NEONATOLOGY Flashcards
SURFACTANT: where is it produced
Type II alveolar cells
SURFACTANT: Role
Keeps alveoli inflated
Maximises SA of alveoli
Increases lung COMPLIANCE
SURFACTANT: When is it produced in gestation?
Between 24-34 weeks gestation
Cardio-respiratory changes at birth
Thorax squeezed as body passes through vagina to help clear fluid from lungs
Adrenaline and cortisol released in response to stress of labour, stimulating respiratory effort
Decreased pulmonary vascular resistance (expansion of alveoli) —> fall in pressure in right atrium —> L atrial pressure higher —> closure of foremen ovale
Prostaglandins keep ductus arteriosus open. At birth there is fall in prostaglandins —> closure of ductus arteriosus (becomes ligamentum arteriosum)
Ductus venosus stops functioning at birth, structurally closes after a few days and becomes ligamentum venosum
Basic principles of neonatal resuscitation
- Warm the baby
- Calculate APGAR score (at 1, 5 and 10 minutes) while resuscitation continues
- Stimulate breathing (e.g. drying vigorously), place baby’s head in neutral position to keep airway open. Check for any airway obstruction (e.g. meconium)
- Inflation breaths (2 x cycles of 5 inflation breaths, if no response - 30 seconds of ventilation can be used, if still no response - chest compressions coordinated with the breaths)
- Chest compressions - if HR < 60bpm despite resuscitation and inflation breaths (3:1 ratio with breaths)
- Severe situations - IV drugs and intubation considered
Consequence of prolonged hypoxia during neonatal resuscitation
Hypoxic-ischeamic encephalopathy
APGAR score
Appearance (blue, blue extremities, pink)
Pulse ( absent, <100, >100)
Grimace (response to stimulation - no response, little response, good response)
Activity (muscle tone) - floppy, flexed arms and legs, active
Respiration (absent, slow/irregular, strong/crying)
Delayed umbilical cord clamping
In healthy, term babies - delay cord clamping for at least 1 minute (improves haemoglobin, iron stores and BP, and reduces intraventricular haemorrhage and necrotising enterocolitis)
- but also increases neonatal jaundice
Normal care after birth
Skin to skin Clamp umbilical cord Dry baby Keep baby warm Vitamin K Label baby Measure weight and length
Importance of Vitamin K after birth
Babies are born with deficiency of vitamin K
IM injection of vit K in thigh shortly after birth
(Important in clotting and preventing bleeding)
Blood spot screening
Screens for 9 congenital conditions
Taken on day 5 (8 at the latest)
Results take 6-8 weeks to come back
What congenital conditions does the blood spot screen for ?
Sickle cell CF Congenital hypothyroidism Phenylketonuria Medium chain acyl-CoA dehydrogenase deficiency Maple syrup urine disease Isovaleric acidaemia Glutamic acidaemia Homocystin
Birth injuries: CAPUT SUCCEDANEUM
Oedema collecting on scalp, outside periosteum
Cause: pressure to specific area of the scalp during traumatic, prolonged, instrumental delivery
Fluid outside the periosteum so can cross suture lines
Generally mild/no discolouration
Doesn’t require treatment - usually resolves
Birth injuries: CEPHALOHAEMATOMA
Collection of blood between skull and periosteum
Cause: damage to BV during delivery
TRAUMATIC SUBPERIOSTEAL HAEMATOMA
Does not cross suture lines !! As below periosteum
Discolouration of affected area
Usually resolves without treatment within a few months - risk of anaemia and jaundice, so baby should be monitored
Birth injuries: FACIAL PARALYSIS
Delivery can cause damage to facial nerve
Associated with forceps delivery
Function usually returns within a few months
Birth injuries: ERB’S PALSY
Result of injury to C5/C6 nerves in the brachial plexus during birth
Associated with shoulder dystocia, traumatic or instrumental delivery and large birth weight
Weakness of: shoulder ABduction and external rotation, arm flexion and finger extension
“Waiters tip” appearance
- internally rotated shoulder
