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
Explain the difference between gastroschisis and exomphalos
gastroschisis = openign in verntral abdominal wall lateral to umbilical cord. bowel in amniotic sac.
exomphalos = bowel in membrane of umbilical cord. liver can also enter it. more likely to be associated with other congenital problems
How can gastroschisis or exomphalos present antenatally
rise in alpha-fetoprotein in the second trimester
abnormality on ultrasound scan.
How are gastroschisis and exomphalos managed?
need closure
if small/medium exomphalos can do primary closure
if large, may need to use plastic sheath - “silo” to create space in abdomen first
in gastroschisis, primary closure may need to be delayed if the intestines are too inflamed and hence too enlarged to be replaced in the abdominal cavity. Too tight closure must be avoided in order to prevent respiratory problems and a reduction in cardiac output
What could be a sign of an anorectal malformation?
failure to pass meconium after 24hrs
What is VACTERL
condition of associated multiple abnormalities, some within and some outside the gut
Vertebral anomolies - single or multiple hemivertebrae, scoliosis, rib deformities
Anorectal malformation - imperforate anus, cloacal deformities
cardiac malformation - VSD, ASD, fallot’s, PDA, coarctation of aorta
Tracheoesophageal fistula
(o)Esophageal atresia
Renal anomalies - ageneis, dysplsaia, horseshoe, polycystic kidneys, urethral atresia
Limb abnormalities - radial dysplasia, absent radius, radial defomities, polydactyly
What investigations should be done if one feature of VACTERL is present
spine xray USS spinal cord examination anus cardiac echo CXR renal USS limb examination
What is Hirchsprung’s disease
absence of parasympathetic ganglion cells in the myenteric and submucosal plexus of the rectum, possibly extending to the colon.
due to failure of Ganglion cells, derived from the neural crest to migrate caudally with the vagal nerve fibres along the intestine.
Arrest in migration leads to an aganglionic segment which is unable to relax, leading to a functional colonic obstruction.
How can Hirchsprung’s disease present in an infant?
Abdominal distention,
failure of passage of meconium within the first 48 hours of life
repeated vomiting.
How can Hirchsprung’s disease present in a child?
chronic constipation that is resistant to the usual treatments and a daily enema may be required.
early satiety,
abdominal discomfort and distension due to the constipation
leads to poor nutrition and poor weight gain.
How is Hirchsprung’s diagnosed?
plain abdominal X-ray - affected segment not dilated, proximal section dliated
rectal biopsy - absence of ganglion cells in the myenteric plexus.
How is Hirchsprung’s managed
resection of affected segment
What is CHARGE syndrome?
most commonly CHD7 mutation causing variety of congential malformations.
Coloboma Heart anomolies - VSD, ASD, Fallot's Atresia - posterior choanal (back of nose) Retardation - physical and developmental Genital hypoplasia Ear abnormalities and deafness
How would you define a floppy infant?
An infant with prominent, generalized decreased muscle tone
What is the difference between postural and phasic tone?
Postural tone = prolonged contraction of muscles in response to the continual low-intensity stretch of gravity. When postural tone is depressed the trunk
and limbs cannot resist gravity and the
infant becomes floppy
Phasic tone = the rapid contraction in response to high-intensity stretch e.g. tendon reflex
Where can a lesion causing hypotonia pccur?
CNS
peripheral nerves
muscles
NMJ
How might an infant with hypotonia present?
floppy
feeding difficulties
breathing difficulties
not meeting developmental milestones
What are the important questions to ask in the history when a child presents with hypotonia
obstetric:
Maternal exposure to toxins and infections (might suggest a CNS cause)
Foetal movement in utero
Foetal presentation - Breech delivery or cervical position may cause spinal cord trauma, Breech delivery is more common in neuromuscular disorders as turning requires motility
Birth trauma
Amniotic fluid volume
Birth anoxia
Now:
- Acquired/Congenital
- Have parents noticed unusual breathing patterns?
- Any swallowing issues?
