Neonatology Flashcards
Definition of prematurity?
Before 37 weeks.
Extreme - <28 weeks
Very preterm - 28-32 weeks
Moderate to late preterm - 32-37 weeks
Causes of prematurity?
Multiple pregnancies
Infections - group B strep, UTI, vaginal infection, foetal/placental infection, pre-eclampsia, cervical incompetence, placental abruption, PPROM, placenta praaevia, chronic maternal conditions - DM, HTN, 40% have no identifiable cause.
Risk factors for prematurity?
Previous preterm delivery
Multiple pregnancy
Smoking and illicit drug use in pregnancy
Being under or overweight in pregnancy
Early pregnancy (within 6 months of previous pregnancy)
Problems involving cervix, uterus or placenta, including infection.
Certain chronic conditions such as DM and HTN.
Physical injury/trauma.
Investigations of prematurity?
Blood gas FBC - preterm infants at high risk of infection, thrombocytopenia and anaemia U&Es, CRP Blood culture Blood group, Direct Coombs Test/Direct Antiglobulin Test. Chest XR - respiratory distress AXR - assess signs of NEC. Crainal USS.
Management of prematurity?
Delivery of extreme preterm infant should be planned for hospital with tertiary level neonatal unit.
Administer course of antenatal steroids
Magnesium sulphate for neuroprotection to baby.
Resuscitation:
<23 weeks - should not be performed
23 - 23+6 - best interest of baby
24 - 24+6 - resus commenced unless baby thought to be severely compromised.
After 25 weeks - appropriate to resuscitate and start intensive care.
Long term respiratory complications of prematurity and management?
Respiratory distress syndrome
Surfactant deficient lung disease
Chronic lung disease/bronchopulmonary dysplasia
Recurrent apnoea
Surfactant administration, endotracheal intubation, mechanical ventilation.
CPAP, high flow oxygen, nasal cannula low flow oxygen, ambient incubator oxygen, caffeine administration.
Long term cardiovascular complications of prematurity and management?
Hypotension
Perfusion abnormalities
PDA
Inotropes
Fluid management
Ibuprofen
Ligation of PDA
Long term neurological complications of prematurity?
Intraventricular haemorrhage Seizures Post haemorrhage ventricular dilatation Neurodevelopmental delay Cerebral palsy
CrUSS
Regular head circumference measurements
Admin of AED
Follow up with neuro.
Long term gastrointestinal complications of prematurity?
Immature gut causing feed intolerance, necrotising enterocolitis (NEC).
TPN, NG feed, breast milk, abx, surgical review if NEC.
Long term renal/electrolyte complications of prematurity?
Immature renal function
Fluid and electrolyte balance monitoring. Catheterisation if indicated.
Long term metabolic complications of prematurity?
Jaundice
Hyperglycaemia
Hypoglycaemia
Inborn errors of metabolism
Phototherapy, exchange transfusion, insulin infusion, increase concentration or volume of glucose given via central IV access, doing heel-prick test.
Long term infection/immune complications of prematurity?
Sepsis
Increased risk of infection due to central lines and multiple procedures
Septic screen
IV abx
Long term skin complications of prematurity?
Immature skin barrier leading to increased insensible losses and increased risk of infection
Nursing in warm, humid incubator, aseptic non-touch technique during procedures.
Long term thermoregulation complications of prematurity?
Immature thermoregulation
Nursing in warm humid incubator, cot warmer, awareness of exposure whilst performing procedures and examinations.
Long term complications of eyes of prematurity?
Retinopathy of prematurity
Avoid excessive oxygen exposure.
Screening for retinopathy of prematurity by ophthalmology team, laser treatment if indicated.
When do anterior and posterior fontanelles close?
Anterior - 9-18 months
Posterior - 6-8 weeks
What are the key changes to respiratory system when child is born?
In utero, airways filled with amniotic fluid. Oligohydramnios can lead to small, underdeveloped lungs.
Amniotic fluid removed by squeezing of thorax during vaginal delivery.
There is also reduced production and increased absorption during labour and after birth.
Surfactant lines alveoli and reduces surface tension. Facilitates lung expansion and first breath.
Surfactant produced between 24 to 34 weeks gestation.
What are the key changes to CVS when baby is born?
