AAAMedicine > Neonates > Flashcards

Neonates Flashcards

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1
Q

What is surfactant?

A

Fluid produced by type II alveolar cells
Contains proteins and fats
Sits on top of the lungs
Increases lung compliance

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2
Q

What causes the closure of ductus arterisosus?

A

Increased blood oxygenation which causes a drop in circulating prostaglandins

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3
Q

Vitamin K - neonates

A

Give babies an IM injection in the thigh
Helps to prevent any bleeding - intracranial, umbilical stump and GI bleeding

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4
Q

What is the blood spot screening

A
  • Screening for 9 congenital conditions
    • Taken on day 5 after consent from parent
    • Heel prick
    • Screening card requires 4 separate drops
      ○ Sickle cell
      ○ Cystic fibrosis
      ○ Congenital hypothyroidism
      ○ Phenylketonuria
      ○ MCADD
      ○ MSUD
      Isovaleric acidaemia
      ○ GA1
      Homocysin
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5
Q

What is caput succedaneum?

A

Oedema collecting on the scalp, outside the periosteum
Caused by pressure to a specific area of the scalp during a traumatic, prolonged or instrumental delivery
Resolves in a few days

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6
Q

What is the periosteum

A

Layer of dense connective tissue that lines the outside of the skull and doesn’t cross the sutures ( gaps in baby’s skull)

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7
Q

What is a cephalohaematoma?

A

Collection of blood between skull and the periosteum
Caused by damage to the blood vessels during a traumatic, prolonged or instrumental delivery

Blood is below the periosteum, so the lump doesnt cross the suture lines of the skull

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8
Q

Facial paralysis - birth injury

A

Delivery can cause damage to the facial nerve
Associated with forceps delivery
Can result in facial palsy - weakness of the facial nerve on one side
Function normally returns spontaneously or within a few months

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9
Q

What is an erb’s palsy?

A

Injury tot he c5/c6 nerves in the brachial plexus during birth
Associated with shoulder dystocia, traumatic or instrumental delivery and a large birth weight

Leads to shoulder weakness abduction and external rotation, arm flexion and finger extension

Function returns spontaneously within a few months

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10
Q

Fractured clavicle - birth injury

A

May be fractured during birth
Shoulder dystocia, traumatic or instrumental delivery and large birth weight

Picked up with lack of movement in the affected arm, asymmetry of the shoulders, pain and distress on movement of the arm

Confirmed with USS or XRAY

Conservative management as usually heals well

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11
Q

What is hypoxic ischaemic encephalopathy?

A

Occurs in neonates as a result of hypoxia during birth
Can lead to permentant damage to the brain, causing cerebral palsy
Severe HIE can result in death

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12
Q

Causes of hypoxic ischaemic encephalopathy?

A

Anything that leads to deprivation of oxygen

Maternal shock, intrapartum haemorrhage, prolapse cord (causing compression of the cord during birth), nuchal cord ( where cord is around the neck)

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13
Q

What are the grades of hypoxic ischaemic encephalopathy

A

Mild, moderate and severe

Mild = Poor feeding, general irritability, hyper alert
Resolves within 24 hours
Normal prognosis

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

Severe= Reduced consciousness, apnoea’s, flaccid and reduced or absent reflexes
Up to 50% mortality and up to 90% cerebral palsy

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14
Q

Management of hypoxic ischaemic encephalopathy

A

Coordinated by specialists in neonatology
Supportive care

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15
Q

What is physiological jaundice?

A

High concentration of RBCs in the foetus and neonate, more fragile than normal RBCs and they also have less developed liver function.
Foetal RBCs break down more rapidly than normal RBCs, releasing lots of bilirubin
Normally this is excreted by the placenta, but at birth the foetus can no longer have access to placenta to excrete bilirubin = rise after birth = yellowing of sclera from 2-7 days. Resolves after 10 days

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16
Q

Neonatal jaundice causes?

A

Increased production of bilirubin
- haemolytic disease of the newborn, ABO incompatibility, haemorrhage, intraventricular haemorrhage, cephalohaematoma, polycyathemia, sepsis and DIC, G6PD deficiency

Decreased clearance of bilirubin
- Prematurity, breast milk jaundice, neonatal cholestasis, extrahetic biliary atresia, endocrine disorders, Gilberts syndrome

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17
Q

Jaundice in premature neonates?

