Paeds 2 Flashcards
What is the difference between GOR, GORD and regurgitation?
Gastro-oesophageal reflux (GOR) = passage of gastric contents into the oesophagus
Gastro-oesophageal reflux disease (GORD) = presence of troublesome symptoms or complications arising from GOR.
Regurgitation/posseting = is the voluntary and involuntary movement of part or all of the stomach contents beyond the oesophagus
Why are infants prone to reflux?
Short, narrow oesophagus.
Delayed gastric emptying.
Shorter, lower oesophageal sphincter that is slightly above, rather than below, the diaphragm.
Liquid diet and high caloric requirement, putting a strain on gastric capacity.
Larger ratio of gastric volume to oesophageal volume.
recumbent posture
What are the risk factors for GORD in infants
premature FH of heartburn or acid regurg obesity hiatus hernia history of diaphragmatic hernia or congenital oesophageal atresia neurodisbility overfed!!!
What are the features of a child with reflux
distressed crying whilst feeding abnormal neck postures chronic cough hoarse feeding difficulties - refusal, gagging, choking failure to thrive aspiration pneumonia
What age has reflux normally developed by?
6 months
if symptoms start after this, probably not reflux!
What are some differentials for reflux and what sets them apart?
pyloric stenosis - projectile vomiting, <2m old
obstruction - bilious vomiting, abdo distension and tenderness
upper GI bleed - heamatemesis
sepsis - unresponsive, focal features of infection
cow’s milk protein allergy - blood in stool, atopy, diarrhoea
How is regurgitation managed
reassure parents that it is normal!
make sure they seek help if child becomes distressed, feeding problems develop or faltering growth
How is GORD managed in a breast fed infant
trial giving gaviscon diluted in water after each feed for 1-2 weeks
if helps, continue
if not, try H2 antagonist or PPI for one month
if fails, seek help of paediatrician
How is GORD managed in a bottle fed infant
if feeds are excessive, decrease amount of milk!
1-2 weeks trial of giving smaller feeds more often (maintaining adequate intake)
if not resolved, 1-2 weeks of thickened feed
if not resolved, 1-2 weeks of gaviscon mixed in with feed
if not resolved, try H2 antagonist or PPI for one month
if fails, seek help of paediatrician
What is the daily milk requirement of an infant
150ml/kg per day
What are some complications of GORD
Reflux oesophagitis.
Recurrent aspiration pneumonia.
Recurrent acute otitis media (more than three episodes in 6 months).
Dental erosion in a child with neurodisability (for example cerebral palsy).
Apnoea
What is pyloric stenosis
diffuse hypertrophy and hyperplasia of the smooth muscle cells of the antrum and pylorus leading to narrowing of the pyloric canal and causing gastric outlet obstruction
What are the risk factors for pyloric stenosis
male
FH
What are the features of pyloric stenosis
infant aged 2-8 weeks vomiting after feeds - projectile, non-bilious, remians hungry and wants more! lethargy dehydration infrequent/absent bowel movements weight loss
What might be found on examination in an infant with pyloric stenosis
Stomach wall peristalsis
An enlarged pylorus, classically described as an ‘olive’, may be palpated in the right upper quadrant or epigastrium of the abdomen.
What is the differential diagnosis for an infant with suspected pyloric stenossi
gastroenteritis food allergy over feeding GORD sepsis UTI malrotation - would be bilious vomiting
What investigations would you do in a child with suspected pyloric stenosis
blood gas
U+E
USS abdomen
What is classically seen on a blood gas in an infant with pyloric stenosis? Why is this?
hypokalaemia, hypochloraemic metabolic alkalosis
due to the loss of hydrochloric acid with the repeated vomiting of stomach acid causing a hypochloraemia and metabolic alkalosis.
The kidneys will then exchange potassium to retain protons to attempt to compensate, leading to a hypokalaemia
What is the management of pyloric stenosis
pre op:
correct hydration and electrolyte abnormalities
NG tube - not for feeds, but aspirated at 4 hourly intervals
operatively: Ramstedt’s pyloromyotomy
post op: recommence feeds 6 hours after op
How is Ramstedt’s pyloromyotomy carried out?
open (supra-umbilical incision) or laparoscopic
pyloric muscle divided down to the mucosa
What are some pre op and post op complications of pyloric stenosis
pre op: hypovolaemia, apnoea
post op: infection, bleeding, wound dehisence, perforation, incomplete myotomy leading to persistent vomiting
Why can an infant vomit post Ramstedt’s pyloromyotomy
gastric distension
dysmotility
incomplete myotomy.
