Paediatrics Flashcards
Childhood vaccinations at age 8 weeks / 2 months
Diphtheria/tetanus/pertussis/Haemophilus influenza type B(HiB)/ Hep B (6 in 1 vaccine)
Men B
Rotavirus (oral)
Childhood vaccinations at age 12 weeks / 3 months
Diphtheria/tetanus/pertussis/Haemophilus influenza type B/ Hep B (6 in 1 vaccine)
Pneumococcal conjugate vaccine (PCV)
Rotavirus
Childhood vaccinations at age 16 weeks / 4 months
Diphtheria/tetanus/pertussis/Haemophilus influenza type B/ Hep B (6 in 1 vaccine)
Men B
Childhood vaccinations at age 12-13 months
Hib B/Men C
PCV
MMR
Men B
Childhood vaccinations at age 3 yrs 4 months
Diphtheria, tetanus, pertussis, polio
MMR
Childhood vaccinations at age 12-13 yrs
HPV types 6,11,16,18 (both boys and girls)
Childhood vaccinations at age 14 yrs
Men ACWY
Tetanus/diphtheria/polio
Developmental milestone: sits without support
7 months (>9 months = red flag)
Developmental milestone: stands independently
12 months (>12 months = red flag)
Developmental milestone: Walks unsupported
13 - 15 months (>18 months = red flag)
Developmental milestone: Pincer grip
10 months (>12 months = red flag)
Developmental milestone: Drawing
2 1/2 yrs
Developmental milestone: 2-3 words / understands name
1 year
Developmental milestone: 6-10 words
15 - 18 months
Developmental milestone: startling at loud noise & follows face
2 months (>3 months = red flag)
Developmental milestone: smiling
6 weeks (>8 weeks = red flag)
Developmental milestone: plays near others but not with them
2 yrs
Developmental milestone: joining two words
2 yrs (>2 yrs = red flag)
Developmental milestone: stranger fear
7 months (>10 months = red flag)
Paeds BLS compression to breath ratio
15:2
First step of paeds BLS
5 rescue breaths before commencing CPR
Peads foreign body airway obstruction (FBAO)
5 back blows 5 thrusts (abdo if >1yr & chest if <1yr)
Neonatal life support Step 1
dry & stimulate baby
Neonatal life support Step 2
5x inflation breaths if still gasping/not breathing with open airway
Neonatal life support Step 3
CPR if not breathing/ HR < 60
ratio 3:1 (compression : ventilation)
APGAR score groups
0-3 = bad 4-6 = moderate 7-10 = good
Risk factors for Sudden Infant Death Syndrome (SIDS)
prone sleeping parental smoking prematurity bed sharing male sex
Protective factors for SIDS
breast feeding
supine sleeping
Most common genetic cause fo trisomy 21
meiotic non-disjunction of chromes 21 (known as full trisomy 21), has 3 full chromosome 21
Risk factors for trisomy 21
↑maternal age, previous child with down syndrome
Physical features of trisomy 21
hypotonia epicanthal folds brushfield spots on iris flat nasal bridge single palmar crease small low set ears short stature
Trisomy 21 investigations to confirm diagnosis
chromosomal karyotype
fluorescent in situ hybridisation (FISH)
Congenital heart defects associated with trisomy 21
atrioventricular septal defect (AVSD) most common
ASD, VSD, tetralogy of fallot
Screening of congenital heart defects in trisomy 21
all neonates require an echo
Congenital GI defects in trisomy 21
duodenal / oesophageal atresia
imperforate anus
How frequent is trisomy 21 related hearing loss
90% of pts have some extend of hearing loss
Hearing screen for trisomy 21
Screen hearing at birth, 6 months, 12 months and annually there after
Trisomy 21 related visual problem at birth
congenital cataracts (absent red reflex - leukocoria)
Thyroids screening for trisomy 21
annual TFTs
↑ risk of hypothyroidism
Trisomy 21 related cancer
↑ risk of acute lymphoid leukaemia & acute myeloid leukaemia
Most common trisomy 21 related sleep problem
Obstructive sleep apnoea (60% of children)
sleep study recommended age 3-4 yrs
Orthopaedics disorders associated with trisomy 21
atlanto-axial instability
scoliosis
Monitoring tests for Trisomy 21 pts
hearing screen: at birth, 6 months, 12 months and then annually
TFTs: at birth, 6 months, annually
Eye screening: at birth, 6 months, then yearly till age 5
Sleep study: age 3-4
echo: at birth
coeliac disease screen
leading cause of death in trisomy 21 pts after age 40
dementia
Trisomy 13 (patau syndrome) presentation
microcephaly
polydactyly
small eyes
midline facial defects
