Neonates Flashcards
Definition of low birth weight?
born weighing less than 5 pounds, 8 ounces (2,500 grams)
less than 3 pounds, 5 ounces (1,500 grams) at birth are considered very low birth weight
extremely low - less than 1000g
Causes of low birth weight?
Often caused by premature birth
Substance use (alcohol, cigarettes, cocaine, heroin)
ACEi, carbamazepine, phenytoin, warfarin
Infections (malaria)
Placental insuff: smoking, DM, HTN, anaemia, AN, APS, SLE, sickle cell, Rh incompatibility, pre-eclampsia
Placenta previa, multiple gest, placenta abruption, umbilical a thrombosis/ infarction, uterine malf e.g. fibroids.
Fetal cyanotic heart defects
Signs and symptoms of low birth weight/small baby?
Asymmetric: more common, abdo circ lower centile than head, due to placenta insuff
Symmetric: head equally ↓, prolonged IUGR. TORCH, drug use, Chr abnormalities.
What is TORCH?
toxoplasmosis, other agents, rubella cytomegalovirus, herpes simplex, and HIV
causes Sx of: fever, difficulty feeding, small areas of bleeding under skin, small reddish or purplish sports, hepatosplenomegaly, jaundice, hearing impairment, abnormalities of eyes
if foetus infected by TORCH agent - outcome of pregnancy may be miscarriage, stillbirth, IUGR, premature birth
Complications of low birth weight/small baby?
Metabolic maladaptation
Use reserves (SC fat, ↓glycogen in liver ↓protein in muscle) to maintain brain growth.
Fetal hypoxia + hypoglycaemia, shunting blood to vital organs.
Anaerobic glycolysis, met acidosis, lactic acid damages organs
Diagnosis of low birth weight/small baby?
Doppler USS: reversed/absent flow suggests fetal distress
Small baby with normal doppler is fine.
Treatment of low birth weight/small baby?
Deliver if sig restriction
Tx of underlying cause
Risk factors for preterm birth?
multiple gest pre-eclamp cervical incompetency, preterm PROM preg HTN IUGR ↑ uterine size bleeding in 1st or 2nd trim placenta previa IU infection polyhydramnios maternal systemic disease (UTI) psychological stress domestic violence
Complications of premature birth?
CP, RDS, NE
LD, behav problems
Chronic health issues: epilepsy, DM
Hypothermia
Infection: maternal IgG crosses 30wk, thin skin, immature immune system
Feeding: no suck/ swallow reflex until 34wks. IV nutritional gradual introduction of breast milk
Diagnosis of premature birth?
Identify risk: cervical assessment, fetal fibronectin (shouldn’t be present > 20 wks), screening for infections
Investigate maternal infection/haem
CTG/USS
Prevention of premature birth?
Abx for asymptomatic bacteriuria
Cervical cerclage, removed 36-37 wks.
Progesterone: antagonises oxytocin, relaxation of smooth muscle
Treatment of premature birth?
Tocolysis: nifedipine, indomethacin etc
24mg betamethasone/ dexamethasone 2 IM injections 24hrs apart.
Delayed cord clamping
What is macrosomia?
Birth weight >4000g
95th centile
Causes of macrosomia?
Mother had previous large baby before
FHx of large babies
BMI >35
Diabetic/gestational diabetes
Diagnosis of macrosomia?
Symphysis-fundal height - greater than expected >2 then offered growth scan
If >90th centime and under 36 wks - GTT
more than 36 wks, monitor BG levels over 7 days
Risks of macrosomia?
Shoulder dystocia > fractured clavicle, Erb’s palsy
PPH
Uterine rupture
C-section, instrumental delivery
Perineum tears
Neonatal hypoglycaemia
Metabolic syndrome
Management of macrosomia?
Induction at 39-40wks
How does GDM cause macrosomia?
increased insulin resistance of the mother
so a higher amount of blood glucose passes through the placenta into the fetal circulation
as a result, extra glucose in the fetus is stored as body fat causing macrosomia
What is hydrops fetalis?
abnormal accumulation of fluid in two or more fetal compartments, including ascites, pleural effusion, pericardial effusion, and skin edema
What causes immune hydrops?