- Alertness
- Spontaneous activity
- Character of cry
- Neonatal seizures
- Apnoeic episodes
- developmental problems
Family history
- Chromosomal abnormalities
- Consanguinity
- Motor milestones
- Premature death
What should you examine in a child presenting with hypotonia
general - dysmorphic features, posture upper and lower limb neuro CN developmental signs truncal tone neck tone shoulder girdle
What are the key examination findings in terms of truncal tone, neck tone and shoulder girdle that prove hypotonia
Truncal tone: suspend the infant with the abdomen held in the hand, the baby will drape
Neck tone: gently pull the baby up and forward by
pulling both arms at the same time, the infant will not be able to resist gravity and the head will become fully
extended
Shoulder girdle: suspend the infant vertically with
hands in the axillae. Floppy infants will slip through the
hands as they will not adduct the arms and fix the
shoulders
How can you differentiate between central and peripheral hypotonia?
central: "strong floppy" ● Truncal weakness, but sustained limb strength ● Increased tendon reflexes ● Upgoing plantars ● Sustained clonus ● Global developmental delay ● Syndromic features - e.g. trisomy 21
peripheral: "weak floppy" Weak cry ● Weak cough ● Poor swallow ● Abnormal breathing pattern ● Frog leg position ● Decreased tendon reflexes ● Downgoing plantars ● Social development may be normal
What are the differentials for a floppy infant?
Central:
Down’s syndrome, Prader-Willi, hypoxic-ischaemic
encephalopathy, congenital infection (e.g. CMV)
Peripheral: Spinal Muscular Atrophy, Charcot-Marie-Tooth, Guillain-Barré,
Myasthenia gravis, Muscular dystrophies
Connective tissue disease: Ehlers Danlos, Marfan’s
Metabolic: Hypokalaemia, hypophosphataemia, rickets
Other: Hypothyroidism, Infection, Benign congenital hypotonia (diagnosis of exclusion)
What are muscular dystrophies?
- > A group of inherited disorders with progressive muscle degeneration.
- > Abnormalities in dystrophin gene, which is part of the muscle fibre cytoskeleton.
- > eg. Duchenne & Becker
What are the jey features of muscular dystrophies?
- > Waddling gait
- > Gower sign (raising from floor in a prone position)
- > Unable to keep up with peers
- > Recurrent LRTIs
- > Nocturnal hypoxia
- > Cardiomyopathy
- > Scoliosis
What investigations are useful in hypotonia
U+E, CK, FBC, CRP, blood cultures MRI head EMG muscle biopsy karyotyping DNA mutation studies
What factors are associated with increased chance of a mother breast feeding?
> 30y
ethnic minority
first time mother
left full time education after 18
What are the benefits of breast feeding for the baby?
reduces risk of: infections eg. otitis media, LRTI, gastroenteritis eczema, asthma, allergic rhinitis SIDS obesity T2DM
transder of antibodies - helps to fight infecions
increases intelligence
changes in response to needs of baby
changes flavour - baby enjoys different flavours
develops microbiota as good bacteria passes via milk/skin
bonding!`
What are the benefits of breast feeding for the mum?
reduces risk of:
breast and ovarian cancer
T2DM
free! no need for sterilizer or bottles no need to pre warm milk can do it anywhere contraceptive no packaging or plastic bonding!
What is croup
viral URTI leading to inflammation of nasopharynx, larynx and trachea
leads to subglottal inflammation, oedema and compromise of airway
movement of vocal cords impaired
What causes croup
parainfluenza types I, II, III and IV RSV adenovirus rhinovirus enterovirus
What are the risk factors for croup
6m-3y (most common 2y)
male
What are the features of croup
pro-dromal coryzal - runny nose, fever, sore throat barking cough hoarse cry worse at night increased work of breathing - recession stridor
if severe: asynchronous chest and abdo movement drowsy lethargy cyanosis reduced air entry
Give some differentials for croup and how they can be distinguished
bacterial tracheitis - high fever, stridor, resp distress, not recovering
epiglottitis - no HiB vaccine!!! sudden onset high fever, dysphagia, drooling, anxiety, non-barking cough, and their preferred posture is sitting upright with head extended.
foreign body - no fever, history of it, non prodrome
retropharyngeal or peritonsillar abscess - dysphagia, drooling, neck dtiffness, cervical lymphadenopathy
allergic reaction - rapid onset, urticaria, history
angioneurotic oedema - acute swelling of the upper airway that may cause dyspnoea and stridor. Fever is uncommon. Swelling of face, tongue, or pharynx may be present
How can croup’s severity be assessed?