Trisomy 13 (patau syndrome) prognosis
very poor, usually stillborn/spontaneously aborted
if born alive usually dead in a week
which is more common Trisomy 18 (edward syndrome) vs Trisomy 13 (patau syndrome)
Trisomy 18 (edward syndrome) is 2nd most common autosomal trisomy Trisomy 13 (patau syndrome) is 3rd most common autosomal trisomy
Most common management of Trisomy 21/18/13 if detected prenatally
abortion of the foetus
Trisomy 18 (edward syndrome) presentation
low birth weight microcephaly micrognathia prominent occiput small facial features (microstomia/micropthalmia) overlapping fingers rocker bottom feet
Trisomy 18 (edward syndrome) prognosis
often stillbirth/death in labour
<10% survive to age 1 year
Fragile X inheritance pattern
X linked dominant inheritance
Fragile X presentation
intellectual disability macrocephaly long face large ears macro-orchidist hyperflexibility
Fragile X genetic cause
expansion of CGG triplet repetition on the FMR1 gene
Noonan syndrome
Autosomal dominate
Features: webbed neck, pectus excavatum, short stature, low set ears
Pierre-Robin syndrome
Features: micrognathia, posterior displaced tongue (can cause airway obstruction)
Prader-Willi syndrome
Features: hypotonia, hypogonadism, obesity, T2DM
Williams syndrome
Features: elfin face, learning difficulties, friendly/extroverted personality, Supravalvular aortic stenosis
Cri du Chat syndrome
Features: characteristic cat like cry, feeding difficulties, poor weight gain
DiGeorge syndrome
Features: CHD, abnormal facies, cleft palate, developmental delay
Turner syndrome genetic cause
complete or partial absence of second X chromosome in females, 45XO/45X
Turner syndrome features
poor growth short stature lymphoedema of hands and feet webbed neck shielded chest wide spaced nipples wide carrying angle absent pubertal development infertility
Turner syndrome associated cardiac abnormalities
bicuspid aortic valve
coarctation of the aorta
Hormone levels in turner syndrome
LH & FHS ↑ Antimullerian hormone↓
Klinefelter’s syndrome genetic cause
males with extra X chromosome (47XXY)
Klinefelter’s syndrome features
tall & slender physique wide hips small firm testes impotence ↓ facial & pubic hair gynaecomastia learning disability
Hormone levels in Klinefelter’s syndrome
↓ testosterone, LH & FHS ↑
Klinefelter’s syndrome associated cardiac abnormalities
↑ risk of mitral valve prolapse
cancer associated with Klinefelter’s syndrome
↑ risk of male breast cancer & germ cell tumours
Klinefelter’s syndrome management
testosterone replacement (as pt enter puberty) intracytoplasmic sperm injection if they are trying to conceive
Neurofibromatosis (NF) types
NF-1:
chromosome 17 gene mutation
NF-2:
chromosome 22 gene mutations
Neurofibromatosis type 1 presentation
cafe au lait spots
axillary & inguinal freckles
neurofibromas
Iris hamartomas
Neurofibromatosis type 2 presentation
bilateral acoustic neuromas/vestibular schwanomas cafe au lait spots juvenile cataracts meningiomas intracranial schwanomas (multiple)
Investigating Neurofibromatosis (NF)
MRI/CT scan
genetic testing
Differentiating Neurofibromatosis (NF) types 1 and 2
NF-1 : more common in children, usually >6 cafe au lait spots
NF-2 : more common in adults, usually <6 cafe au lait spots
Neurofibromatosis (NF) differential diagnosis
tuberous sclerosis
which is differentiated by presence of ash-leaf spots (seen under UV light), retinal hamartomas, epilepsy
Cystic fibrosis (CF) genetics
abnormalities in salt and water transport across epithelial surfaces due to mutations in CF transmembrane conductance regulator (CFTR) gene on chromes 7
most common mutation in caucasians = DF508 (delta F508)
Ethnic group is at ↑ risk of cystic fibrosis
white population
↓ incidence in africans/hispanic/asian
Pathophysiology of cystic fibrosis
impaired salt & water transport by epithelial cells leads to thick sticky excretions, which can affect the pancreas/GI tract/Bilairy tree/resp system/sweat
Presentation of cystic fibrosis in neonates
meconium ileus/delayed passage of meconium
prolonged jaundice
Presentation of cystic fibrosis in older children