Rh incompatiblity - Rh positive baby, Rh -ve mother
Causes haemolytic anaemia. If baby cannot overcome this, causes hydrops as heart starts to fail.
What causes non-immune hydrops?
Severe anemia
Infections present before birth
Heart or lung defects
Chromosomal abnormalities and birth defects
Liver disease
S+S of hydrops fetalis?
During pregnancy:
- polyhydramnios
- thickened placenta
- US shows enlarged liver, spleen, heart, may show fluid build-up
After birth:
- pale colouring
- severe swelling - especially in abdomen
- trouble breathing
- hepatosplenomegaly
Diagnosis of hydrops fetalis?
USS
Increased abdominal fluid
Fetal blood sampling
Amniocentesis
Treatment of hydrops fetalis?
Depends on cause
Early delivery
Newborn - O2/ventilator, paracentesis
How long for baby to breath after vaginal and C-section?
Normal vaginal: breathing in 30s.
CS: several hrs to clear fluid from lungs
Causes of failure to develop normal respirations?
Asphyxia > lack of O2 to developing brain > prevents infant breathing
Prolonged uterine contractions /delivery, birth trauma
Preterm
Cong malformation
Poor oxygenation in delivery: maternal ↓BP, poor maternal oxygenation (anaesthesia induced hypoventilation, resp/heart disease), XS oxytocin, placental insuff, umbilical prolapse.
What is persistent pulmonary hypertension of the newborn?
Disorder in which the arteries to the lungs remain narrowed after delivery, and so limits the amount of blood flow to the lungs
Pathophysiology of PPHN?
RV pressure increases
Then LV
FO and DA don’t close as body chooses low pressures over high
Causes of PPHN?
Severe distress during delivery - meconium aspiration syndrome
Respiratory distress syndrome
Other causes of low O2 in foetus before, during or after delivery > infection, diaphragmatic hernia, collapsed lung, underdeveloped lungs, pneumonia
Primary PPHN - hypertrophy of muscular layer in PA. Placenta insuff, maternal NSAID use, poor prognosis
Congen abnormalities of heart + lungs eg diaphragmatic hernia, blocked heart valve, smaller lungs, pul hypoplasia
Pleural effusions
Risk factors for PPHN?
perinatal asphyxia
prolonged PROM
more common among new-borns who are full term (37-42) or post-term (>42)
Features of PPHN in new-born?
Persistently low sats despite intensive O2 therapy Cyanosis Tachypnoea Retractions, Within 24hr of birth, Systolic murmur, Low APGAR. Meconium staining
Diagnosis of PPHN?
ECHO: R>L shunting, patent FO + DA/
Difference of > 10% between pre + postductal O2 sat. Pre-ductal measured R hand, blood before DA, post-ductal > measured feet. If there is difference in them, means mixing of blood through duct
CXR: assess lung disease, congen diaphragmatic hernia
Treatment of PPHN?
Supplemental oxygen - environment with 100% O2
Sometimes a ventilator
Sometimes nitric oxide gas - opens arteries in newborn’s lungs and reduces pulmonary HTN
Sometimes extracorporeal membrane oxygenation - machine adds O2, removes CO2, slowly opens vessels
Causes of apnoea in newborn?
Prematurity, LBW Hypothermia, hypo/HTN Aspiration, airway obstruction Congenital HD, PDA Anaemia Infections Pain GORD ↑↓Ca/Na Maternal drugs Abnormal responses to hypoxia, hypercapnia, obstructed airflow or reflex laryngospasm
S+S of apnoea in newborn?
O2 sats typically <85% + HR <80 BPM, apnoeic spells.
Resp pauses at least 20 secs, or under 20s associated with bradycardia,
Cyanosis, pallor.
Treatment of apnoea in newborn?
HF nasal cannula, PEEP, CPAP, ventilation
Dry bay, rub back + feet, head neutral
Incubator
Suction secretions
Methylxanie: caffeine/ theophylline: stim resp centre, CNS, + CVS. ↑sensitivity to CO2 ↑skeletal muscle tone. Enhanced diaphragm contractility, ↑ventilation, MR, O2 consumption.
Supplementary O2 to maintain sats.
Usually settles within 1-2 days.
Prevention: CS
What is transient tachypnoea of newborn?
benign, self-limited condition that can present in infants of any gestational age, shortly after birth.