Westley clinical scoring system
What differentiates between mild, moderate and severe croup
Mild – seal-like barking cough but no stridor or sternal/intercostal recession at rest.
Moderate – seal-like barking cough with stridor and sternal recession at rest; no agitation or lethargy.
Severe – seal-like barking cough with stridor and sternal/intercostal recession associated with agitation or lethargy.
Which children with croup require hospital assessment
Moderate or severe croup, or impending respiratory failure.
Any suspicion of epiglottitis, bacterial tracheitis, peritonsillar abscess, retropharyngeal abscess, or laryngeal diphtheria.
Any suspicion of inhaled foreign body, angioneurotic oedema, hypocalcaemic tetany, or ingestion of corrosives.
Which children with croup need consideration of admission to hospital for treatment?
moderate or severe illness
impending respiratory failure.
respiratory rate of over 60 breaths/minute.
Children with mild illness may require admission if they have factors that warrant a lower threshold for admission, such as:
Chronic lung disease (including bronchopulmonary dysplasia).
Haemodynamically significant congenital heart disease.
Neuromuscular disorders.
Immunodeficiency.
Age under three months.
Inadequate fluid intake (50 to 75% of usual volume, or no wet nappy for 12 hours).
Factors that might affect a carer’s ability to look after a child with croup, such as adverse social circumstances, or concerns about the skill and confidence of the carer in looking after a child with croup at home, or the carer being able to spot deteriorating symptoms.
Longer distance to healthcare in case of deterioration.
What are the features of Impending respiratory failure?
increasing upper airway obstruction,
sternal/intercostal recession,
asynchronous chest wall and abdominal movement,
fatigue,
pallor or cyanosis,
decreased level of consciousness.
The degree of chest wall recession may diminish with the onset of respiratory failure as the child tires.
A respiratory rate of over 70 breaths/minute
What is the treatment for mild croup
in the community
give one dose of oral dexamethasone - 150micrograms/kg
safety net
paracetamol or ibuprofen if distressed by fever
adequate fluid intake
check them during the night
What is the treatment for moderate/severe croup
admission!
o2 if low sats
PO dexamethasone 150micrograms/kg or nebulised budenoside
adrenaline nebuliser
adequate oral fluid intake
paracetamol or ibuprofen if distressed by fever
What is gastroenteritis?
transient disorder due to enteric infection with viruses, bacteria, or parasites. It is characterized by the sudden onset of diarrhoea, with or without vomiting
Define diarrhoea
three or more episodes of partially-formed or watery stool in a day
What is the difference between acute and persistent diarrhoea
Acute diarrhoea is defined as three or more episodes of partially-formed or watery stool in a day, lasting for less than 14 days
Persistent diarrhoea is an acutely starting episode of diarrhoea that lasts for more than 14 days
What are the causes of gastroenteritis?
viruses - most common
Rotavirus
adenovirus
norovirus
bacteria Campylobacter jejuni/coli E coli Salmonella Shigella
parasites
Cryptosporidium
Entamoeba histolytica
Giardia
bacterial toxins
Staphylococcus aureus — usually found in cooked meats and cream products.
Bacillus cereus — mainly found in reheated rice.
Clostridium perfringens — usually found in reheated meat dishes or cooked meats.
What are the symptoms of gastroenteritis?
Diarrhoea (loose or watery stools, usually at least three times in 24 hours) is the main symptom of gastroenteritis.