Foetal circulation - pulmonary pressure exceeds systemic pressure causing right to left shunt through foramen vale and ductus arteriosus. Allows bypass of lungs.
At birth, these relationships change:
- systemic pressure increases with clamping of umbilical vessels
- pulmonary pressure reduced as lungs expand (oxygen increase and prostaglandin mediated vasodilation).
Foramen vale and ductus arteriosus close functionally after birth due to changes in pressure.
Key features of GI system at birth?
35 weeks gestation, develop coordination to latch on/suck from breast/bottle
Meconium usually passed at day 1
With effective feeding meconium is replaced by yellow stool by day 3-4
Immaturity of liver enzymes responsible for conjugation of bilirubin is responsible for physiological jaundice which can occur from day 2 of life.
Key features of GU system at birth?
Infant should void within 24 hours of life.
Often occurs during delivery so may go unnoticed.
Renal concentrating ability is reduced in neonates.
Key features of haem/immunity at birth?
Neonates have faetal Hb which has high affinity for oxygen.
Neonates have impaired neutrophil reserves, reduced phagocytosis, reduced complement, low IgG.
Maternal IgA crosses the placenta and are found in breast milk, providing some immune protection.
Key features of CNS at birth?
Myelination does not complete until 2 years of life.
Babies are born with primitive reflexes
Newborns sleep for 16-20 hours each day.
Apgar score factors?
Pulse Respiratory effort Colour Muscle tone Reflex/irritability
Apgar score ranges?
0-3 - very low
4-6 - moderately low
7-10 baby is in good state
Breast feeding in first few days of life?
Colostrum produced by breast in first few days, then replaced by milk.
Colostrum has high protein and Ig content.
Breast feeding intervals gradually lengthen from 2-3 hours to approx 4-hourly schedule.
What are contraindications to breast feeding?
What drugs are CI?
Galactosaemia
HIV
Aspirin Carbimazole Methotrexate Sulfonylureas Cytotoxic drugs Amiodarone Psychiatrics drugs - lithium, benzodiazepines Abx - ciprofloxacin, tetracycline, chloramphenicol, sulphonamides.
Advantages to breast feeding?
Reduced infection, atopy, constipation, maternal breast cancer, sudden infant death syndrome. Convenient, promotes bonding between mum and baby.
Disadvantages to breast-feeding?
Volume of intake uncertain.
Transmission of some drugs.
Nutrient deficiencies (vit D, vit K).
Failure to establish breast feeding results in emotional upset and guilt.
Difficulties with breastfeeding?
Sleepy baby
Difficulty latching
Cracked nipples
Poor milk supply
Problems with bottle feeding?
Incorrect reconstitution -> electrolyte abnormalities.
Over feeding -> reflux and vomiting
Inadequate sterilisation -> gastroenteritis.
Foetal causes of IUGR?
Symmetrical
Chromosomal disorders
Congenital infections
Maternal causes of IUGR?
Asymmetrical Pre-eclampsia Increased maternal age Smoking Multiple pregnancy
Risk of IUGR?
Death Hypoxia Hypothermia Hypoglycaemia (low fat and glycogen stores) Polycythaemia NEC.
Management of Group B strep
Antepartum maternal IV benzylpenicillin to women in preterm labour or with previous GBS pregnancy.
High vaginal swab offered at 35-37 weeks to detect GBS.
Women with pyrexia during labour given IV benzylpenicillin
At-risk neonates are given benzylpenicillin.
Risk factors for neonatal jaundice?
Gestational age <38 weeks (premature babies).
Small for date babies.
Previous sibling with neonatal jaundice requiring phototherapy.
Mothers intention to breastfeed exclusively.
Visible jaundice in first 24 hours of life.
What is physiological jaundice?
Normal rise in bilirubin, causing mild yellowing of skin and sclera from day 2-7 and usually resolves completely by 10 days.
Baby remains otherwise healthy and well.
Causes of neonatal jaundice?
First 24 hours - pathological
- excessive haemolysis - rhesus incompatibility, ABO incompatibility, G6PD deficiency, pyruvate kinase deficiency, hereditary spherocytosis.
2 days to 2 weeks:
- physiological
- breast milk jaundice
- UTI
- Excess haemolysis, bruising or polycythaemia
Prolonged jaundice >14 days - always investigate biliary atresia needs urgent surgery.