It is caused due to delay in resorption of fluid in lungs after birth which leads to ineffective gas exchange, respiratory distress, and tachypnea
Commonest cause of resp distress in newborn
More common after CS, fluid not squeezed out by contractions.
Diagnosis of TTN?
CXR: hyperinflation of lungs, fluid in horizontal fissure.
Management of TTN?
Supplementary O2 to maintain sats.
Usually settles within 1-2 days.
What is choanal atresia?
Congen narrowing of back of nasal cavity. Unilat or bilat.
Completely bony or composed of both bone + membranes.
1 in 7000 births
What is CHARGE syndrome?
coloboma heart defects atresia choanae (also known as choanal atresia) growth retardation genital abnormalities ear abnormalities.
Symptoms of choanal atresia?
Immediately after birth, later if unilat Cyclical RD Improved with crying Worse when feeding Noisy breathing
Unilateral - persistent nasal drainage, recurrent sinus infections
B/L - respiratory distress, cyanosis
Diagnosis of choanal atresia?
Laryngeal mirror - fogging to suggest air flow or nasal obstruction
Inability to pass catheter into nasopharynx
CT for specifics
Diagnosis late in unilateral
Treatment of choanal atresia?
Surgical repair ASAP in bilat, can wait in unilat > Transnasal endoscopic surgery, placing stent for few wks
Bilat intubation ASAP
Unilat > supplemental O2 nasal saline, keep nasal linings free of discharge.
What is congenital cystic lung disease?
a benign lung lesion that appears before birth as a cyst or mass in the chest.
It is made up of abnormal lung tissue that does not function properly, but continues to grow.
CCAM is also frequently referred to as a congenital pulmonary airway malformation (CPAM)
Complications of congenital cystic lung disease?
Lung hypoplasia
Recurrent infections
HF
Compression of heart
Investigations and treatment of congenital cystic lung disease?
Prenatal USS
Steroid prevent growth
Prenatal removal of fluid/shunt placement
Prenatal surgery
CS with resection
Summary of pneumothorax in neonates?
Can be spontaneous or secondary to: meconium, RDS, cystic lung disease, high pressure ventilation
Features - tachypnoea, grunting, cyanosis, chest on affected side more prominent
Investigations - CXR, ABG, positive transillumination
Management - give O2, aspirate, chest tube
What is meconium aspiration syndrome?
refers to respiratory distress in the newborn as a result of meconium in the trachea.
It occurs in the immediate neonatal period
It is more common in post-term deliveries
Resp distress > meconium in trachea, airway obstruction > surfactant dysfunction > pul vasoconstriction > pul HTN.
Higher rates occur where there is a history of maternal hypertension, pre-eclampsia, chorioamnionitis, smoking or substance abuse.
Features of meconium aspiration syndrome?
Immediate neonatal period
Post-maturity: green/ yellow skin + UC, long, stained nails, dry peeling skin, loss of SC tissue
Cyanosis
Systolic murmur. Rales, ↓BS, rhonchi
↑RR + HR, ↓BP
Chest wall asymmetry ↓air entry > pneumothorax
Barrel shaped chest, retractions. Grunting
Complications of meconium aspiration syndrome?
Infection,
Chemical pneumonitis (oedema),
Pneumothorax,
Atelectasis.
Diagnosis of meconium aspiration syndrome?
CXR: patchy infiltrations, atelectasis, hyperexpanded lung fields, areas of collapse, consolidation, pneumothorax
Management of meconium aspiration syndrome?
Endotracheal suction only if flat at birth
Surfactant
O2 therapy, ventilation > CPAP, ECMO, mechanical ventilation + inhaled NO
Abx: ampicillin + gentamicin
Chest drain
Vasopressor: dopamine, dobutamine
What is retinopathy of prematurity?
Disorder of developing retina
Abnormal fibrovascular prolif of retinal vessels > retinal detachment > visual loss
Risk factors for retinopathy of prematurity?
prematurity (<31 wks), anaemia, blood transfusions, LBW (<1500g), hypotension, exposure to supplemental oxygen + fluctuations in O2
Features of retinopathy of prematurity?