Other symptoms may include: Nausea. Sudden onset of vomiting. Blood or mucus in stool. Systemic features (for example fever or malaise). dehydration shock
Give some differentials for gastroenteritis
Systemic infection (UTI, pneumonia, meningitis, sepsis).
Appendicitis.
Other surgical causes (intussusception, sub-acute bowel obstruction, Hirschsprung’s colitis).
Gastro-oesophageal reflux.
What investigations should be done in gastroenteritis
obs
FBC U+E
stool MC+S
blood cultures
What is the management of gastroenteritis if there is no sign of dehydration
continue to breast feed/bottle feed
maintain fluid intake
no fizzy drinks or fruit juice
if at risk of dehydration, consider 5ml/kg oral rehydration solution after watery stool
What are the signs of dehydration in gastroenteritis
decreased responsiveness/alertness sunken eyes dry mucous membranes reduced urine output tachypnoea tachycardia reduced skin turgor appear unwell/deteriorating
Which children are most at risk of dehydration from gastroenteritis
<1yr
low BW
>5 diarrhoeal stools in the previous 24 hours.
>2 vomits in previous 24 hours.
Children who have not been offered, or have not been able to tolerate, supplementary fluids before presentation.
Infants who have stopped breastfeeding during their illness.
Children with signs of malnutrition.
What is the management of gastroenteritis if there are signs of dehydration
50ml/kg oral rehydration solution in 4 hours resuscitation
maintenance fluids
continue to breast feed/give usual drinks
ondansetron if vomiting continues
ORS via NG if vomit continues
monitor!
What is the management of gastroenteritis if there are signs of shock
IV/IO access 20ml/kg 0.9% saline repeat if no response SENIOR REVIEW consider other diagnoses
How should children be rehydrated orally?
50ml/kg over 4h
When might an NG tube be required for rehydration
vomiting oral rehydration solution
feed refusal
no red flag symptoms
What are the red flags for dehydration
inherited metabolic disorder appears unwell/deteriorating irritable or lethargic sunken eyes tachycardia tachypnoea decreased skin turgor
What are the indications for IV fluid resuscitation
Confirmed or suspected shock
Presence of red flag signs/symptoms, and deterioration despite oral rehydration
Persistent vomiting of oral rehydration solution (orally or via NG)
Nil by mouth (e.g. surgical patients)
How is IV resuscitation given to children
20ml/kg of 0.9% sodium chloride reassess 20ml/kg of 0.9% sodium chloride reassess SENIOR CICU REVIEW
What maintenance fluids are given to children
0.9% sodium chloride + 5% dextrose
100ml/kg/24h for the first 10kg
50ml/kg/24h for next 10kg
20ml/kg/24h for each additional kg
add 10mmol KCl per 500ml of dex/saline
What is whooping cough
respiratroy infection caused by Bordatella pertussis
What kind of organism is Bordatella pertussis
gram -ve coccobacillus
What are the feaures of whooping cough
Catarrhal phase: 1-2 weeks mild resp infection. Nasal discharge, Conjunctivitis, Malaise. Sore throat. Low-grade fever. Dry, unproductive cough
Paroxysmal phase: 1-6 weeks. prolonged dry hacking cough followed by whoop. choking, gasping, flailing, cyanosis. post-tussive vomiting
Convalescent phase: lasts up to 3 months, during which there is a gradual improvement in cough frequency and severity.
What is a whoop?
breathing in through partially closed vocal cords after a coughing paroxysm
Give some differentials for whooping cough
croup bronchiolitis other resp infection - adenovirus, Mycoplasma asthma post infectious cough
What investigatons are done for whooping cough
it is a clinical diagnosis!
needs PHE notification
What investigations do PHE suggest upon notification of a potential whooping cough diagnosis
If the cough is of 2 weeks’ duration or less, culture of a nasopharyngeal aspirate or nasopharyngeal/pernasal swabs is recommended for people of all ages. However, a negative result does not exclude pertussis.
Real-time PCR testing of nasopharyngeal or throat swabs can also be used to confirm infection in people of all ages with symptoms of less than three weeks’ duration.