- uncongugated - breast milk jaundice, UTI, excess haemolysis
- conjugated - biliary atresia, neonatal hepatitis, alpha-1 antitrypsin deficiency.
Features of rhesus incompatibility?
Haemolysis, anaemia, jaundice
Severe cases - foetal hydrops and death.
Rhesus status now screened antenatally, and anti-D Ig given to rhesus neg mothers.
Features of ABO incompatibility?
Anaemia, jaundice, positive direct antiglobulin test (haemolysis). Less severe than rhesus incompatibility.
Features, investigations and management of biliary atresia?
Destruction or absence of extra hepatic biliary tree.
Rare but life-threatening, so much always investigate prolonged jaundice (urgent surgery).
Prolonged jaundice - dark urine, pale stools.
Failure to thrive as disease progresses due to:
- malabsorption
- enlargement of liver and spleen
Bleeding tendency might develop due to vitamin K deficiency.
Abdominal USS, liver biopsy, cholangiography.
Kasai surgical procedure - ideally <6 weeks.
Prognosis - often requires transplant by aged 20.
Investigations for prolonged jaundice?
Conjugated fraction FBC TFT, LFT, U&E, blood film Blood group of mum and baby Coombs test Urine culture.
Management of neonatal jaundice?
Plot serial bilirubin measurements on a treatment threshold graph within 2 hours in all babies with suspected or obvious jaundice in first 24 hours of life, and when bilirubin levels exceed threshold, initiate treatment.
Phototherapy - blue light breaks down bilirubin in the skin
Exchange transfusion - used if phototherapy doesn’t work - involves removing some of baby’s blood and swapping it with donor blood.
What is kernicterus?
Complication of unconjugated hyperbilirubinaemia.
Can deposit in basal ganglia and cerebellum, causing bilirubin encephalopathy.
Early signs - lethargy and hypotonia
Later signs - seizures, irritability, hypertonia.
What is transient tachypnoea of newborn, features, management?
Delayed resorption of fluid in lungs.
Most common following C sections, possibly due to lung fluid not being squeezed out during passage through birth canal.
CXR shows hyperinflation and fluid in horizontal fissure.
Management - supplementary oxygen may be required.
Usually settles within 1-2 days.
What is surfactant deficiency/RDS of prematurity? Features?
Present at birth or develop over 4 hours
Tachycardia Tachypnoea Intercostal and subcostal recession Accessory muscles Expiratory grunting Cyanosis/reduced o2 sats. Nasal flare Grunting
Risk factors for surfactant deficiency?
Male sex Diabetic mothers C-section Second born of premature twins Prematurity: - 50% of infants born at 26-28 weeks - 25% of infants born at 30-31 weeks
Investigations and management of surfactant deficiency?
Chest X-ray - ground-glass appearance, indistinct heart border, air bronchogram.
Antenatal management - maternal corticosteroids induce foetal lung maturation.
Foetal management -
- artificial surfactant therapy via ET
- oxygen
Assisted ventilation.
Features and management of chronic lung disease?
RDS babies can develop chronic lung disease, due to need of prolonged assisted ventilation with high pressures and high concentrations of oxygen.
Defined as requiring oxygen beyond 36 weeks corrected gestation age or 28 days of age.
CXR - widespread opacities with patchy translucent areas.
Respiratory support - CPAP, oxygen, mechanical ventilation
Steroids to wean from ventilatory support
Strict nutrition
What is chronic lung disease major risk factor for?
Bronchiolitis - therefore prophylaxis against RSV required - palivizumab.
Name 3 vascular birth marks?
Salmon patches (stork mark) - flat red/pink patches on baby's eyelids, neck or forehead at birth. Most common. Fades within a few months.
Infantile haemangioma (Strawberry birth mark) - Red raised marks. Increase in size first 6 months, then shrinks and disappears around 7 years of age. Only treat if blocks aiways.
Capillary malformation (port wine stain) - flat red purple marks. Face chest and back - usually affects one side of body. Sensitive to hormones, may become more noticeable around puberty, pregnancy and menopause.
Examples of pigmented birth marks?
