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Flashcards in Paeds 2 Deck (174)
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1
Q

What is the difference between GOR, GORD and regurgitation?

A

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

2
Q

Why are infants prone to reflux?

A

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

3
Q

What are the risk factors for GORD in infants

A
premature
FH of heartburn or acid regurg
obesity
hiatus hernia
history of diaphragmatic hernia or congenital oesophageal atresia
neurodisbility
overfed!!!
4
Q

What are the features of a child with reflux

A
distressed
crying whilst feeding
abnormal neck postures
chronic cough
hoarse
feeding difficulties - refusal, gagging, choking
failure to thrive
aspiration pneumonia
5
Q

What age has reflux normally developed by?

A

6 months

if symptoms start after this, probably not reflux!

6
Q

What are some differentials for reflux and what sets them apart?

A

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

7
Q

How is regurgitation managed

A

reassure parents that it is normal!

make sure they seek help if child becomes distressed, feeding problems develop or faltering growth

8
Q

How is GORD managed in a breast fed infant

A

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

9
Q

How is GORD managed in a bottle fed infant

A

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

10
Q

What is the daily milk requirement of an infant

A

150ml/kg per day

11
Q

What are some complications of GORD

A

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

12
Q

What is pyloric stenosis

A

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

13
Q

What are the risk factors for pyloric stenosis

A

male

FH

14
Q

What are the features of pyloric stenosis

A
infant aged 2-8 weeks
vomiting after feeds - projectile, non-bilious, remians hungry and wants more!
lethargy
dehydration
infrequent/absent bowel movements
weight loss
15
Q

What might be found on examination in an infant with pyloric stenosis

A

Stomach wall peristalsis

An enlarged pylorus, classically described as an ‘olive’, may be palpated in the right upper quadrant or epigastrium of the abdomen.

16
Q

What is the differential diagnosis for an infant with suspected pyloric stenossi

A
gastroenteritis
food allergy
over feeding
GORD
sepsis
UTI
malrotation - would be bilious vomiting
17
Q

What investigations would you do in a child with suspected pyloric stenosis

A

blood gas
U+E
USS abdomen

18
Q

What is classically seen on a blood gas in an infant with pyloric stenosis? Why is this?

A

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

19
Q

What is the management of pyloric stenosis

A

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

20
Q

How is Ramstedt’s pyloromyotomy carried out?

A

open (supra-umbilical incision) or laparoscopic

pyloric muscle divided down to the mucosa

21
Q

What are some pre op and post op complications of pyloric stenosis

A

pre op: hypovolaemia, apnoea

post op: infection, bleeding, wound dehisence, perforation, incomplete myotomy leading to persistent vomiting

22
Q

Why can an infant vomit post Ramstedt’s pyloromyotomy

A

gastric distension
dysmotility
incomplete myotomy.

23
Q

What is intussusception and why does it lead to obstruction

A

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!!!

24
Q

When is intussusception most common?

A

aged 5-10 months

25
Q

What causes intussusception to occur?

A

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.
26
Q

What are the symptoms of intussusception

A
sudden onset of colicky abdo pain 
paroxysmal - every 20mins
vomiting
dehydration
lethargy, irritability, hypotonia, reduced conscious level
27
Q

What can be found on examination in intussusception

A

sausage shaped mass in RUQ

lack of bowels in RLQ - Dance’s sign

28
Q

What investigations should be done in suspected intussusception

A

U+E, FBC, clotting,

USS, AXR

29
Q

What are the management options for intussusception

A

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!

30
Q

What is CMPA

A

cow’s milk protein allergy

immune mediated abnormal allergic response to harmless proteins in milk

31
Q

Which components of milk can a child be allergic to?

A

casein - 5 components
whey - 5 components

can be allergic to any of these!

32
Q

What different kinds of CMPA are there? What is the difference between them?

A

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

33
Q

What are the risk factors for CMPA

A

atopy
other allergies
FH of atopy
formula fed

34
Q

What are the features of IgE mediated CMPA

A

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
35
Q

What are the features of non IgE mediated CMPA

A

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
36
Q

What are some differentials for CMPA

A

other allergies
lactose intolerance
Meckel’s diverticulum
GORD

37
Q

What are the key features of lactose intolerance

A

due to an inability to digest lactose due to inadequate lactase
typically >6y
leads to abdo pain and diarrhoea

38
Q

What investigations can be done to diagnose CMPA

A

skin prick test

IgE blood test

39
Q

What is the management of CMPA

A

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

40
Q

What is hydrolysed milk?