If the cough is of more than 2 weeks’ duration, anti-pertussis toxin immunoglobulin G (IgG) serology may be employed in people aged over 17 years. Anti-pertussis toxin IgG detection in oral fluid can be used in children aged 5 to 16 years.
What is the management of whooping cough
NOTIFY PHE
admit if <6mand acutely unwell, respiratory compromise, complications
Abx if onset <21 days ago.
<1m = clarithromycin
>1m = clarithromycin/azithromycin
pregnant women = erithromycin
supportive
no work/school fo >48hrs after stopped abx/21 days after onset
What is the vaccination schedule for whooping cough
at 8w
at 3y 4m
booster in pregancy >20w gestation
What is the incubation period for whooping cough
7 to 20 days.
What are some complications of whooping cough
Serious complications of pertussis include:
Apnoea.
Pneumonia (usually caused by secondary bacterial infection).
Seizures.
Encephalopathy (rare in adults).
Increased intra-thoracic and intra-abdominal pressure due to violent and/or prolonged coughing can cause:
Pneumothorax.
Umbilical and inguinal hernias, and rectal prolapse.
Rib fracture and herniation of lumbar intervertebral discs.
Urinary incontinence.
Subconjunctival or scleral haemorrhage, and facial and truncal petechiae.
Frequent post-tussive vomiting can lead to severe dehydration and/or malnutrition.
What is IUGR?
intrauterine growth restriction
clinical definition used to describe a neonate born with clinical features of malnutrition and growth restiction, irrespective of birth weight centile
fetal growth slows or stops in utero
What is SGA
small for gestational age
defined as having a birth weight below the 10th centile
does not take into account growth in utero or characteristics at birth
What are the three kinds of SGA
growth at all ages has been low, but the infant is otherwise healthy. constitutionally small
normal growth, which then slows down - due to IUGR
non placental mediated growth restriction - strucutal, chromosomal, inborn error of metabolism, fetal infection
What are the risk factors for SGA
Minor risk factors: Maternal age ≥35 years. IVF singleton pregnancy. Nulliparity. BMI <20 or 25-34.9. Smoker - 1-10 cigarettes per day. Low fruit intake pre-pregnancy. Pregnancy interval <6 months or ≥60 months.
Major risk factors: Maternal age >40 years. Smoker - ≥11 cigarettes per day. Paternal or maternal SGA. Cocaine use. Daily vigorous exercise. Previous SGA baby. Previous stillbirth. Chronic hypertension. Diabetes with vascular disease. Renal impairment. Antiphospholipid syndrome. Heavy bleeding similar to menses. Pregnancy associated plasm protein-A (PAPP-A) <0.4 multiples of the median (MOM).
How is the diagnosis of SGA made?
Symphysis fundal height measurement after 24w
plotted on customised chart
if SFH plots <10th centile or growth slows and crosses a centile line
then an USS is used to measure the size
When is symphysis fundal height an inaccurate measure?
BMI >35
large fibroids
hydraminos - oligo or poly
How is SGA monitored during pregnancy
if major risk factor - serial USS and umbilical artery dopplers to monitor from 26 weeks
if >=3 minor risk factors - uterine artery doppler at 20-24 weeks. if abnormal, need further USS and doppler monitoring after 26 weeks
What are the maternal risk factors for IUGR
Maternal age <16 years or >35 years
Low socio-economic status.
Parity (none or more than five births).
Inter-pregnancy interval <6 months or >120 months
Previous delivery of an SGA newborn.
Maternal substance abuse (smoking, alcohol, illicit drugs such as marijuana or cocaine).
Maternal medication (eg, warfarin, steroids, anticonvulsants, antineoplastic, antimetabolite, and folic acid antagonists).
Maternal pre-pregnancy BMI <20, weight <45 kg or >75 kg.
Assisted reproductive technologies.
Pregnancy: moderate to heavy physical work, severe maternal starvation, poor weight gain, high-altitude and maternal hypoxia, poor medical care.