May appear normal, visual loss as child grows
1) Mildly abnormal BV growth, normal vision, no Tx
2) Mod abnormal, normal vision, no Tx
3) Severely abnormal, BVs grow towards centre of eye instead of along surface of retina. Tx to prevent retinal detachment
4) Partially detached retina, traction from scar produced by bleeding, abnormal vessels pull retina away from wall of eye
5) Completely detached retina, severe visual impairment + blindness
Diagnosis of ROP?
Regular ophthalmology screening of high risk = wkly <32 wks / <1500g, until risk of developing ROP requiring Tx has passed
Management of ROP?
Tx: laser therapy
photocoagulation > less myopia than cryotherapy,
Intravitreal anti-VEGF monoclonal antibodies (bevacizumab),
Vitrectomy with lensectomy
What is Phenylketonuria?
an autosomal recessive condition caused by a disorder of phenylalanine metabolism.
This is usually due to defect in phenylalanine hydroxylase, an enzyme which converts phenylalanine to tyrosine
High levels of phenylalanine lead to problems such as learning difficulties and seizures.
The gene for phenylalanine hydroxylase is located on chromosome 12.
The incidence of PKU is around 1 in 10,000 live births.
Features of PKU?
Presents by 6 mnths > developmental delay
Blue eyes, blonde hair
Seizures - typically infantile spasms
Eczema
Musty odour to urine + sweat
Microcephaly
Diagnosis of PKU?
Guthrie test: the ‘heel-prick’ test done at 5-9 days of life - also looks for other biochemical disorders such as hypothyroidism
Hyperphenylalaninaemia
Phenylpyruvic acid in urine
Management of PKU?
Restriction of dietary protein + phenylalanine.
Supplementation with phenylalanine-free AA mixtures
Dietary restrictions are however important during pregnancy as genetically normal fetuses may be affected by high maternal phenylalanine levels
What is haemorrhagic disease of newborn?
aAbleeding problem that occurs in a baby during the first few days of life
Babies are normally born with low levels of vitamin K
Early or later (1-8 wks PP)
Risk factors for haemorrhagic disease of newborn?
BF
Symptoms of haemorrhagic disease of newborn?
Mild in most: melena/ haematemesis, bruising, prolonged bleeding of umbilical stump
Severe: IC haem, permanent disability, death
Diagnosis and management of haemorrhagic disease of newborn?
↑PTT + PT
Platelets normal
It’s why vit K IM is given to all newborn infants (IM or oral)
Vit K 1mg ± FFP
Jaundice in neonate in first 24 hours?
Always pathological
Causes of jaundice in the first 24 hrs:
- rhesus haemolytic disease
- ABO haemolytic disease
- hereditary spherocytosis
- glucose-6-phosphodehydrogenase
- sepsis
- CNJ syndrome
- Gilbert’s
- Red cell abnormalities
- pyruvate kinase deficiency
- congenital infection
Investigations for jaundice in neonate in first 24 hours?
Direct coombs,
Maternal IgA,
AntiA AntiB for Rh
FBC,
Blood film,
Syphilis, TORCH
May rise >15mg/dL, 5mg/dL/day
Causes of jaundice in neonate from days 2-14?
Common (up to 40%) and usually physiological
It is due to a combination of factors, including more red blood cells, more fragile red blood cells and less developed liver function.
It is more commonly seen in breastfed babies due to decreased fluid intake and inadequate bowel movements to remove bilirubin from body
Hepatic immaturity in BR conjugation, removal/ haemolysis of fetal RBCs. If ↓albumin, UBR unbound
Infection. Dehydration
Absence of gut flora impedes elimination of bile pigment
Total peak <15mg/L
<5mg/dL/day
Causes of jaundice in neonate 14+ days?
If there are still signs of jaundice after 14 days (21 days if premature) a prolonged jaundice screen is performed, including:
- conjugated and unconjugated bilirubin: the most important test as a raised conjugated bilirubin could indicate biliary atresia which requires urgent surgical intervention
- direct antiglobulin test (Coombs’ test)
- TFTs
- FBC and blood film
- urine for MC&S and reducing sugars
- U&Es and LFTs
Causes of prolonged jaundice:
- biliary atresia (conjugated and pale stools!)