- extended elbow
- flexed wrist facing backwards
- lack of movement in affected arm
Birth injuries: Fractured clavicle
Picked up during newborn examination
- lack of movement or asymmetry of movement in the affected arm
- asymmetry of shoulders, with affected lower than normal shoulder
- pain and distress on movement of arm
Confirmed by USS or X-ray
Conservative management, might need immobilisation, usually heals well
Main complication: brachial plexus injury
Neonatal sepsis: common organisms
Group B strep E. Coli Listeria Klebsiella Staphylococcus aureus
Neonatal sepsis: Risk factors
Vaginal GBS colonisation
GBS sepsis in a previous baby
Material sepsis, chorioamnionitis or fever above 38
Prematurity (<37 weeks)
Early (premature) rupture of the membrane
Prolonged rupture of membranes (PROM)
Neonatal sepsis: Clinical features
Fever Reduced tone/activity Poor feeding Respiratory distress/apnoea Vomiting Tachycardia or bradycardia Hypoxia Jaundice within 24hrs Seizures Hypoglycaemia
Neonatal sepsis: RED FLAGS
Confirmed or suspected sepsis in mother
Signs of shock
Seizures
Term baby needing mechanical ventilation
Respiratory distress starting more then 4hours after birth
Presumed sepsis in another baby in a multiple pregnancy
Neonatal sepsis: TREATMENT
Risk factor or clinical feature present: monitor the observations and clinical condition for at least 12hrs
2 or more risk factors or clinical features: START ABX within 1 hour
1 single red flag: START ABX within 1 hour
Blood cultures taken before abx given
Check baseline FBC and CRP
If any signs of meningitis: LP
Early onset neonatal sepsis: Antibiotic choice
1st line: BENZYLPENICILLIN IV & GENTAMICIN IV
2nd line/gram -ve cover: CEFOTAXIME IV
if gram negative confirmed stop benzylpenicillin !
Late onset neonatal sepsis (after 72 hours): antibiotic choice
Evidence of localised infection:
FLUCLOXACILLIN IV & GENTAMICIN IV
Suspected sepsis AND meningitis:
add CEFOTAXIME to any current antibiotics or commence AMOXICILLIN, CEFOTAXIME, and GENTAMICIN
MENINGITIS abx choice when causative pathogen unknown
AMOXICILLIN & CEFOTAXIME
MENINGITIS abx choice - confirmed gram -ve infection
CEFOTAXIME (stop amoxicillin)
for at least 21 days
MENINGITIS - group b strep
abx choice
BENZYLPENICILLIN (for at least 14 days) plus GENTAMICIN (for 5 days)
Group B strep septicaemia
abx choice
BENZYLPENICILLIN (stop gentamicin)
for at least 10 days
Hypoxic-ischaemic encephalopathy: consequences
Permanent damage to the brain —> Cerebral palsy
Sever HIE —> death
Hypoxic-ischaemic encephalopathy: CAUSES
Anything that leads to asphyxia
- maternal shock
- intrapartum haemorrhage
- Prolapsed cord, causing compression of the cord during birth
- nuchal cord, cord wrapped around baby’s neck
Hypoxic-ischaemic encephalopathy: staging system
SARNAT STAGING
HIE: THERAPEUTIC HYPOTHERMIA
Baby cooled in neonatal ICU - target 33-34 degrees
- aim is to reduce inflammation and neurone loss after the acute hypoxic injury to reduce risk of neurological condition
Continued for 72 hours
Then carefully warmed over 6 hours
Neonatal jaundice causes: INCREASED PRODUCTION
Haemolytic disease of the newborn ABO incompatibility Haemorrhage Intraventricular haemorrhage Cephalo-Haematoma Polycythaemia Sepsis and DIC G6PD deficiency
Neonatal jaundice causes: DECREASED CLEARANCE
Prematurity Breast milk jaundice Neonatal cholestasis Extra-hepatic biliary atresia Endocrine disorders (hypothyroid and hypopituitary) Gilbert syndrome
Consequence of high bilirubin levels
Kernicterus - permanent damage to the nervous system as bilirubin can cross BBB
—> Cerebral palsy, learning disability, deafness
Prematurity: definition
Prematurity = birth before 37 weeks gestation
Under 28 weeks: EXTREME PRETERM
28-32 weeks: VERY PRETERM
32-37: MOD TO LATE PRETERM
Prematurity: associations
Social deprivation Smoking Alcohol Drugs Overweight or underweight mother Maternal co-morbidities Twins Personal or FH of prematurity
Options for delaying birth