What is intussusception and why does it lead to obstruction
one section of bowel invaginates into a distal section of bowel
mesentery becomes compressed as it is drawn between the layers
lymphatic and venous obstruction leads to ischaemia
therefore, bowel wall distends and obstructs lumen
peristalsis is disrupted
OBSTRUCTION!!!
When is intussusception most common?
aged 5-10 months
What causes intussusception to occur?
90% - non-pathological lead point eg. rotavirus, adenovirus, HHV6, amoeba, shigella
10% pathological eg. Meckel's diverticulum (75%). Polyps and Peutz-Jeghers syndrome (16%). Henoch-Schönlein purpura (3%). Lymphoma and other tumours (3%). Reduplication - a process by which the bowel wall is duplicated (2%). Cystic fibrosis. An inflamed appendix. Ascariasis. Nephrotic syndrome. Foreign body. Hyperperistalsis. Exclusive breast-feeding. Weight above average. Rotavirus vaccine. Abdominal tuberculosis.
What are the symptoms of intussusception
sudden onset of colicky abdo pain paroxysmal - every 20mins vomiting dehydration lethargy, irritability, hypotonia, reduced conscious level
What can be found on examination in intussusception
sausage shaped mass in RUQ
lack of bowels in RLQ - Dance’s sign
What investigations should be done in suspected intussusception
U+E, FBC, clotting,
USS, AXR
What are the management options for intussusception
drip adn suck firstly - for dehydration
radiologist managed reduction by air or barium enema - if no sign of peritonitis, perforation or shock.
if any sign of peritonitis, perforation, pathological lead point >24 history or failed enema, laparotomy is needed!
What is CMPA
cow’s milk protein allergy
immune mediated abnormal allergic response to harmless proteins in milk
Which components of milk can a child be allergic to?
casein - 5 components
whey - 5 components
can be allergic to any of these!
What different kinds of CMPA are there? What is the difference between them?
IgE mediated - associated with histamine from mast cells and basophils. acute rapid onset - mins - 2 hours
non-IgE mediated - T cells. delayed onset - 48 hours-1 week
What are the risk factors for CMPA
atopy
other allergies
FH of atopy
formula fed
What are the features of IgE mediated CMPA
within 2 hours of ingestion
skin: pruritis erythema urticaria angio-oedema
GI: N+V oral pruritis colicky abdo pain diarrhoea
resp: cough chest tightness wheeze SOB URT symptoms - nasal itching, sneeze
What are the features of non IgE mediated CMPA
48 hours to 2 days after ingestion
skin:
pruritis
erythema
atopic eczema
GI: food aversion or refusal GORD abdo pain constipation loose/freq stools perianal redness failure to thrive
resp: cough chest tightness wheeze SOB
What are some differentials for CMPA
other allergies
lactose intolerance
Meckel’s diverticulum
GORD
What are the key features of lactose intolerance
due to an inability to digest lactose due to inadequate lactase
typically >6y
leads to abdo pain and diarrhoea
What investigations can be done to diagnose CMPA
skin prick test
IgE blood test
What is the management of CMPA
trial avoidance:
bottle fed - hydrolysed or amino acid formula
breast fed - mother omits all milk products from diet
children - omit from diet under care of dietitian
Challenge test:
every 6-12 months to see if remission has occurred
use ‘milk ladder’ baked goods to glass of milk
What is hydrolysed milk?