recurrent chest infections/chronic pulmonary disease wet sounding cough purulent sputum wheezes nasal polyps failure to thrive steatorrhoea
Investigating cystic fibrosis
found on heelprick test (day 5-7 after birth)
Sweat test (↑ Cl- concentration >60mmol/L)
genetic testing
CXR
Lung function test (FEV1/FVC ↓)
stool elastase (for pancreatic dysfunction)
Common pathogens in cystic fibrosis pts
staph aureus H influenzas pseudomonas aeroginosa aspergillus Burkholderia cepacia
Managing respiratory problems in cystic fibrosis pts
chest physio & mucous clearance techniques
ABx
mucolytics e.g. dornase alfa
Management of pancreatic insufficiency in cystic fibrosis
confirm via stool elastase test
pancreatic enzyme therapy
Recommended diet for cystic fibrosis pts
high fat, high protein, high calorie diet
Fertility problems related to cystic fibrosis
almost all males suffer from azoospermia so should be counselled on IVF for conception
Biological treatments of cystic fibrosis
lumacaftor & Ivacaftor
to treat homozygous pts for DF508, help increase CFTR protein numbers
Presentation of meconium ileus
24-48h post birth with failure to pass meconium, abdo distension and bilious vomiting
NB seen in ~20% of CF pts
Management of meconium ileus
surgical decompression
Genetic cause of sickle cell disease
autosomal recessive gene defect of the 17th nucleotide of the beta chain leading to the substitution of valine instead of glutamic acid
screening for sickle cell disease
part of the routine heel prick test screening on day 5-7 after birth
timeline of presentation for sickle cell disease
symptomatic presentation between age 3-6 months as HbF levels fall
presentation of sickle cell disease
jaundice pallor anaemia growth restriction failure to thrive lethargy systolic flow murmur
The spleen in sickle cell disease
↑ risk of infection by encapsulated organisms e.g. pneumococcus
highest risk of overwhelming infection in <3y/o
recurrent infections lead to autosplenectomy
Vaso-occlusive crisis in sickle cell
most common type of crisis
obstruction of micro circulation by sickle cells leading to ischaemia
precipitating factors of vaso-occlusive crisis in sickle cell
cold, infection, dehydration, exertion
presentation of vaso-occlusive crisis in sickle cell
swollen joints
pain
tachypnoea
priapism
if major vessels may present as thrombotic stroke/acute sickle chest syndrome
aplastic crisis in sickle cell
temporary cessation of erythropoiesis leading to severe anaemia
trigger of aplastic crisis in sickle cell
parvovirus B19 infection
presentation of aplastic crisis in sickle cell
generally rapid drop in Hb over 1 week with spontaneous recovery
may have high output congestive HF
sequestration crisis in sickle cell
sudden enlargement of spleen leading to ↓ Hb & circulatory collapse which causes hypovolaemic shock
at risk groups for sequestration crisis in sickle cell
young children snd babies
presentation of sequestration crisis in sickle cell
↓ Hb, ↑reticulocytes, splenomegaly
management of recurrent sequestration crisis in sickle cell
splenectomy
differentiating sequestration crisis in sickle cell & aplastic crisis in sickle cell
aplastic = ↓ Hb but no ↑reticulocytes
sequestration ↓ Hb, ↑reticulocytes, splenomegaly
Acute chest crisis in sickle cell
vaso-occlusive crisis of the lungs
diagnostic criteria for Acute chest crisis in sickle cell
new pulmonary infiltrates on CXR + ≥ 1 of
- cough
- fever
- sputum production
- tachypnoea
- dyspnoea
- hypoxia
investigating sickle cell disease
FBC (↓ Hb, ↑reticulocytes) blood film (sickle cells) haemoglobin electrophoresis (to confirm diagnosis, absence of HbA, but presence of HbS)
general management of sickle cell disease
Patient & parental education
folic acid/zinc/Vit D supplementation
unconjugated pneumococcal vaccine (from age 2)
oral penicillin prophylaxis
hydroxycarbamide (,2y/o to ↓ frequency of crisis by stimulation HbF)
blood transfusion
treatment of sickle cell disease in pregnancy
prophylactic LMWH due ↑ risk of prematurity/neonatal death/low birth weight
low dose aspirin 75mg from 12 weeks
Duchenne muscular dystrophy (DMD) inheritance
X-linked recessive
Duchenne muscular dystrophy (DMD) pathophysiology