A

eg nutramigen

milk proteins broken down into peptides

41
Q

What causes Down’s syndrome

A

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

42
Q

What are the risk factors for down’s syndrome

A

family history

increasing maternal age - 15% by 40, 30% by 45

43
Q

What are some features of down’s syndrome in the neonate

A

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

44
Q

What screening tests need to be carried out on neonates with Down’s syndrome

A

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

45
Q

Which cardiac conditions are associated with down’s

A
atrioventicular canal defects
VSD
ASD
PDA
tetralogy of fallot
46
Q

Which ENT conditions are associated with down’s

A

sensorineural or conductive hearing loss
increased risk otitis media, sinusitis, pharyngitis
obstructive sleep apnoea

47
Q

Which eye conditions are associated with down’s

A
congenital cataracts
refractive errors
strabismus
nystagmus
congenital glaucoma
keratoconus
48
Q

Which GI conditions are associated with down’s

A
dental problems
oesophageal atresia
tracheooesophageal fistula
GORD
pyloric stenosis
duodenal atresia
Meckel's diverticulum
Coeliac disease
imperforate anus
49
Q

Which orthopaedic conditions are associated with down’s

A
atlanto-axial instability
hyperflexibility
scoliosis
hip dislocation
patellar subluxation/dislocation
foot deformities
50
Q

Which endocrine conditions are associated with down’s

A

hypothyroid

51
Q

Which neuro/psych conditions are associated with down’s

A

learning difficulties
behavioural problems
seizures
dementia after 40y

52
Q

Which haem conditions are associated with down’s

A

increased risk of infections due to immature immune system
increased risk ALL, AML, AMegL
polycythemia
transient myloproliferative disorder

53
Q

Describe the screening programme available for Down’s

A

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

54
Q

When can serum screening for Down’s syndrome be done?

What does it measure?

A

10 - 14+1 gestation

betaHCG - raised in down’s
PAPP-A - decreased in down’s

55
Q

When can fetal nuchal translucency screening for Down’s syndrome be done?
What does it measure?

A

11+2 - 14+1 gestation

56
Q

What screening for down’ can be done after 14+1 weeks gestation? When until?

A

quadruple testing
involves beta HCG, AFP, inhibin A, uE3

up to 20+0

57
Q

When can chorionic villus sampling and amniocentesis be carried out?

A

chorionic villus sampling - <13weeks

amniocentesis >15 weeks

58
Q

What is the risk of miscarriage with chorionic villus sampling and amniocentesis?

A

chorionic villus sampling - 1-2%

amniocentesis - 0.5-1%

59
Q

What is oesophageal atresia

A

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)

60
Q

What is the most common kind of TOF

A

blind ended oesophagus

fistula between distal oesophagus and trachea

61
Q

What conditions are associated with oesophageal atresia

A
VACTERL
CHARGE
Down's
Patau's - trisonomy 13
Edward's - trisonomy 18
Di george
62
Q

How might oesophageal +-TOF present?

A
polyhydraminos antenatally
SGA
respiratory distress
feeding problems
not avle to swallow!
lots of secretions - frothing
not able to pass NG tube
63
Q

What investigations should be done in an infant with oesophageal atresia?

A
CXR
bronchoscopy to assess for fistulae
cardiac echo
renal scan
limb xrays
USS spine
64
Q

What can be seen in CXR in oesophageal atresia

A

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.

65
Q

What is the management of oesophageal atresia?

A

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).

66
Q

What is duodenal atresia

A

either atresia, stenosis or web in duodenum leading to obstruction

67
Q

How does duodenal atresia present?

A

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

68
Q

What investigations are done in duodenal atresia

A

CXR/AXR

barium enema

69
Q

What would an xray show in duodenal atresia

A

fewer air levels than expected

classical double bubble sign - due to stomach, pylorus and dilated duodenum then atresia

70
Q

Explain the difference between gastroschisis and exomphalos

A

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

71
Q

How can gastroschisis or exomphalos present antenatally

A

rise in alpha-fetoprotein in the second trimester

abnormality on ultrasound scan.

72
Q

How are gastroschisis and exomphalos managed?

A

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

73
Q

What could be a sign of an anorectal malformation?

A

failure to pass meconium after 24hrs

74
Q

What is VACTERL

A

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

75
Q

What investigations should be done if one feature of VACTERL is present

A
spine xray
USS spinal cord
examination anus
cardiac echo
CXR
renal USS
limb examination
76
Q

What is Hirchsprung’s disease

A

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.

77
Q

How can Hirchsprung’s disease present in an infant?

A

Abdominal distention,
failure of passage of meconium within the first 48 hours of life
repeated vomiting.

78
Q

How can Hirchsprung’s disease present in a child?