- hypothyroidism
- galactosaemia
- urinary tract infection
- breast milk jaundice (thought to be due to high concentrations of beta-glucuronidase → increase in intestinal absorption of unconjugated bilirubin)
- prematurity
- due to immature liver function
- increased risk of kernicterus
- congenital infections e.g. CMV, toxoplasmosis
- CF, Hirschsprung’s, pyloric stenosis
- bile duct obstruction
- neonatal hepatitis
- Gilberts, CNJ syndrome, rotor syndrome
Investigations for prolonged jaundice in neonate?
CBR/UBR: ↑conjugated = biliary atresia
Direct Coombs’ test
TFTs
FBC + blood film
Urine MC+S + reducing sugars
U+Es
LFTs
What is Kernicterus?
a type of brain damage that can result from high levels of bilirubin in a baby’s blood
UBR crosses BBB, permanent neurological damage, deposits in BG or brain stem nuclei.
if smaller levels - less likely permanent, little effect on IQ unless preterm or SGA
Risk factors for Kernicterus?
premature, co-morbid hypoalbuminaemia
Symptoms of Kernicterus?
Sleepy ± poor suck/ feed
Setting sun lid traction
No moro reflex
Apnoea
Hypotonia
Odd movements
CP > choreoathetoid
Sensorineural deafness
Vertical gaze palsy
Movement (athetosis)
Dental enamel hypoplasia
Low IQ, LD
Irritability
Opisthotonos: UMN damage, seizures, coma
Bronze baby syndrome: rare, ↑BR following phototherapy, accumulation of bronze-coloured pigments (photoisomers of bilirubin) within skin
Management of Kernicterus?
Phototherapy
Exchange transfusion
IV immunoglobulin
What is neonatal hypoglycaemia?
Normal term babies often have hypoglycaemia especially in the first 24 hrs of life but without any sequelae, as they can utilise alternate fuels like ketones and lactate
< 2.6 mmol/L
Transient hypoglycaemia in the first hours after birth is common.
Persistent/severe: premature, SGA, poor stores, GDM, IUGR, hypothermia, neonatal sepsis, inborn errors of metabolism, Nesidioblastosis (β cell hyperplasia), maternal BB, Beckwith-Wiedemann synd, illness, ↑ demand, GH def, congen adrenal hypoplasia
Sx of neonatal hypoglycaemia?
May be asymptomatic
Autonomic: jittery, irritable, ↑RR, pallor
Neuroglycopenic: poor feed/suck, weak cry, drowsy, hypotonia, seizures
Apnoea
Hypothermia
Management of neonatal hypoglycaemia?
asymptomatic:
- encourage normal feeding (breast or bottle)
monitor blood glucose
symptomatic or very low blood glucose:
- admit to the neonatal unit
intravenous infusion of 10% dextrose
If <1.6 - give immediate glucose
What is hypoxic ischaemic encephalopathy?
Sub-acute brain damage due to systemic hypoxaemia, causes ↓cerebral perfusion
Causes of HIE?
↓placental gas exchange: abruption/ uterine rupture, prolonged contractions
UC: compressed, prolapsed, nuchal (wrapped around neck of baby)
Maternal hypotension (shock, intrapartum haemorrhage)
Fetal issues: cardioresp/ asphyxia
Metabolic issues: inborn errors of metabolism. hypoglycaemia,
Congenital infections
Maternal: DM, PE, CHD
Traumatic delivery, CS with GA
Grading of HIE? (Sarnat staging)
Mild - weak sucking reflex, impaired feeding, good prognosis, hyperalert, resolves within 24 hrs, normal prognosis
Moderate - lethargic, ↓tone periodic apnoea, weak reflexes, feeding issues, seizures within 24 hrs birth, recovery possible after 1-2 wks, up to 40% develop cerebral palsy
Severe - reduced consciousness, flaccid tone, decerebrate, absent reflexes, irreg breathing and apnoeas, generalised seizures ↑ 24 – 48hrs after birth. Pupil abnormalities, death (50% mortality) or disability (90% develop CP)
Diagnosis of HIE?
MRI: deep nuclear gray matter injury, parasagittal injury of cerebral cortex + watershed cortical injury
Clinical + cerebral function monitor (EEG).
MRI at 1 wk = dysfunction suggests highly likely CP
Management of HIE?