mutation leads to absence of dystrophin protein leading to muscle degeneration/necrosis with muscle being replaced by adipose tissue
Presentation of Duchenne muscular dystrophy (DMD)
delayed motor milestones calf hypertrophy waddling gait/inability to run Gower's sign (climbing up legs when standing up) heel contractures lordosis ↓ tendon reflexes ↓muscle tone
Investigating Duchenne muscular dystrophy (DMD)
Creatine kinase (↑10-100x normal levels) genetic testing muscle biopsy (check for dystrophin protein)
Normal test result excluding Duchenne muscular dystrophy (DMD)
normal creatine kinase excludes diagnosis of DMD
Managing Duchenne muscular dystrophy (DMD) early stages
Physiotherapy
knee-foot-ankle orthosis
corticosteroids e.g. prednisolone (prolongs ambulation)
Managing Duchenne muscular dystrophy (DMD) late stages
mobility aids
respite care
NIV
regular cardiology reviews (6 monthly)
Spinal muscular atrophy (SMA)
slow progressive atrophy & weakness of limb muscles due to SMN1 gene mutation, leading to lower motor neurone weakness
generally autosomal recessive
Features of Spinal muscular atrophy (SMA)
muscle weakness & wasting preserved intellect flaccid weakness hypotonia ↓ tendon reflexes fasciculation's
most common type of Spinal muscular atrophy (SMA)
SMA type II most common (chronic infantile SMA)
Investigating Spinal muscular atrophy (SMA)
creatine kinase (normal) genetic testing
Charcot-Marie-Tooth disease
heterogenous group of peripheral neuropathies which is the most common inherited neuromuscular disorder
usually autosomal dominant inheritance
Presentation of Charcot-Marie-Tooth disease
slowly progressive (CMT1 most common onset by age 10)
muscle weakness & wasting (starting in intrinsic foot muscles)
muscle weakness spreads to lower legs & thigh
sensory loss following same pattern as muscle weakness (especially ↓vibration & light touch)
generalised tendon areflexia
Necrotising enterocolitis (NEC)
ischaemic inflammatory bowel necrosis
most common GI emergency in neonates
Risk factors for necrotising enterocolitis (NEC)
prematurity
↓ birth weight
PDA
presentation of Necrotising enterocolitis (NEC)
classically in preterm infants within first 2 weeks of life abdo distension altered stool pattern bloody mucoid stool bilious vomiting ↓ bowel sounds lethargy
investigating necrotising enterocolitis (NEC)
FBC
ABG/VBG
baseline biochem
AXR (dilated bowel loops, intramural gas, Ringler sign)
AXR findings in necrotising enterocolitis (NEC)
dilated bowel loops
bowel wall oedema
intramural gas (pneumatosis intestinalis)
portal venous gas
Rigler sign
Football sign (air outlining falciform ligament)
managing necrotising enterocolitis (NEC)
Nil by mouth NG tube to decompress bowel IV fluids/parenteral nutrition IV ABx (cefotaxime +metronidazole/clindamycin) surgery
Exomphalos (omphalocele)
abdo contents herniated into umbilical cord via umbilical ring, viscera covered by a membrane
Gastroschisis
abdominal contents herniating into amniotic sac without covering membrane
usually to right side of umbilicus
Investigating gastroschisis & exomphalos
maternal AFP (↑) USS
Managing exomphalos
surgical repair fo defect, abdominal contents returned to abdomen
Managing gastroschisis
surgical repair
requires more pre-op care than exomplhalos with IV fluids, radiant heaters etc
congenital diaphragmatic hernia
incomplete fusion of diaphragm leading to herniation of abdo contents into thorax which causes pulmonary hypoplasia
common side of congenital diaphragmatic hernia
left side
liver plugs space on right
congenital diaphragmatic hernia prenatal presentation
often prenatal diagnosis (polyhydraminos & via routine USS)
congenital diaphragmatic hernia presentation
presents soon after birth cyanosis tachypnoea chest wall asymmetry absent breath sounds on affected side bowel sounds audible on chest wall
Managing congenital diaphragmatic hernia
intubate & venitalte at minimal pressures orogastric tube (to locate stomach on X-ray) surgery to fix diaphragm
Hirschsprung’s disease
congenital condition characterised by partial/complete colonic functional obstruction associated with absence of parasympathetic ganglion cells = tonically constricted lamina = functional obstruction