Prophylactic vaginal progesterone - suppository in the vagina to discourage labour
Prophylactic cervical cerclage - suture in cervix to hold it closed
Options to improve outcomes in suspected preterm labour
Tocolysis with NIFEDIPINE: CCB which suppresses labour
Maternal CORTICOSTEROIDS: offered before 35w to reduce neonatal morbidity and mortality
IV MAGNESIUM SULPHATE: offered before 34 weeks to help protect baby’s brain
Delayed cord clamping or cord milking: increase circulating blood volume and haemoglobin in the baby
Prematurity: issues in early life
Respiratory distress syndrome Hypothermia Hypoglycaemia Poor feeding Apnoea and bradycardia Neonatal jaundice Intraventricular haemorrhage Retinopathy of prematurity Immature immune system/infection
Prematurity: Long term effects
Chronic lung disease of prematurity Learning/behavioural difficulties Hearing/visual difficulties Cerebral palsy Susceptibility to infections
Apnoea of prematurity: causes
Immaturity of autonomic nervous system (controls HR and RR)
Apnoea of prematurity: incidence
Occur in almost all babies less than 28 weeks
Incidence decreases with increased gestational age
Apnoea of prematurity: definition
Breathing stops for more than 20 seconds
Or shorter periods with oxygen desaturation or bradycardia
Often accompanied by bradycardia
Apnoea of prematurity: management
Apnoea monitors
Tactile stimulation to prompt baby to start breathing
IV CAFFEINE can be used to prevent apnoea and bradycardia in babies with recurrent episodes
Retinopathy of prematurity: when does retinal BV development occur
Starts around 16 weeks and complete by 37-40 weeks
Retinopathy of prematurity: cause
Vessel formation stimulated by hypoxia (normal condition in retina during pregnancy)
- this stimulant removed when exposed to higher oxygen concentrations particularly supplementary oxygen
When hypoxic environment reoccurs - retina responds by producing XS BV (neovascularisation) as well as scar tissue
Abnormal BV may regress and leave retina without a blood supply
Scar tissue may cause retinal detachment
Retinopathy of prematurity: Assessment
Retina divided into 3 zones
- Optic nerve and macula
- Edge of zone 1 to ora serrated (pigmented border between retina and ciliary body)
- Ora serrata
Stage 1 (slightly abnormal vessel growth) —> stage 5 (complete retinal detachment)
“Plus disease” describes additional findings e.g. tortuous vessels and hazy vitreous humour
Retinopathy of prematurity: Screening
Babies born before 32 weeks or under 1.5kg should be screened for ROP
Screen at 30-31 weeks in babies born under 27 weeks
4-5 weeks of age in babies born after 27 weeks
Screening at least every 2 weeks and stop once vessels enter zone 3 (usually 36 weeks gestation)
Retinopathy of prematurity: Treatment
Systematically targeting areas of the retina to stop new BV developing
TRANSPUPILLARY LASER PHOTOCOAGULATION - to halt and reverse neovascularistion
CRYOTHERAPY
Injections of VEGF INHIBITORS
Surgery - if retinal detachment occurs
Respiratory distress syndrome: CXR appearance
“Ground glass” appearance
Respiratory distress syndrome: Pathophysiology
Inadequate surfactant —> high surface tension within alveoli
—> atelectasis (lung collapse)
—> hypoxia, hypercapnia, resp distress
Respiratory distress syndrome: Management
Antenatal steroids (dexamethasone) - mothers with expected or confirmed preterm labour to increase surfactant
- intubation and ventilation
- endotracheal surfactant delivered to the lungs
- continuous positive airway pressure (CPAP)
- supplementary oxygen (aim for between 91-95% stats)
Respiratory distress syndrome: short term complications
Pneumothorax Infection Apnoea Intraventricular haemorrhage Pulmonary haemorrhage Necrotising enterocolitis
Respiratory distress syndrome: Long term complications
Chronic lung disease of prematurity
Retinopathy of prematurity
Neurological, hearing or visual impairment
Necrotising enterocolitis: what it it?
