Paeds - Neonatology Flashcards
1
Q
Neonatal Resuscitation
Pathophysiology
Risk Factors for Requiring Resuscitation
Principles of Neonatal Resuscitation
A
- ) Pathophysiology - extended hypoxia upon delivery can cause the baby to become unconscious
- hypoxia –> anaerobic respiration and bradycardia
- hypoxia –> ↓respiratory effort and ↓consciousness
- extended hypoxia to the brain leads to hypoxic-ischaemic encephalopathy (HIE) –> cerebral palsy - ) Risk Factors for Requiring Resuscitation
- fetal: pre-term, IUGR, oligo/polyhydramnios, twins, serious congenital abnormality
- maternal: infection, gestational HTN, pre-eclampsia, GDM, high BMI, short stature, lack of antenatal steroids
- delivery: C-section, vaginal breech, instrumental delivery
- intrapartum: fetal compromise, meconium-stained amniotic fluid, significant bleeding, general anaesthesia - ) Principles of Neonatal Resuscitation
- warm the baby: dry baby ASAP, warm delivery room, manage under a heat lamp, <28wkers are placed in a plastic bag while still wet
- calculate the APGAR Score: at 1/5/10 mins as an indicator of progress in the first minutes after birth
- stimulate breathing: vigorous drying with a towel, keep head in a neutral position to keep the airway open, check airways if gasping or unable to breath
2
Q
Method of Resuscitation
Inflation Breaths
Chest Compressions
APGAR Score
Delayed Umbilical Cord Clamping
A
- ) Inflation Breaths
- inflation breaths are given when the neonate is gasping or not breathing despite the initial simulation
- 2 cycles of 5 inflation breaths (last 3s each) can be given to stimulate breathing and heart rate
- if there is no response and the heart rate is low, 30 seconds of ventilation breaths can be used
- air is used in term or near-term babies whilst a mix of air and oxygen is used in pre-term babies
- O2 sats are monitored throughout, aiming for a gradual rise in oxygen saturations, not exceeding 95%. - ) Chest Compressions - start chest compressions if HR remains <60 despite resus and inflation breaths
- performed at a 3:1 ratio with ventilation breaths
- severe situations: consider intubation and IV drugs, consider therapeutic hypothermia in possible HIE - ) APGAR Score - scoring between 0-10
- assesses Appearance (skin colour), Pulse, Grimace (response to stimulation), Activity (tone), Respiration - ) Delayed Umbilical Cord Clamping
- uncompromised neonates should have delayed UC clamping of at least 60 seconds following birth
- placental transfusion: this provides time for fetal blood in the placenta to enter the baby’s circulation
- neonates requiring resuscitation should have their UC clamped sooner to prevent delays in getting the baby to the resuscitation team
3
Q
Normal Care After Birth
Immediately After Birth
Out of the Delivery Room
Blood Spot Screening
A
- ) Immediately After Birth
- dry the baby, keep baby warm w/ hat and blankets
- provide skin to skin contact: warms and calms baby, improves mother-baby interaction and breastfeeding
- clamp the umbilical cord (delayed clamping in most)
- label the baby, measure weight and height
- administer IM vitamin K: help prevent bleeding (esp intracranial, umbilical stump, GI) as all babies have vitK deficiency (not produced in GI as there are no bacteria) - ) Out of the Delivery Room
- initiate feeding as soon as the baby is alert enough
- first bath is delayed until this baby is warm and stable,
- newborn exam w/in 72hrs, repeated by GP at 6-8wks
- blood spot (Guthrie’s) test in 5 days
- hearing test: otoacoustic emission test w/in 4-5wks, auditory brainstem response test if ^^ is abnormal OR are at risk for hearing loss due to various factors, such as family history - ) Blood Spot Screening - a screening test for 9 congenital conditions taken on day 5 (latest day 8)
- results take 6-8 weeks to come back
- cystic fibrosis (↑immunoreactive trypsinogen/IRT)
- hypothyroidism, sickle cell disease
- phenylketonuria (PKU), homocysteinuria (HCU)
- medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