A

Physiological jaundice is exaggerated due to the immature liver
Increases the risk of complications, particularly kernicterus

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18
Q

What is kernicterus?

A

Brian damage due to high bilirubin

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19
Q

What is breast milk jaundice?

A

Babies that are breastfed are more likely to have neonatal jaundice
Components of the breast milk inhibit the ability for liver to process bilirubin

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20
Q

What is haemolytic disease of the newborn?

A

Caused by haemolysis ( RBCs breaking down) and jaundice in the neonate

Caused by incompatibility between the rhesus antigens of the surface of the RBCs of the mother and foetus

When a women that is rhesus D negative becomes pregnant, need to consider the possibility that the child will be rhesus D positive. The babies red blood cells display the rhesus D antigen. Mothers immune system will recognise this rhesus D antigen as foreign and produce antibodies to the rhesus D antigen

Mother has then become sensitised to the rhesus D antigen

Usually, this sensitisation process doenst cause any problems during first pregnancy - unless the sensitisation happens ealry on, such as during antepartum haemorrhage

During subsequent pregnancies, the mother’s anti D antibodies can cross the placenta into the fetus. If that fetus is rhesus positive, these antibodies attach themselves to the RBCs of the fetus and cause the fetus immune system to attack their own RBCs

Leads to haemolysis, causing anaemia and high bilirubin levels

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21
Q

What is prolonged jaundice?

A

When is lasts longer than it would be expected in physiological jaundice
More than 14 days in full term babies
More than 21 days in premature babies

e.g. biliary atresia, hypothyroidism, g6pd deficiency

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22
Q

Investigations for neonatal jaundice?

A

RBC and blood film
Conjugated bilirubin
Blood type testing of mother and baby for ABO or rhesus incompatibility
Direct combs test for haemolysis
Thyroid function

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23
Q

Phototherapy - neonatal jaundice

A
  • Converts unconjugated bilirubin into isomers that can be excreted in the bile and urine without requiring conjugation in the liver
    • Blue light
      Rebound bilirubin is measured 12-18 hours after stopping to ensure the levels do not rise about the treatment threshold again
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24
Q