Cafe-au-lait spots
- coffee coloured. Can have one or two. If more than 6 appear by time child is 5, neurofibromatosis should be excluded.
Mongolian blue spots
- blue-grey or bruised-looking birthmarks, present from birth.
- commonly on dark skinned people. Over lower back or buttocks. Looks like bruise.
Congenital melanocytic nevi (congenital mole)
- large brown/black moles present from birth. Overgrowth of pigmented cells. Becomes smaller and darker. Risk of developing cancer low, but risk increases the larger it is.
Risk factors of birth trauma?
Breech presentation
Cephalopelvic disproportion
Macrosomia
Instrumental delivery
Common birth trauma injuries?
Bruising
Cephalohaematoma
Brachial plexus injury - eg erbs palsy, especially following shoulder dystocia.
Facial palsy - especially following forceps delivery, often resolves spontaneously, may cause feeding difficulties.
Clavicle fracture - most common fracture
Subaponeurotic haemorrhage - rare but life-threatening.
- haematoma between skull periosteum and scalp galea aponeurosis, caused by instrumental delivery. Can result in large volume of blood loss and haemodynamic instability.
Features and management of cephalohaematoma?
Swelling on newborn head, more common following prolonged, difficult deliveries.
Due to bleeding between periosteum and skull -> does not cross suture lines. Parietal region most common.
Develops several hours after delivery and may take up to 3 months to resolve.
Jaundice may occur as Bloods in haematoma gets broken down.
Self limiting, but may require drainage.
Risk factors of congenital abnormalities?
Familial
Low and middle income countries
Possible lack of access to sufficient nutritious foods, alcohol, drugs, poor access to healthcare.
Advanced maternal age
Exposure to pesticides or chemicals in pregnancy.
Maternal infections.
Maternal nutritional status (folate deficiency)
Features of toxoplasmosis?
Ingestion of raw or undercooked meat, or from oocytes in faeces of infected cats.
Transmission more likely if seroconversion occurs later in pregnancy. But more serious disease occurs if transmission in first trimester.
Features: Chorioretinitis Hydrocephalus Asymptomatic Intracranial calcification Neurological damage (including cerebral palsy).
Diagnosis of toxoplasmosis?
Antibody test (IgG passes transplacentally from mum). Neurological exam and ophthalmological exam of retina in at risk neonates.
CT brain with IV contrast or MRI brain.
Management of toxoplasmosis?
Pyrimethamine plus sulfadiazine plus calcium folinate for 12 months.
Features of neonatal rubella?
SNHL Congenital cataracts and glaucoma Congenital heart disease - PDA, pulmonary stenosis Growth retardation Hepatosplenomegaly Salt and petter chorioretinitis Cerebral palsy
Diagnosis of rubella?
Always consider in growth-restricted neonates with SNHL.
IgM antibodies are raised in women recently exposed to virus.
Management of rubella?
No longer screened at booking. If mother tested and has no immunity, should be advised to keep away from people who have rubella.
Non-immune mothers should be offered MMR vaccine in post-natal period.
Features of neonatal CMV?
IUGR Early onset jaundice Hepatosplenomegaly Thrombocytopenia Microcephaly Purpuric skin lesions SNHL Intracranial calcification Chorioretinitis.
Whats the long term sequele of CMV?
Cerebral palsy
Epilepsy
Learning difficulty
Diagnosis and treatment of CMV?
Virus isolation (urine and saliva) Specimens of viral isolation must be taken within 3 weeks of birth
Treat with gangciclovir.
Features, diagnosis and treatment of HSV?
Risk highest if mother acquired HSV during 3rd trimester.
Fever, seizures, lethargy, sepsis, vesicular blisters of skin/eye/mucous membranes.
CSF or serum HSV PCR testing.
Eye/mouth/nasopharynx/rectal cultures
Manage with acyclovir for 21 days if disseminated/CNS disease
Manage with acyclovir for 14 days if disease limited to skin/mucous membranes
How to reduce risk of passing HIV to baby?
Maternal antiretroviral therapy in pregnancy.
Elective C-section if detectable viral load. (vaginal delivery if viral load undetectable)
Give antiretroviral therapy to neonates for first 6 weeks.
Avoid breast feeding.
Features of foetal varicella syndrome?