- maple syrup urine disease (MSUD)
- isovaleric acidaemia (IVA)
- glutaric aciduria type 1 (GA1)
4
Q
Newborn Examination
Oxygen Saturations
Head Examination
Examination of Other Body Parts
Reflexes
A
- ) Oxygen Saturations
- check pre-ductal (right hand) and post-ductal (foot) sats, should be >96% and <2% difference in both
- abnormal sats require further investigations
- >2% difference in sats suggests a duct-dependent congenital heart disease - ) Head Examination
- general appearance: size, shape, head circumference, dysmorphology, facial injury
- scalp: fontanelles, sutures, caput succedaneum, cephalohaematoma
- ears: skin tags, low set ears and asymmetry
- eyes: red reflex, squints, epicanthic folds (Down’s), purulent discharge could indicate infection
- mouth: cleft lip/palate or tongue-tie, suckling reflex - ) Examination of Other Body Parts
- shoulders and arms: symmetry/clavicle, Erb’s palsy, brachial/radial pulses, palmar creases, digits
- chest: symmetry, SATS, respiratory distress, noises, heart sounds, breath sounds
- abdomen: shape, umbilical stump, palpation
- genitals: sex, testes descent, hernias, hydroceles, hypospadias, epispadias and urination, patent anus
- legs: observe, Barlows and Ortolani’s (DDH),
- back: curvature, spina bifida, pilonidal sinus
- skin: acne, erythema toxicum, moles, milia, cradle cap, haemangiomas, desquamation, port-wine stains, Mongolian blue spot, transient pustular melanosis - ) Reflexes
- moro: limbs extend when rapidly tipped backwards
- suckling: suck with a finger in the mouth
- rooting: tickling the cheek –> turn towards stimulus
- grasp: grasp a finger placed in the palm
- stepping: stepping motion when feet touch surface
5
Q
Birth Injuries
Caput Succedaneum Cephalohaematoma Facial Paralysis Erb's Palsy Clavicular Fracture
A
- ) Caput Succedaneum - a collection of fluid on the scalp, due to pressure to a specific area of the scalp during a traumatic, prolonged or instrumental delivery
- fluid is above the periosteum, therefore the lump can cross the suture lines of the skull
- there is no (or mild) discolouration of the skin
- resolves within a few days without any treatment - ) Cephalohaematoma - traumatic subperiosteal haematoma due to damage to blood vessels
- blood is below the periosteum, therefore the lump does not cross the suture lines of the skull
- blood can cause discolouration of the skin
- resolves within a few months without any treatment
- the risk of anaemia and jaundice is because as the blood breaks down, bilirubin can be released - ) Facial Paralysis - facial nerve injury –> facial palsy
- often associated with a forceps delivery
- function normally returns spontaneously within a few months, if not, consider required neurosurgical input - ) Erb’s Palsy - C5/6 nerve injury due to shoulder dystocia, traumatic or instrumental delivery and LGA
- weakness of shoulder abduction and external rotation, arm flexion and finger extension
- ‘waiter’s tip’: internally rotated shoulder, extended elbow, flexed wrist (pronated), lack of movement
- function normally returns spontaneously within a few months, if not, consider required neurosurgical input - ) Clavicular Fracture - due to shoulder dystocia, traumatic/instrumental delivery and large birth weight
- movement: reduced or asymmetrical, painful
- shoulder asymmetry, the affected shoulder is lower
- confirmed w/ US or X-Ray conservative management (immobilisation), nerve injury/palsy is main complication
6
Q
Neonatal Sepsis
Pathophysiology Criteria for Investigation/Treatment Differential Diagnoses Investigations Management
A
- ) Pathophysiology - sepsis w/in first 48-72hrs of life
- the spread of GBS from maternal chorioamnionitis and E.coli are the most common causes
- other organisms: S.auerus, Listeria, Klebsiella
- low birth weight and prematurity are risk factors for increased mortality - ) Criteria for Investigation/Treatment
- 1 red flag risk factor or clinical indicator
- 2 non-red flag risk factors or clinical indicators