Disease associated with Hirschsprung’s disease
Down’s syndrome
Hirschsprung’s disease initial presentation
failure to pass meconium in first 48h of life
repeated bilious vomiting
abdo distension
explosive passage of liquid & foul smelling stools (especially post PR exam)
failure to thrive
later presentation of Hirschsprung’s disease
chronic constipation resistant to treatment
investigating Hirschsprung’s disease
AXR
contrast enema (contracted distal bowel & dilated proximal bowel)
rectal biopsy
Hirschsprung’s disease treatment
Surgery
Hirschsprung’s disease prognosis
most pts acquire normal fecal continence & normal bowel habits
Meckel’s diverticulum
true diverticulum due to failure of the vitelline duct to obliterate
most common congenital abnormality of the small bowel
Location of Meckel’s diverticulum
in distal ileum close to ileocaecal valve
Meckel’s diverticulum rule of 2’s
occurs in 2% of population
within 2 feet from ileocaecal valve
2 inches long
Meckel’s diverticulum presentation
generally asymptomatic
painless Gi bleeding = haematochezia
intractable constipation
Meckel’s diverticulum investigations
AXR (for bowel obstruction)
Meckel’s scan
CT abdo
Intussusception epidemiology
usually seen age 3-12 months
peak age 9 months
commonest part of bowel affected by Intussusception
ileocaecal region
lead point is often an enlarged lymph node (peters patch) in terminal ileum
Intussusception presentation
paroxysmal colicky abdo pain drawing knees up to chest crying early vomiting blood PR (red current jelly stools) child normal between bouts of pain
Investigating Intussusception
Abdo USS (target sign/doughnut sign)
AXR
diagnostic enema
Mangement of Intussusception
drip & suck (IV fluids & NG tube)
radiological reduction via air enema
surgical reduction
Umbilical hernia
herniation of peritoneal sac covered with skin
generally spontaneously resolves in most children
Umbilical hernia presentation
bulge at umbilicus with overlying skin
easily reducible
Umbilical hernia management
generally observed till age 4-5 yrs if small
surgical closure if large (if asymptomatic then by age 2-3 yrs)
Inguinal hernia
due to patent processus vaginalis allowing abdominal contents to herniate into inguinal canal, presenting as bulge lateral to pubic tubercle
Inguinal hernia management
urgent surgical management indicated due to ↑ risk of strangulation
pyloric stenosis
infantile hypertrophic pyloric stenosis due to hypertrophy of the pyloric sphincter narrowing the pyloric canal
risk factors for pyloric stenosis
first born
male
family history
exposure to erythromycin in first 2 weeks of life
time of presentation of pyloric stenosis
between 2-8 weeks of age
rare after 12 weeks of age
Presentation of pyloric stenosis
non bilious vomiting within 30-60 minute of feeding projectile vomit
upper abdominal mass (olive)
baby remains hungry after feed
frequency/intensity of vomiting ↑ over several days
investigating pyloric stenosis
ABG/VBG (hypochloraemic, hypokalaemic metabolic alkalosis)
Abdo USS
classic blood gas finding for pyloric stenosis
hypochloraemic, hypokalaemic metabolic alkalosis
Management of pyloric stenosis
Ramstedt’s pyloromyotomy
Biliary atresia
progressive idiopathic necroinflammatory process involving the extra hepatic biliary tree leading to fibrosis
time of presentation of biliary atresia
usually between 2-8 weeks after birth
presentation of biliary atresia
usually seen in term infant with normal birth weight persistent jaundice play stools/dark urine failure to thrive hepatosplenomegaly
Investigations for biliary atresia
total & conjugated bilirubin (↑ conjugated bilirubin)
LFTs (generally ↑, disproportionate ↑ GGT)
Liver histology (gold standard)
management biliary atresia
surgery (portoenterostomy), best outcome if surgery before 8 weeks of age ursodeoxycholic acid (to encourage bile flow)
oesophageal atresia
blind ending oesophagus presenting with frothing at mouth, feeding difficulties, chocking, respiratory distress
oesophageal atresia investigation
antenatal USS (polyhydraminos, smaller/no stomach bubble) antenatal MRI (small stomach, oesophageal pouch)