Scars, lesions, malformed digits and limbs, eye defects, learning disabilities.
Severe neonatal varicella - if mother gets infection near time of delivery, foetus receives high viral load but little maternal antibodies -> increased risk of infection and death.
Management of foetal varicella syndrome?
If doubt mother has had chicken pox, check ab’s in maternal blood.
Non-immune - give varicella zoster Ig ASAP. Effective up to 10 days post exposure.
If pregnant women with chickenpox present within 24 hours - give oral acyclovir.
Neonates exposed in high-risk period should be treated with varicella zoster Ig.
Features of neonatal syphilis?
Early congenital syphilis - presents before 2 years of age - prematurity, IUGR, highly infectious rhinitis, hepatosplenomegaly, skin rash, osteochondritis, neurological symptoms.
Late congenital syphilis - presents after 2 years of age - craniofacial malformation, dental abnormalities, interstitial keratitis, deafness, neurosyphilis.
Investigations of neonatal syphilis?
Serology at first antenatal booking appointment.
Repeated syphilis serology in third trimester and at delivery if serology was positive.
Foetal USS - hepatomegaly, ascites, hydrops.
Infants born to mothers with syphilis require a non-treponemal blood test.
Dark-field microscopy on lesions or nasal discharge.
Management of neonatal syphilis?
First line for neonates - IV aqueous benzylpenicillin or IM procaine benzylpenicillin.
Pregnant women should be treated with benzylpenicillin
All pregnant women who have syphilis should be tested for HIV.
What is erythema toxicum? Treatment?
Common rash in neonates -> blotchy red spots on skin with overlying white or yellow papule or pustules.
Does not cause any discomfort to infant.
Appears in up to half of term neonates, usually 2-5 days after birth, and resolves within 2 weeks of life.
No treatment indicated, as eruption is transient and self-limiting.
Causes of failure to feed?
Premature birth
Congenital causes - herpes, jaundice, ifnections
Congenital hypothyroidism
Down syndrome
Beckwith-Wiedemann syndrome
Temporary conditions - diarrhoea, ear infection, coughs and colds, teething.
Red flags for failure to feed?
Not fed in over four hours Fever Vomiting after feeding Vomiting blood Persistent and worsening cough Constant crying Bloody stool Wheeze Becoming unresponsive to touch.
Treatment of failure to feed?
Treat underlying cause.
Change feeding schedule - smaller, more frequent meals.
Change feeding formula - breast to bottle.
Screening for Hep B and treatment?
All pregnant women should have antenatal screening for HBsAg -> babies born to positive mothers should have hep B vaccine within 24 hours of birth.
- Baby should also receive hepatitis B-specific Ig, unless mother is known to be anti-HBe positive.
What is Hypoxic Ischaemic Encephalopathy? Features?
Acute or subacute brain injury due to perinatal asphyxia.
Acute injury caused by hypoxia, repercussion injury occurs 6-72 hours later.
Mild - lethargy followed by period of hyper-alertness with irritability but normal tone. Impaired feeding for 1-2 days. No focal signs or seizures. Good prognosis.
Moderate - hypotonia with reduced movements and consciousness. Seizures may be seen. Variable prognosis.
Severe - Coma with absence or spontaneous movement and reflexes. Seizures usually seen and may be frequent. Prognosis poor.
Diagnosis of hypoxic Ischaemic Encephalopathy (HIE)
Bloods - U&E, cardiac enzymes, LFTs, clotting screen, ABG
Imaging - MRI brain, cranial USS, echo
Additional - EEG, hearing test, retinal and ophthalmic examination
Metabolic or mixed acidosis in umbilical artery sample.
Apgar score 0-3 for longer than 5 minutes
Neonatal neurological signs (seizure, coma, hypotonia)
Multiple organ involvement.
Management of HIE?
Interventions needed within 6 hours of initial hypoxic insult to prevent repercussion injury (can occur 6-72 hours later). Total body cooling Respiratory support Anticonvulsants for seizures Fluid restriction Circulatory support with inotropes.
Cerebral function monitoring for seizures and neurological function.
MRI and electroencephalogram may reveal cystic lesions or cerebral atrophy.
How does total body cooling help with HIE?
Reduces risk of neurodisability - induce hypothermia for 72 hours followed by gradual rewarming to protect the brain from reperfusion injury.