Supportive care - neonatal resuscitation, ongoing optical ventilation, circulatory support, nutrition, acid base balance and Tx of seizures
Therapeutic hypothermia - actively cooling the core temperature of the baby. emperature is carefully monitored with a target of between 33 and 34°C, measured using a rectal probe. This is continued for 72 hours, after which the baby is gradually warmed to a normal temperature over 6 hours. It reduces the inflammation and neurone loss after the acute hypoxic injury. It reduces the risk of cerebral palsy, developmental delay, learning disability, blindness and death.
What is Rhesus haemolytic disease?
Rh- mother gives birth to RH+, sensitisation event (mother + baby’s blood mixing)
Mother produces anti-D IgG, in later pregnancies, can cross placenta in successive Rh+ preg
Events: APH, CVS, threatened miscarriage, amnio, ECV, abdo trauma, termination, ectopic, miscarriage gestation >12wks
Features of foetus in Rhesus haemolytic disease?
Oedematous: hydrops fetalis, liver devoted to RBC production albumin↓
Jaundice, anaemia, hepatosplenomegaly
HF
Kernicterus
Investigations of Rhesus haemolytic disease?
All babies born to Rh- mother have cord blood taken RBC, blood group, direct coombs test.
Coombs test: direct antiglobulin, IG on RBCs of baby
Kleihauer test: add acid to maternal blood, fetal cells are resistant
Management of Rhesus haemolytic disease?
Anti-D: within 72hrs of senitising events, + at 28 +34wks. Neutralises RhD pos antigens that enter mother’s blood in so mother doesn’t produce antibodies.
Tx of affected fetus: transfusions, UV phototherapy. Drain ascites + pleural effusion, limit IV fluids
What are neural tube defects?
Failure of NT to close 3-4th wk IU.
Spina bifida: incomplete vertebral arch, spine split - cystica (meningocele and myelomeningocele) and occulta (when meninges do not herniate through opening)
Myelocele: failure of cord fusion - open spinal cord with meningeal cyst
Meningocele: herniation of dura + arachnoid through bony defect - protrusion of meninges through defect in skull/spine
Anencephaly: most common, incompatible with life - open brain and lack of skull vault
Encephalocele - herniation of meninges and brain
Craniorachischisis - completely open brain and spinal cord
RF: maternal folate def, vit B2 def, prev Hx of infant with NTD, smoking, DM, obesity + AED (valproic acid, carbamazepine, methotrexate)
Open (not covered by skin), closed (covered by skin)
Features of neural tube defect?
Variable paralysis, sensory loss in legs
Scoliosis
Neurogenic bladder/ bowel.
Absence of anal wink/ rectal tone
Stool/ meconium leakage
Hydrocephalus: bulging fontanelle, rapid head growth, downward deviation of eyes, abnormal/ stridulous cry
Arching of neck: pressure on brainstem, shunt malfunction/ dysfunction
Asymmetry of spont arm + leg movements. Pain in limbs, muscle weakness, atrophy
Complications of neural tube defect?
Fecal + urinary incontinence, sexual dysfunction
If higher than lumbosacral might never walk
Facial asymmetry > CN lesion
Club foot: common deformity with lumbar or ↑ lesions imbalance of muscles around foot + ankle.
Abnormal muscle tone + bulk in arms + legs, spasticity
Investigations for neural tube defect?
USS: mostly found IU. Size, location, hydrocephalus. Flattened/ inwardly scalloped frontal bones (lemon sign), obliteration of cisterna magna + loss of roundness of cerebellar hemispheres (banana sign)
Antenatal/quadruple test: elevated
Fetal MRI
Management of neural tube defects?
Termination offered at any stage
Surgical closure shortly after birth > prevent CNS infx
Further ops = fix spinal deformity
Hydrocephalus = ventriculoperitoneal CSF shunts
Prevention: 400mg folic acid normally until 13 wks, high risk mothers = 5mg folic acid
What is umbilical granuloma?
a type of scar tissue that forms in the belly button. Most umbilical granulomas form when the belly button is healing after the umbilical cord falls off. They look like small red lumps in your child’s navel
Usually separates around day 7 but can persist up to 6 wks
Cherry red lesion surrounding umbilicus
May bleed on contact
Seropurulent discharge
Apply salt
Don’t cauterise with silver nitrate