- if only 1 non-red flag sign, monitor obs for 24 hours - ) Differential Diagnoses
- respiratory distress: TTN, RDS (esp if pre-term), meconium aspiration (can cause a rise in CRP)
- HDN: can cause neonatal jaundice in the first 24hrs - ) Investigations
- bloods: FBC, CRP (repeat after 18-24hrs), cultures
- blood gases: metabolic acidosis very concerning
- relevant swabs/cultures e.g. urine, eye discharge
- LP: if strong suspicion of sepsis or >10 rise in CRP, ideally before starting abx (or ASAP after abx) - ) Management
- empirical abx: IV benzylpenicillin + IV gentamicin
- duration: 7-10d (positive cultures), 14d (positive CSF), 5d if negative cultures but a rise in CRP
- can consider stopping the antibiotics at 36 hours if:
- blood culture is negative, weak initial suspicion, baby’s clinical condition is reassuring (inc CRP)
7
Q
Signs Suggestive of Neonatal Infection
Red Flag Signs/Risk Factors
Other Risk Factors for Neonatal Infection
Other Signs of Neonatal Infection
A
- ) Red Flag Signs/Risk Factors
- respiratory distress starting >4hrs after birth (most common presentation, roughly 85% of neonates)
- seizures, haemodynamic shock
- mechanical ventilation required in a term baby
- suspected maternal sepsis treated w/ Abx (intra or postpartum)
- suspected/confirmed infection in a co-twin - ) Other (Minor) Risk Factors for Neonatal Infection
- suspected chorioamnionitis/intrapartum fever >38°C
- maternal GBS colonisation (urine MC+S or HVS)
- invasive GBS infection in a previous baby
- PROM, PPROM for > 18 hours - ) Other Signs of Neonatal Infection
- unexplained abnormal temp (<36°C or >38°C)
- localised signs of infection (e.g. skin or eye)
- feeding difficulties/intolerance (refusal, vomiting etc)
- abnormal HR, hypoxia, respiratory distress, apnoea
- oliguria, metabolic acidosis, hypo/hyperglycaemia
- altered behaviour, muscle tone (floppiness)
- jaundice w/in 24hrs of birth, signs of encephalopathy
- need for CPR, mechanical ventilation in a pre-term
- persistent fetal circulation (PPHTN)
- excessive bleeding, thrombocytopenia, INR >2
8
Q
Hypoxic Ischaemic Encephalopathy
Pathophysiology
Clinical Features
Management
Therapeutic Hypothermia
A
- ) Pathophysiology - prolonged hypoxia to the brain during birth causing ischaemic brain damage
- HIE can cause permanent brain damage causing cerebral palsy and if severe, can even cause death
- causes: maternal shock, intrapartum haemorrhage, cord compression, nuchal cord (wrapped around neck) - ) Clinical Features - grades uses Sarnat staging
- HIE is suspected in hypoxic events, acidosis on umbilical artery blood gas, poor APGAR scores, features of HIE, or evidence of multi-organ failure
- mild: poor feeding, irritability, hyper-alertness, resolves w/in 24hrs and has a normal prognosis
- mod: poor feeding, lethargy, hypotonia, seizures, can take weeks to resolve, up to 40% get cerebral palsy
- severe: ↓consciousness, apnoeas, flaccid and areflexia, up to 50% mortality, 90% get cerebral palsy - ) Management - by neonatology specialists
- supportive: resuscitation, ventilation, circulatory support, nutrition, treatment of seizures
- F/U: assess development and support any disabilities - ) Therapeutic Hypothermia - used to reduce the risk of developing cerebral palsy and other complications
- active cooling to 33-34°C using cooling blankets/hats
- done for 72hrs, then slowly warmed `over 6hrs
- reduces inflammation and reduces metabolic activity
9
Q
Pathophysiology of Neonatal Jaundice
Physiological Jaundice
Pathological Jaundice
Jaundice due to Increased Bilirubin Production
Jaundice due to Reduced Bilirubin Clearance
Prolonged Jaundice
A
- ) Physiological Jaundice - starts on day 2/3, peaks at day 5 and is usually resolved by day 10
- due to ↑RBCs/Hb in a neonate which breakdown easier causing ↑bilirubin, the immature liver cannot process it all as it’s was done by the placenta in utero - ) Pathological Jaundice - jaundice which requires treatment or further investigation