A

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.

79
Q

How is Hirchsprung’s diagnosed?

A

plain abdominal X-ray - affected segment not dilated, proximal section dliated

rectal biopsy - absence of ganglion cells in the myenteric plexus.

80
Q

How is Hirchsprung’s managed

A

resection of affected segment

81
Q

What is CHARGE syndrome?

A

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
82
Q

How would you define a floppy infant?

A

An infant with prominent, generalized decreased muscle tone

83
Q

What is the difference between postural and phasic tone?

A

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

84
Q

Where can a lesion causing hypotonia pccur?

A

CNS
peripheral nerves
muscles
NMJ

85
Q

How might an infant with hypotonia present?

A

floppy
feeding difficulties
breathing difficulties
not meeting developmental milestones

86
Q

What are the important questions to ask in the history when a child presents with hypotonia

A

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
87
Q

What should you examine in a child presenting with hypotonia

A
general - dysmorphic features, posture
upper and lower limb neuro
CN
developmental signs
truncal tone
neck tone
shoulder girdle
88
Q

What are the key examination findings in terms of truncal tone, neck tone and shoulder girdle that prove hypotonia

A

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

89
Q

How can you differentiate between central and peripheral hypotonia?

A
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
90
Q

What are the differentials for a floppy infant?

A

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)

91
Q

What are muscular dystrophies?

A
  • > A group of inherited disorders with progressive muscle degeneration.
  • > Abnormalities in dystrophin gene, which is part of the muscle fibre cytoskeleton.
  • > eg. Duchenne & Becker
92
Q

What are the jey features of muscular dystrophies?

A
  • > Waddling gait
  • > Gower sign (raising from floor in a prone position)
  • > Unable to keep up with peers
  • > Recurrent LRTIs
  • > Nocturnal hypoxia
  • > Cardiomyopathy
  • > Scoliosis
93
Q

What investigations are useful in hypotonia

A
U+E, CK, FBC, CRP, blood cultures
MRI head
EMG
muscle biopsy
karyotyping
DNA mutation studies
94
Q

What factors are associated with increased chance of a mother breast feeding?

A

> 30y
ethnic minority
first time mother
left full time education after 18

95
Q

What are the benefits of breast feeding for the baby?

A
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!`

96
Q

What are the benefits of breast feeding for the mum?

A

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!
97
Q

What is croup

A

viral URTI leading to inflammation of nasopharynx, larynx and trachea
leads to subglottal inflammation, oedema and compromise of airway
movement of vocal cords impaired

98
Q

What causes croup

A
parainfluenza types I, II, III and IV
RSV
adenovirus
rhinovirus
enterovirus
99
Q

What are the risk factors for croup

A

6m-3y (most common 2y)

male

100
Q

What are the features of croup

A
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
101
Q

Give some differentials for croup and how they can be distinguished

A

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

102
Q

How can croup’s severity be assessed?

A

Westley clinical scoring system

103
Q

What differentiates between mild, moderate and severe croup

A

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.

104
Q

Which children with croup require hospital assessment

A

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.

105
Q

Which children with croup need consideration of admission to hospital for treatment?

A

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.

106
Q

What are the features of Impending respiratory failure?

A

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

107
Q

What is the treatment for mild croup

A

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

108
Q

What is the treatment for moderate/severe croup

A

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

109
Q

What is gastroenteritis?

A

transient disorder due to enteric infection with viruses, bacteria, or parasites. It is characterized by the sudden onset of diarrhoea, with or without vomiting

110
Q

Define diarrhoea

A

three or more episodes of partially-formed or watery stool in a day

111
Q

What is the difference between acute and persistent diarrhoea

A

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

112
Q

What are the causes of gastroenteritis?

A

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.

113
Q

What are the symptoms of gastroenteritis?

A

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
114
Q

Give some differentials for gastroenteritis

A

Systemic infection (UTI, pneumonia, meningitis, sepsis).
Appendicitis.
Other surgical causes (intussusception, sub-acute bowel obstruction, Hirschsprung’s colitis).
Gastro-oesophageal reflux.

115
Q

What investigations should be done in gastroenteritis

A

obs
FBC U+E
stool MC+S
blood cultures

116
Q

What is the management of gastroenteritis if there is no sign of dehydration

A

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

117
Q

What are the signs of dehydration in gastroenteritis

A
decreased responsiveness/alertness
sunken eyes
dry mucous membranes
reduced urine output
tachypnoea
tachycardia
reduced skin turgor
appear unwell/deteriorating
118
Q

Which children are most at risk of dehydration from gastroenteritis

A

<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.