Maternal medical disorders - eg, asthma, cyanotic congenital heart disease, hypertensive disorders, pre-eclampsia, diabetes associated with vasculopathy, chronic kidney disease, systemic lupus erythematosus, antiphospholipid syndrome, sickle cell disease; acquired thrombophilia - eg, anti-cardiolipin antibodies and lupus anticoagulant.
Maternal infection and parasite infestations: TORCH syndrome (= toxoplasmosis, other, rubella, cytomegalovirus, herpes simplex), malaria, tuberculosis, urinary tract infections and bacterial vaginosis).
What are some fetal risk factors for IUGR
Chromosomal abnormalities - eg, trisomies 13, 18, or 21, autosomal deletions, triploidy, ring chromosomes and uniparental disomy.
Genetic syndromes - eg, Russell-Silver syndrome, Rubinstein-Taybi syndrome, Dubowitz’s syndrome, Seckel’s syndrome, Fanconi’s syndrome.
Major congenital anomalies - eg, tracheo-oesophageal fistula, congenital heart disease, congenital diaphragmatic hernia, abdominal wall defects (omphalocele or gastroschisis), neural tube defect (eg, anencephaly), anorectal malformation.
Multiple gestation.
Congenital infections (TORCH syndrome, malaria, congenital HIV infection, syphilis).
Metabolic disorders - eg, congenital lipodystrophy, galactosaemia, generalised gangliosidosis type I, hypophosphatasia, fetal phenylketonuria.
Give some placental risk factors for IUGR
placental dysfunction (including pre-eclampsia) placental abruption.
What are the featues of an IUGR baby once born?
Large head when compared to the rest of the body (brain sparing effect).
Large and wide anterior fontanelle.
Anxious and hyper-alert infant.
Absence of buccal fat (old man look).
Long fingernails.
Loose, dry and easy peelable skin.
Loose fold of skin in the nape of the neck, axilla, interscapular area and gluteal region.
Poor skeletal muscle mass and subcutaneous fat with thin arms and legs.
Small or scaphoid abdomen.
Poor breast bud formation and immature female genitalia.
Relatively large and thin hands and legs compared with the body.
Thin umbilical cord, often stained with meconium.
Describe the features of symmetrical IUGR in utero and at birth
hypoplastic
occurs early in pregnancy
head circumference, abdominal circumference, biparietal diameter and fetal length are all proportionally reduced
post natal weight, length and head circumference reduced
poor prognosis
Describe the features of asymmetrical IUGR in utero and at birth
malnourisehd
occurs later in pregnancy
reduced abdominal circumference. biparietal, head circumference and femur length all normal. HEAD SPARING GROWTH
reduced postnatal weight, length and head circumference normal
good prognosis
What are the neonatal complications of an IUGR baby?
Birth/perinatal asphyxia. Meconium aspiration. Hypothermia. Retinopathy of prematurity. Persistent pulmonary hypertension. Pulmonary haemorrhage. Feed intolerance, necrotising enterocolitis. Polycythaemia, hyperviscosity. Renal dysfunction. Immunodeficiency. Hypoglycaemia, hyperglycaemia, hypocalcaemia, low serum ferritin.
What are some of the long term neurodevelopmental problems an IUGR baby can have?
Lower scores on cognitive testing.
Difficulties in schools or requiring special education.
Gross motor and minor neurological dysfunction.
Behavioural problems (attention deficit hyperactivity disorder).
Lower strength and work capacity.
Cerebral palsy.
Low social competence.
Poor academic performance.
Lower levels of intelligence.
Hyperactive behaviour.
Poor perceptual performance.
Poor visuo-motor perception; motor incompetence and difficulties with reading and with learning mathematics.
What long term health problems does IUGR increase the risk of?
attaining an adult height below their target height,
developing metabolic disorders (obesity, metabolic syndrome, type 2 diabetes) and cardiovascular diseases.
precocious pubarche,
exaggerated precocious adrenarche,
an earlier onset of menarche,
faster progression of puberty
What is volvulus?
complete twisting of a loop of intestine around its mesenteric attachment site
results in a closed loop bowel obstruction
Where is it most common for a volvulus to occur in an infant?