- jaundice w/in first 24hrs, prolonged jaundice
- haemolytic disease, bilirubin > phototherapy threshold
- unwell neonate: jaundice becomes a sign of infection - ) Jaundice due to Increased Bilirubin Production
- haemolysis: HDN/rhesus, ABO incompatibility
- neonatal sepsis and DIC
- haemorrhage (inc intraventricular), cephalohaematoma
- polycythemia, G6PDH deficiency - ) Jaundice due to Reduced Bilirubin Clearance
- prematurity: immature liver worsens physiological
- breast milk jaundice: components of breast milk inhibit the ability of the liver to process bilirubin, the baby is well and may take 1.5 to 4 months to resolve
- neonatal cholestasis, extrahepatic biliary atresia
- metabolic: hypothyroid/pituitarism, galactosaemia
- Gilbert syndrome - ) Prolonged Jaundice - >14 days in term infants OR >21 days in preterm infants, causes include:
- breast milk jaundice, hypothyroidism/hypopituitarism, biliary atresia, G6PDH deficiency, galactosaemia, choledhocal cyst
10
Q
Clinical Management of Neonatal Jaundice
Clinical Features
Investigations
Phototherapy
Kernicterus
A
- ) Clinical Features
- jaundiced: yellow colouring of skin, sclera, gums
- drowsy: difficult to rouse, difficulty feeding
- neurological: altered muscle tone, seizures
- other: signs of infection, poor urine output, abdo mass or organomegaly, black stools (not changing colour) - ) Investigations - infants jaundiced to the naked eye
- transcutaneous bilirubinometer (TCB): used most of the time unless when you have to use serum bilirubin
- serum bilirubin: used if <35wks, <24hr old, TCB >250
- FBC, blood groups and direct Coombs test
- others: sepsis screen, U+Es, LFTs, TFTs, consider TORCH screen, G6PDH deficiency - ) Phototherapy - use depends on bilirubin level
- converts unconjugated bilirubin into isomers that can be excreted in the bile and urine (don’t need liver)
- started if level is above the phototherapy threshold
- stop when >50 below threshold and repeat in 12-18hrs to check for rebound hyperbilirubinemia
- if <50 below the threshold, repeat in 18-24hrs
- alternatives: exchange transfusion (if signs of encephalopathy), IVIG in haemolysis (HDN/ABO) - ) Kernicterus - main complication
- bilirubin is neurotoxic and can accumulate in the CNS grey matter causing irreversible neurological damage
- affects basal ganglia causing dyskinetic cerebral palsy (shows extrapyramidal signs)
- can also cause learning disabilities and deafness
11
Q
Prematurity
Definition
Risk Factors
Complications in Early Life
Complications in Later Life
A
1.) Definition - birth <37wks, <28w is extreme, 28-32w is very preterm and 32-37w is mod-late pre-term
- ) Risk Factors
- smoking, alcohol, drugs, social deprivation
- twins, personal or FH of prematurity
- maternal co-morbidities (inc over/underweight) - ) Complications in Early Life
- respiratory distress syndrome, apnoea and bradycardia,
- hypothermia, hypoglycaemia, poor feeding
- intraventricular haemorrhage (IVH)
- neonatal jaundice (immature liver), infection (immature immune system) e.g. sepsis or NEC
- retinopathy of prematurity: affects <32wkers, abnormal development of retinal blood vessels can lead to scarring, retinal detachment and blindness - ) Complications in Later Life
- chronic lung disease of prematurity (CLDP)
- ↑susceptibility to infections, esp respiratory infection
- learning and behavioural difficulties, hearing and visual impairment, cerebral palsy
12
Q
Respiratory Distress Syndrome
Pathophysiology
Clinical Features
Management
Complications
A
1.) Pathophysiology - inadequate surfactant leads to inadequate gas exchange –> hypoxia, hypercapnia
- ↓surfactant –> ↑surface tension within alveoli making it more difficult to expand –> atelectasis (lung collapse)
- very common in infants <32wks gestation
- an alternative rare cause is a diaphragmatic hernia where bowel loops are in the thoracic cavity
- risk factors: male sex, maternal diabetes, C-section,
second born of premature twins
- ) Clinical Features - signs of respiratory distress