Complications of perinatal asphyxia?
Brain - HIE
Heart - hypoxic cardiomyopathy, hypotension
Lungs - persistent pulmonary hypertension
Gut - ileus and necrotising enterocolitis
Kidneys - acute tubular necrosis
Blood - DIC
Causes of hypothermia?
Preterm infants, due to lack of brown fat, little muscle activity and high body surface area to volume ratio.
Management of hypothermia?
Radiant heat
Ambient temperature and humidity
Insulation with clothing (including a hat)
Plastic bags - effectively steaming the baby.
What is meconium aspiration and why does it occur?
Neonates pass meconium before delivery -> respiratory distress in new born as result of meconium in trachea.
Occurs in immediate neonatal period.
More common in post-term deliveries.
Risk factors for meconium aspiration?
Maternal hypertension Pre-eclampsia Chorioamnionitis Smoking Substance abuse
Management of meconium aspiration?
If thick meconium causing obstruction, suction meconium from trachea under direct vision after delivery.
Most cases are due to aspiration in utero, cannot be prevented by suction at delivery.
Causes and management of meconium delay?
Hirschsprung’s disease - requires surgery
Meconium ileus/cystic fibrosis - enema, IV fluids, surgery
Meconium plus syndrome - requires rectal stimulation and enema
Anorectal malformations - dilatation, surgery
Small left colon syndrome - enema, colostomy.
What is neonatal apnoea? Features?
Baby doesn’t breathe for >20 seconds.
More common in premature babies than full-term, due to immaturity of respiratory centre of brain, occurring days 2-7 of life.
More common when in REM sleep.
Often idiopathic in premature babies, but almost always pathological in term infants.
May be followed by bradycardia.
Management of neonatal apnoea?
> 34 weeks - need cardio-resp/sats monitoring if unstable.
<34 weeks - monitoring for first week of life or until absence of apnoeic episodes for at least 7 days.
Apnoea monitors used in perinatal nurseries to alert staff when to act on apnoea.
Prone position reduced apnoea of prematurity.
Step-up treatment of neonatal apnoea after sats monitoring?
First line - oral/IV caffeine. Given routinely <34 weeks neonates. Smooth muscle relaxant and cardiac muscle and CNS stimulant.
If this doesn’t work - high flow nasal cannula.
Then nasal CPAP
Last resort - mechanical ventilation.
What are the most common causes of neonatal collapse?
Sepsis and cardiac disease. Both present as shock.
Features of neonatal collapse?
Hypothermia, respiratory distress, poor pulses.
Management of neonatal collapse?
Initial evaluation and resuscitation - high flow O2, IV access, 20ml/kg normal saline, abx
What immediate investigations do you do for neonatal collapse?
ABG, FBC, U&E, glucose, LFTs, clotting, blood cultures, consider LP
CXR, ECG if tachycardic.
Ammonia (if seizures/encephalopathy)
Causes of neonatal hypoglycaemia?
Hyperinsulinism
Inadequate hepatic glycogen stores - prematurity, IUGR.
Increased glucose use (hypothermia, sepsis)
Reduced glycogenolysis, gluconeogenesis (inborn errors of metabolism, adrenal insufficiency.
Risk factors for hypoglycaemia?
Maternal DM Prematurity IUGR Hypothermia Neonatal sepsis Inborn errors of metabolism Neisioblastosis (beta cell hyperplasia) Beckwith-Wiedemann syndrome
What neurological damage can hypoglycaemia cause?
Mental retardation
Recurrent seizures
Developmental delay
Personality disorders
Presentation of hypoglycaemia in neonates?
Asymptomatic Hypotonia Lethargy, apathy Poor feeding Seizures, jitteriness Congestive heart failure Cyanosis Apnoea Hypothermia Tachycardia
Diagnosis of hypoglycaemia?
Serum or plasma glucose levels
Serum insulin
Urine - first-voided urine dipstick for ketones
Screen for metabolic errors.
Management of hypoglycaemia?
Early feeding of newborn with breastmilk or formula
NG/IM/IO/IV 10% dextrose
IV 10% dextrose drip if hypoglycaemia is recurrent
Surgery if appropriate (eg pancreas resection).