Kernicterus- symptoms

A
  • Less responsive, floppy, drowsy baby with poor feeding.
    Damage to CNS is permanent, causing cerebral palsy, learning disability and deafness
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25
What is prematurity?
Being born before 37 weeks gestation
26
Associations with prematurity?
Social deprivation, smoking, alcohol, drugs, overweight or underweight mother, maternal co-morbities, twins, personal or family history of prematurity
27
Management before birth - prematurity - in women with a history of preterm brith or USS demonstrating 25mm cervical length or less before 24 weeks gestation
2 options of trying to delay birth: - Prophylactic vaginal progesterone: progesterone suppository in the vagina to discourage labour Prophylactic cervical cerclage: putting a suture in the cervix to hold it closed
28
When preterm labour is suspected/confirmed, what are the options for improving outcomes?
- Tocolysis with nifedipine: CCB 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 to help protect the babys brain - Delayed cord clamping or cord milking: can increase the circulating blood volume and haemoglobin in the baby
29
Issues in early life - prematurity
- Respiratory distress syndrome - Hypothermia - Hypoglycaemia - Poor feeding - Apnoea and bradycardia - Neonatal jaundice - Intraventricular haemorrhage - Retinopathy of prematurity - Necrotising enterocolitis Immature immune system and infection
30
Long term effects- prematurity
- Chronic lung disease of prematurity - Learning and behavioural difficulties - Susceptibility to infections, particularly respiratory tract - Hearing and visual impairment - Cerebral palsy
31
What is apnoea of prematurity?
Periods where breathing stops spontaneously for more than 20 seconds, or shorter periods with oxygen desaturation or bradycardia Can occur in neonates of all gestational ages Often accompanied by a period of bradycardia Common in premature neonates Occur in almost all babies less than 28 weeks gestation
32
Causes of apnoea of prematurity?
- Immaturity of the autonomic nervous system - Sign of a developing illness e.g. ○ Infection ○ Anaemia ○ Airway obstruction ○ CNS pathology such as seizures of haemorrhage ○ GORD ○ Neonatal abstinence syndrome
33
Management of apnoea of prematurity?
- Units attach apnoea monitors to premature babies, these make a sound when an apnoea is occurring - Tactile stimulation is used to prompt the baby to restart breathing - IV caffeine can be used to prevent apnoea and bradycardia in babies with recurrent episodes - Episodes will settle as the baby grows and develops
34
What is retinopathy of prematurity?
Typically affects babies born before 32 weeks gestation Abnormal development of the blood vessels in the retina can lead to scarring, retinal detachment and blindness Treatment can prevent blindness
35
Pathophysiology behind retinopathy of prematurity?
Retinal blood vessel development starts at around 16 weeks and is complete by 37 – 40 weeks gestation. The blood vessels grow from the middle of the retina to the outer area. This vessel formation is stimulated by hypoxia, which is a normal condition in the retina during pregnancy. 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.
36
Screening for retinopathy of prematurity?
Babies born before 32 weeks or under 1.5kg should be screened for ROP. Screening is performed by an ophthalmologist. Screening starts 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, usually at around 36 weeks gestation
37
Treatment of retinopathy of prematurity?
Treatment involves systematically targeting areas of the retina to stop new blood vessels developing. First line is transpupillary laser photocoagulation to halt and reverse neovascularisation. Other options are cryotherapy and injections of intravitreal VEGF inhibitors. Surgery may be required if retinal detachment occurs.
38
What is respiratory distress syndrome?
Affects premature neonates, born before the lungs start producing adequate surfactant Commonly occurs below 32 weeks Ground glass appearance on CXR
39
Pathophysiology of respiratory distress syndrome?
Inadequate surfactant leads to high surface tension within alveoli Leads to ateclasis - lung collapse - as its more difficult for the alveoli and the lungs to expand Leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia and respiratory distress
40
Management of respiratory distress syndrome?
Antenatal steroid e.g. dexamethasone given to mothers Premature neonates may need support
41
Complications of respiratory distress syndrome?- long and short term
Short term: pneumothorax, infection, apnoea, intraventricular haemorrhage, pulmonary haemorrhage, necrotising enterocolitis Long term: chronic lung disease of prematurity, retinopathy of prematurity, neurological, hearing and visual impairment
42
What is necrotising enterocolitis?
Affects premature neonates Part of the bowel becomes necrotic Life threatening emergency Death of bowel tissue can lead to perforation = peritonitis and shock
43
Risk factors for necrotising entercolitis?
Low birth weight or premature Formula feeds Respiratory distress Sepsis Patent ductus arteriosus
44
Presentation of necrotising enterocolitis?
Intolerance to feeds Vomiting with green bile Generally unwell Distended tender abdomen Absent bowel sounds Blood in stool
45
Investigations for necrotising enterocolitis?