Why?
midgut
due to malrotation
Describe hte normal rotation of the midgut
herniation of midgut into umbilical cord
3 x 90 degree turns anticlockwise (looking at body)
the cranial portion returns first to create posterior lie of small bowel
What does malrotation of the midgut result in?
incomplete rotation (only 1 x 90 degree turn) leads to left sided colon
reversed rotation (1 x 90 degree turn clockwise) leads to transverse colon lying posterior to duodenum
what are the features of malrotation
failure to thrive anorexia constipation bloody stools bilious vomiting recurrent abdo pain (due to ischaemia)
What are the features of volvulus
distended abdomen bilious vomiting peritonitits metabolic acidosis oliguria hypotension
What investigations need to be done in malrotation/volvulus
ABG/VBG, FBC, U+E, LFT, CRP, clotting, G+S if severe volvulus
AXR
upper GI contrast study
CT abdo
What would you expect to see on upper GI contrast study in volvulus
dilation of proximal duodenum
bird beak/spiral/corkscrew obstruction
How would you manage volvulus
NG tube - decompresssion of stomach
surgery - Ladd’s procedure
How would you manage malrotation
elective Ladd’s procedure
due to risk of volvulus
Describe Ladd’s procedure
detorsion of bowel
resect any necrotic section
dissect away Ladd’s bands - attach displaced caecum to upper right anterior abdominal wall
place caecum to left
small bowel to right - this spreads out the mesenteric base
What are the complications of chronic intermittent volvulus
malabsorption
constipation
diarrhoea
What are the complications of acute volvulus
ischaemia necrosis of mucosa perforation peritonitis sepsis death
What causes chicken pox?
varicella zoster virus
Describe the transmission, incubation and infectious period of chicken pox
90% Transmission rate by personal contact or droplet spread,
incubation period of 1–3 weeks
Chickenpox is infectious from 1–2 days before the rash appears until the vesicles are dry or have crusted over usually 5 days after the onset of the rash
What are the risk factors for developing severe chicken pox
immunocompromised
steroids
older age
malignancy
What are the features of chicken pox
prodrome: includes nausea, myalgia, anorexia, and headache
General malaise, loss of appetite, and feeding problems.
Fever.
Rash: Small, erythematous macules appear on the scalp, face, trunk, and proximal limbs, which progress over 12–14 hours to papules, clear vesicles (which are intensely itchy), and pustules.
Vesicles can also occur on the palms and soles, and mucous membranes can also be affected, with painful and shallow oral or genital ulcers.
Crusting occurs usually within 5 days of the onset of the rash, and crusts fall off after 1–2 weeks.
Give some differentials for chicken pox
Other vesicular viral rashes, such as:
Herpes simplex (not usually disseminated).
Herpes zoster (usually unilateral and localized to dermatomes).
Hand, foot, and mouth disease (caused by Coxsackie virus).
Other infections, such as: Impetigo. Scabies. Syphilis. Meningococcaemia (can be confused with haemorrhagic varicella). Toxic shock syndrome.
Skin disorders, such as: Guttate psoriasis. Drug eruption. Insect bites. Papular urticaria. Erythema multiforme. Stevens–Johnson syndrome. Henoch–Schönlein purpura. Dermatitis herpetiformis.
What is the management of chicken pox
if otherwise healthy: supportive management
if immunocompromosied: oral/IV aciclovir
> 14y - oral aciclovir if present within 24 hrs of onset
What are the potenital complications of chicken pox
Secondary infection of lesions can occur, especially group A streptococcal infection. can produce necrotising fasciitis and toxic shock syndrome.
Viral pneumonia
Encephalitis
Other CNS complications - eg, benign cerebellar ataxia, myelitis, vasculitis causing strokes (may occur several months after the chickenpox
Which people should people with infectious chicken pox avoid?
immunocompromised
neonates
pregnant women