Disorder in preterm neonates
Part of bowel becomes necrotic
LIFE THREATENING EMERGENCY
Death of bowel —> bowel perforation —> peritonitis —> shock
Necrotising enterocolitis: risk factors
V low birth weight / v premature
Formula feeds (less common in breast fed babies)
Sepsis
Respiratory distress and assisted ventilation
Patient ductus arteriosus and other congenital heart defects
Necrotising enterocolitis: Presentation
Intolerance to feeds Vomiting green bile Generally unwell Distended, tender abdomen Absent bowel sounds Blood in stools
If perforation: severely unwell and shock
Necrotising enterocolitis: X-ray findings
Dilated loops of bowel
Bowel wall oedema
Pneumatics is interstinalis (gas in bowel wall)
Pneumoperitoneum - indicates perforation
Gas in portal veins
Necrotising enterocolitis: Management
NBM IV fluids TPN Antibiotics NG tube - to drain fluid and gas from stomach and intestines SURGICAL EMERGENCY Bowel may need to be removed
Neonatal abstinence syndrome: what is it
Neonates of mothers that used substances during pregnancy
Neonatal abstinence syndrome: substances that cause NAS
Opiates Methadone Benzodiazepines Cocaine Amphetamines Nicotine and cannabis Alcohol SSRI antidepressants
Neonatal abstinence syndrome: Management
Babies kept on monitoring for at least 3 days with NAS chart
Urine sample to test for substances
Oral MORPHINE SULPHATE - for opiate withdrawal
Oral PHENOBARBITONE - for non-opiate withdrawal
Then gradually weaned off
*SSRI withdrawal doesn’t typically require medical treatment
Neonatal abstinence syndrome: additional considerations
Test for HepB, HepC and HIV
Safeguarding and social services
Safety net advice for re admission if withdrawal signs and symptoms occur
Support mother to stop using substances
Check suitability for breast feeding in mothers
Feta alcohol syndrome: characteristics
Microcephaly (small head)
Thin upper lip
Smooth flat philtrum (groove between nose and upper lip)
Short palpable disuse (short horizontal distance from one side of eye to the other)
Learning & behavioural difficulties
Hearing and visual problems
Cerebral palsy
Congenital rubella syndrome: features
Congential cataracts
Congenital heart disease (PDA, pulmonary stenosis)
Learning disability
Hearing loss
Congenital varicella syndrome
1% of cases of chickenpox in pregnancy - infection in the first 28 weeks.
Features:
- feral growth restriction
- microcephaly, hydrocephalus and learning disability
- Scars and significant skin changes following the dermatomes
- Limb hypoplasia (under developed limes)
- Cataracts and inflammation in the eye (chorioretinitis)
Varicella zoster virus infection during pregnancy: management
If mother not immune they may be given prophylaxic IV varicella immunoglobulins within 10 days of exposure
If infected during pregnancy - may be given oral aciclovir if they present within 20 hours and are more than 20 weeks gestation
Infection during pregnancy can lead to fatal varicella syndrome and more severe infection in the mother (pneumonitis, hepatitis, encephalitis)
Congenital cytomegalovirus
Fetal growth restriction Microcephaly Hearing loss Vision loss Learning disability Seizures
Congential Zika Syndrome
Sudden infant death syndrome
Usually in first 6 months of life Risk factors: - prematurity - low birth weight - smoking during pregnancy - male gender (slightly higher)
Measures to minimise risk of SIDS
Put baby on back when not directly supervised
Keep baby head uncovered
Place feet at foot of bed to prevent them sliding under blancket
Keep cot clear of lots of toys and blankets
Maintain comfortable room temp
Avoid smoking
Avoid co-sleeping