eg nutramigen
milk proteins broken down into peptides
What causes Down’s syndrome
trisonomy 21
Due to:
additional copy of 21 - error in cell division = non-dysjunction
mosaicism - segment of 21 had three copies, whole chromosome triplicated
translocations
What are the risk factors for down’s syndrome
family history
increasing maternal age - 15% by 40, 30% by 45
What are some features of down’s syndrome in the neonate
hypotonia
hyperreflexia
brachycephaly - short/flat head oblique palpebral fissures epicanthal folds Brushfield spots - white spots in iris flat nasal bridge low set ears protruding tongue high arched palate
loose skin at back of neck
congenital heart defects
duodenal atresia
single palmar crease
short little finger
short broad hands
gap between hallux and second toe
What screening tests need to be carried out on neonates with Down’s syndrome
cardiac echo - CHD
radiographic swallowing assessment - duodenal/oesophageal atresia
red reflex - congenital cataracts
hearing test - sensorineural or conductive hearing loss
TFT - risk of hypothyroid
FBC - risk of transient myelodysplasia of newborn
Which cardiac conditions are associated with down’s
atrioventicular canal defects VSD ASD PDA tetralogy of fallot
Which ENT conditions are associated with down’s
sensorineural or conductive hearing loss
increased risk otitis media, sinusitis, pharyngitis
obstructive sleep apnoea
Which eye conditions are associated with down’s
congenital cataracts refractive errors strabismus nystagmus congenital glaucoma keratoconus
Which GI conditions are associated with down’s
dental problems oesophageal atresia tracheooesophageal fistula GORD pyloric stenosis duodenal atresia Meckel's diverticulum Coeliac disease imperforate anus
Which orthopaedic conditions are associated with down’s
atlanto-axial instability hyperflexibility scoliosis hip dislocation patellar subluxation/dislocation foot deformities
Which endocrine conditions are associated with down’s
hypothyroid
Which neuro/psych conditions are associated with down’s
learning difficulties
behavioural problems
seizures
dementia after 40y
Which haem conditions are associated with down’s
increased risk of infections due to immature immune system
increased risk ALL, AML, AMegL
polycythemia
transient myloproliferative disorder
Describe the screening programme available for Down’s
identify those at high risk of having a child with Down’s - combined test using ultrasound nuchal translucency and serum markers
offer invasive testing if risk >1 in 150 - chorionic villus sampling or amniocentesis
When can serum screening for Down’s syndrome be done?
What does it measure?
10 - 14+1 gestation
betaHCG - raised in down’s
PAPP-A - decreased in down’s
When can fetal nuchal translucency screening for Down’s syndrome be done?
What does it measure?
11+2 - 14+1 gestation
What screening for down’ can be done after 14+1 weeks gestation? When until?
quadruple testing
involves beta HCG, AFP, inhibin A, uE3
up to 20+0
When can chorionic villus sampling and amniocentesis be carried out?
chorionic villus sampling - <13weeks
amniocentesis >15 weeks
What is the risk of miscarriage with chorionic villus sampling and amniocentesis?
chorionic villus sampling - 1-2%
amniocentesis - 0.5-1%
What is oesophageal atresia
there is a blind ending oesophagus.
It can occur in isolation or there may be one or more fistulae communicating between the abnormal oesophagus and the trachea, known as a tracheo-oesophageal fistula (TOF)
What is the most common kind of TOF
blind ended oesophagus
fistula between distal oesophagus and trachea
What conditions are associated with oesophageal atresia
VACTERL CHARGE Down's Patau's - trisonomy 13 Edward's - trisonomy 18 Di george
How might oesophageal +-TOF present?
polyhydraminos antenatally SGA respiratory distress feeding problems not avle to swallow! lots of secretions - frothing not able to pass NG tube
What investigations should be done in an infant with oesophageal atresia?
CXR bronchoscopy to assess for fistulae cardiac echo renal scan limb xrays USS spine
What can be seen in CXR in oesophageal atresia
If there is no air seen in the gastrointestinal tract, it is likely that there is isolated oesophageal atresia with no TOF.
Air can also be injected to distend the upper oesophageal pouch prior to X-ray so that the blind ending pouch may be seen.
If attempt has been made to pass a nasogastric tube, it can be seen curling up in the upper oesophageal pouch.
What is the management of oesophageal atresia?
Surgery is carried out either immediately, as a delayed repair or as a staged repair depending on other factors such as birth weight and other associated conditions (principally cardiac abnormalities).
What is duodenal atresia
either atresia, stenosis or web in duodenum leading to obstruction
How does duodenal atresia present?
polyhydraminos
persistent vomiting, often bilious (if below level of entry of bile duct), after feeds in first few days of life
if stenosis can occur as failure to thrive
What investigations are done in duodenal atresia
CXR/AXR
barium enema
What would an xray show in duodenal atresia
fewer air levels than expected
classical double bubble sign - due to stomach, pylorus and dilated duodenum then atresia