oesophageal atresia management
surgery
suctioning oesophageal pouch till surgery
Risk factors of duodenal/oesophageal atresia
related to trisomy 21/13/18
twins
NB duodenal atresia is particularly related to trisomy 21
duodenal atresia presentation
abdo distension
bilious/non-bilious vomiting
presents in first days of life
Investigations for duodenal atresia
AXR (double bubble sign)
Volvulus/midgut rotation
a spectrum of rotation & fixation disturbances of the intestines occurring during embryonic development,
volvulus is complete twisting of a loop of intestines
Presentation of volvulus
rapid onset bilious/non bilious vomiting lactataemia metabolic acidosis oligouria hypotension feeding intolerance
Volvulus/midgut rotation investigations
Volvulus = clinical diagnosis AXR (double bubble sign, air fluid levels) contrast studies (duodenojejunal junction displaced in malrotation)
Managing Volvulus/midgut rotation
surgical treatment (even of asymptomatic malrotation due to risk fo volvulus) Ladd's procedure = treatment of choice
hydrocele
collection of serous fluid between the layers of tunica vaginalis around testicles/along spermatic cord
usually disappears age 1-2 yrs
most common hydrocele in children
communicating hydrocele i.e. patent processus vaginalis allowing fluid to drain into scrotum from peritoneum
presentation of hydrocele
scrotal enlargement (non tender, smooth cystic swelling, below/anterior to testicle)
transluminates with pen torch
swelling confined to scrotum i.e. able to get above it
managing hydrocele
clinical diagnosis
usually self limiting, so observe
repair if not resolves after 2 yrs of age
cryptorchidism
unilateral/bilaterally undescended testes, i.e. not present within the dependent portion of the scrotal sac
when to refer cryptorchidism
specialist referral age 6 months (corrected) if still undescended with surgical correction in next year
presentation of cryptorchidism
testes may be palpable in upper portion of scrotum/inguinal canal or may be absent (indicates intra-abdominal location)
Management of cryptorchidism
if still undescended by age 3 months =pathological
referral to specialist before 6 months
surgical repair by 12-18 months of age
cryptorchidism complications
risk of infertility if delayed diagnosis (especially >2y/o)
↑ risk of testicular torsion
↑ of testicular cancer
Hypospadias
congenital abnormality of penis where urethral opening is somewhere along ventral aspect of penis
Hypospadias common location
90% have meatus on/near glans = distal hypospadias
Hypospadias associated condition
if associated with cryptorchidism then may suggest disorder of sexual differentiation
Posterior urethral valves
cause obstruction of urethra
most common cause if UTI in male infants
Posterior urethral valves presentation
poor, intermittent dribbling urine stream
±frequent UTIs
Posterior urethral valves complications
can cause high pressure & detrusor hypertrophy leading to vesicoureteric reflux causing hydronephrosis
Posterior urethral valves diagnostics
voiding cystourethrography (VCUG) = gold standard postnatally NB most prenatal diagnosis
Posterior urethral valves treatment
endoscopic ablation = gold standard
meconium aspiration syndrome (MAS)
respiratory distress in the newborn due to presence of meconium in the trachea usually secondary to foetal hypoxia
meconium aspiration syndrome (MAS) risk factors
post term infants (>42 weeks) fetal distress oligohydramnios chorioamnionitis NB rare in <34 weeks gestation
meconium aspiration syndrome (MAS) presentation
meconium/green stained amniotic fluid green/blueish staining of skin at birth floppy baby ↓ APGAR score rapid/laboured/absent breathing bradycardia signs of post maturity (skin peeling, long stained nails)
managing meconium aspiration syndrome (MAS)
suctioning
O2/ventilatory support
surfactant (if severe)
infant respiratory distress syndrome (IRDS)
know as surfactant deficient lung disease or hyaline membrane disease
usually seen in preterm infants due to surfactant deficiency
Risk factors for infant respiratory distress syndrome (IRDS)
prematurity
male infant
c-section delivery without maternal labour
maternal diabetes