present within 24 hours and > 20 weeks

59
Q

features of congenital varicella syndrome

A

if infection in first 28 weeks of gestation
- small head
- growth restriction
- significant skin changes following dermatomes
- limb hypoplasia -

60
Q

features of congenital toxoplasmosis infection

A

TRIAD -

  1. intracranial cacification
  2. hydrocephalus
  3. chorioretinitis
61
Q

when does sudden infant death syndrome occur

A

within the first 6 months of life

62
Q

risk factor for SIDS - sudden infant death syndrome

A
  • prematurity
  • low birth weight
  • smoking during pregnancy
  • slight risk when male