FBC for thrombocytopenia and neutropenia CRP for inflammation Capillary blood gas will show metabolic acidosis Blood culture for sepsis XRAY for the abdomen
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What does abdo XRAY look like for necrotising enterocolitis?
- Dilated loops of bowel - Bowel wall oedema - Pneumatosis intestinalis - Pneumoperitoneum - Gas in the portal veins
47
Management of necrotising enterocolitis?
Nil by mouth, IV fluids, TPN, ABX Surgical emergency
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Complications of necrotising enterocolitis?
Perforation, peritonitis Sepsis Strictures Abscess formation Recurrence Long term stoma Short bowel syndrome after surgery
49
What is neonatal abstinence syndrome?
Withdrawal symptoms that happens in neonates of mothers that used substances in pregnancy
50
Substances - neonatal abstinence syndrome
Opiates, methadone, benzos, cocaine, amphetamines, nicotine/cannabis, alcohol, SSRIs
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Signs and symptoms of neonatal abstience
CNS- irritability, increased tone, high pitched cry, not settling, tremors, seizures Vasomotor and respiratory - yawning, sweating, unstable temperature and pyrexia, tachypnoea Metabolic and GI - poor feeding, regurgitation and vomiting, hypoglycaemia, loose stools with sore nappy area
52
Management of neonatal abstience?
- Kept in hospital on a NAS chart for at least 3 days - Urine sample Medical treatment options for moderate to severe symptoms are: * Oral morphine sulphate for opiate withdrawal - Oral phenobarbitone for non-opiate withdrawal
53
Risk factors for SIDS?
Prematurity, low birth weight, smoking during pregnancy, male baby
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Measures to minimise the risk of SIDS?
* Put the baby on their back when not directly supervised * Keep their head uncovered * Place their feet at the foot of the bed to prevent them sliding down and under the blanket * Keep the cot clear of lots of toys and blankets * Maintain a comfortable room temperature (16 – 20 ºC) * Avoid smoking. Avoid handling the baby after smoking (smoke stays on clothes). * Avoid co-sleeping, particularly on a sofa or chair If co-sleeping avoid alcohol, drugs, smoking, sleeping tablets or deep sleepers
55
What are signs of congenital zika syndrome?
Microcephaly, foetal growth restriction, other intracranial abnormalities
56
What is congenital toxoplasmosis?
Infection with the toxoplasma gondii parasite Faeces from a cat that is host of the parasite Triad: - Intracranial calcification - Hydrocephalus - Chorioretinitis
57
What is CMV? ( in neonates)?
Occurs due to maternal CMV infection during pregnancy Mostly spread via infected saliva or urine of asymptomatic children Most cases in pregnancy do not cause congenital CMV Features; - Fetal growth restriction - Microcephaly - Hearing loss - Vision loss - Learning disability Seizures
58
What is congenital varicella syndrome? What do you give?
Chickenpox Dangerous in pregnancy as can lead to: - More severe cases in the mother e.g. pneumonitis, hepatitis or encephalitis - Foetal varicella syndrome - Severe neonatal varicella infection if mum is infected around delivery If mother has previously had chickenpox they are safe IV varicella immunoglobulins can be given as prophylaxis If chickenpox rash starts in pregnancy - give oral acyclovir
59
Features of Congenital varicella syndrome?
- Foetal growth restriction - Microcephaly, hydrocephalus, learning disability - Scars and significant skin changes following the dermatomes - Limb hypoplasia Cataracts and inflammation in the eye
60
What is congenital rubella syndrome?
Caused by maternal infection with the rubella virus during pregnancy Highest risk during first 3 months of pregnancy Women planning to become pregnant should have the MMR vaccine. Can be tested for rubella immunity Pregnant women SHOULD NOT RECEIVE IT as it’s a live vaccine
61
Features of congenital rubella syndrome?
- Congenital cataracts - Congenital heart disease - Learning disability Hearing loss
62
What is foetal alcohol syndrome? What can it lead to?
Alcohol in pregnancy can cross the placenta and enter the fetus, where it disrupts fetal development Greatest effects in the first 3 months Can lead to: - Miscarriage - Small for dates Preterm delivery
63
Features of foetal alcohol syndrome?
- Microcephaly ( small head) - Thin upper lip - Smooth flat philtrum - Short palpebral fissure - short distance from one side of the eye and the other - learning disability - Behavioural difficulties - Cerebral palsy
64
Jaundice in the first 24 hours of life?Causes?
ALWAYS PATHOLOGICAL Causes - Rhesus haemolytic disease, ABO haemolytic disease, hereditary spherocytosis
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Jaundice in neonate from 2-14 days
Common Usually physiological more RBCs, more fragile RBCs less developed liver function
66
What do you do if Jaundice after 14 days? (prolonged) in the neonate?Causes?
Do a screen- conjugated and unconjugated bilirubin ( conjugated =? biliary atresia) Direct antiglobulin test (Coombs test) TFTs FBC and blood film. Urien for MC+S and reducing sugars U+Es and LFTs
67
Causes of prolonged jaundice?
Biliary atria, hypothyroidism, galactosaemia, uTI, breast milk jaundice, prematurity, congenital infections
68
Most likely cause of worsening neurological function in a premature infant
Intraventricular haemorrhage
69
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