- raised respiratory rate, cyanosis (due to low sats)
- use of accessory muscles: SCM, abdo, intercostal
- intercostal and subcostal recessions, inflated chest
- nasal flaring, head bobbing, tracheal tugging
- abnormal airway noises: inspiratory crackles, expiratory wheeze, grunting, stridor
- CXR: ‘ground-glass’ appearance - ) Management
- prevention: IM antenatal steroids + IV magnesium during labour for mothers to ↑surfactant production
- 1°: CPAP via a nasal mask to help keep lungs inflated
- supplementary O2 to keep SATS between 91-95% (can take 10mins to reach adult levels)
- I+V to fully assist breathing if severe, can give endotracheal surfactant (Curosurf) into the lungs
- caffeine to help breath more effectively
- breathing support is gradually stepped down until the baby can support themselves in just air
- infant requiring oxygen therapy after 36wks gestation suggests bronchopulmonary dysplasia (CLDP) - ) Complications
- short-term: pneumothorax, infection, apnoea, IVH, pulmonary haemorrhage, necrotising enterocolitis
- long-term: chronic lung disease of prematurity, retinopathy of prematurity, neurological, hearing and visual impairment
13
Q
Apnoea of Prematurity
What is It?
Pathophysiology
Management
A
- ) What is It? - where breathing stops spontaneously for >20secs OR shorter if there are O2 desaturations
- often accompanied by a period of bradycardia
- lasts >20s OR periods of O2 desats or bradycardia
- very common/normal in premature neonates, usually indicates underlying pathology in term infants - ) Pathophysiology - due to immaturity of autonomic nervous system that controls respiration and heart rate
- often a sign of a developing illness, such as:
- airway obstruction, GORDs, infection, anaemia, CNS pathology, neonatal abstinence syndrome - ) Management
- premature babies are attached to apnoea monitors
- tactile stimulation is used to prompt the baby to restart breathing whenever apnoea is occurring
- IV caffeine for prevention if the apnoea is recurrent
- often settles as the baby grows and develops
14
Q
Retinopathy of Prematurity
Pathophysiology
Screening
Treatment
A
- ) Pathophysiology - blood vessel formation in the retina is stimulated by hypoxia, so early O2 exposure leads to neovascularization and scar tissue formation
- this can leave the retina without a blood supply and the scar tissue can cause retinal detachment
- affects preterm (typically <32wks) and LBW babies - ) Screening - monitoring of the development of retinal vessels and looking for any additional (plus) disease
- done for babies <32wks or under 1.5kg
- done at 4-5wks of age for babies born after 27wks OR 3-4wks of age for babies born before 27 weeks
- screening occurs at least every 2wks and until retinal vessels enter zone 3 (often around 36wks) - ) Treatment - prevent neovascularization
- 1°: transpupillary laser photocoagulation
- other: cryotherapy, intravitreal VEGF inhibitors, may require surgery if retinal detachment occurs
15
Q
Necrotising Enterocolitis (NEC)
Pathophysiology
Clinical Features
Differential Diagnosis
A
1.) Pathophysiology - not yet entirely understood
- immune response to an infant’s gut microbiota where:
part of the bowel becomes necrotic which can lead to bowel perforation –> peritonitis –> shock –> death
- main risk factor is prematurity or very LBW (VLBW)
- other RF: formula feeding, resp distress, assisted ventilation, sepsis, PDA (+other heart diseases), IUGR, polycythaemia, exchange transfusion, hypoxia
- ) Clinical Features
- feeding intolerance, vomiting (often w/ green bile)
- abdominal distension/tenderness, blood in stools
- ↓bowel sounds, erythema, palpable bowel loops
- non-GI: apnoea, bradycardia and decreased peripheral perfusion, temperature instability, lethargy - ) Differential Diagnosis - non-specific so broad DDx
- medical: neonatal sepsis, infectious enterocolitis, reflux
- surgical: Hirschsprung’s, intussusception, intestinal malrotation or volvulus, spontaneous intestinal perforation