119
Q

What is the management of gastroenteritis if there are signs of dehydration

A

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!

120
Q

What is the management of gastroenteritis if there are signs of shock

A
IV/IO access
20ml/kg 0.9% saline
repeat if no response
SENIOR REVIEW
consider other diagnoses
121
Q

How should children be rehydrated orally?

A

50ml/kg over 4h

122
Q

When might an NG tube be required for rehydration

A

vomiting oral rehydration solution
feed refusal
no red flag symptoms

123
Q

What are the red flags for dehydration

A
inherited metabolic disorder
appears unwell/deteriorating
irritable or lethargic 
sunken eyes
tachycardia
tachypnoea
decreased skin turgor
124
Q

What are the indications for IV fluid resuscitation

A

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)

125
Q

How is IV resuscitation given to children

A
20ml/kg of 0.9% sodium chloride
reassess
20ml/kg of 0.9% sodium chloride
reassess
SENIOR CICU REVIEW
126
Q

What maintenance fluids are given to children

A

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

127
Q

What is whooping cough

A

respiratroy infection caused by Bordatella pertussis

128
Q

What kind of organism is Bordatella pertussis

A

gram -ve coccobacillus

129
Q

What are the feaures of whooping cough

A

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.

130
Q

What is a whoop?

A

breathing in through partially closed vocal cords after a coughing paroxysm

131
Q

Give some differentials for whooping cough

A
croup
bronchiolitis
other resp infection - adenovirus, Mycoplasma
asthma
post infectious cough
132
Q

What investigatons are done for whooping cough

A

it is a clinical diagnosis!

needs PHE notification

133
Q

What investigations do PHE suggest upon notification of a potential whooping cough diagnosis

A

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.

134
Q

What is the management of whooping cough

A

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

135
Q

What is the vaccination schedule for whooping cough

A

at 8w
at 3y 4m

booster in pregancy >20w gestation

136
Q

What is the incubation period for whooping cough

A

7 to 20 days.

137
Q

What are some complications of whooping cough

A

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.

138
Q

What is IUGR?

A

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

139
Q

What is SGA

A

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

140
Q

What are the three kinds of SGA

A

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

141
Q

What are the risk factors for SGA

A
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).
142
Q

How is the diagnosis of SGA made?

A

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

143
Q

When is symphysis fundal height an inaccurate measure?

A

BMI >35
large fibroids
hydraminos - oligo or poly

144
Q

How is SGA monitored during pregnancy

A

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

145
Q

What are the maternal risk factors for IUGR

A

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).

146
Q

What are some fetal risk factors for IUGR

A

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.

147
Q

Give some placental risk factors for IUGR

A
placental dysfunction (including pre-eclampsia)
placental abruption.
148
Q

What are the featues of an IUGR baby once born?

A

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.

149
Q

Describe the features of symmetrical IUGR in utero and at birth

A

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

150
Q

Describe the features of asymmetrical IUGR in utero and at birth

A

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

151
Q

What are the neonatal complications of an IUGR baby?

A
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.
152
Q

What are some of the long term neurodevelopmental problems an IUGR baby can have?

A

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.

153
Q

What long term health problems does IUGR increase the risk of?

A

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

154
Q

What is volvulus?

A

complete twisting of a loop of intestine around its mesenteric attachment site
results in a closed loop bowel obstruction

155
Q

Where is it most common for a volvulus to occur in an infant?
Why?

A

midgut

due to malrotation

156
Q

Describe hte normal rotation of the midgut

A

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

157
Q

What does malrotation of the midgut result in?

A

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

158
Q

what are the features of malrotation

A
failure to thrive
anorexia
constipation
bloody stools
bilious vomiting
recurrent abdo pain (due to ischaemia)
159
Q

What are the features of volvulus

A
distended abdomen
bilious vomiting
peritonitits
metabolic acidosis
oliguria
hypotension
160
Q

What investigations need to be done in malrotation/volvulus

A

ABG/VBG, FBC, U+E, LFT, CRP, clotting, G+S if severe volvulus
AXR
upper GI contrast study
CT abdo

161
Q

What would you expect to see on upper GI contrast study in volvulus

A

dilation of proximal duodenum

bird beak/spiral/corkscrew obstruction

162
Q

How would you manage volvulus

A

NG tube - decompresssion of stomach

surgery - Ladd’s procedure

163
Q

How would you manage malrotation

A

elective Ladd’s procedure

due to risk of volvulus

164
Q

Describe Ladd’s procedure

A

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

165
Q

What are the complications of chronic intermittent volvulus

A

malabsorption
constipation
diarrhoea

166
Q

What are the complications of acute volvulus

A
ischaemia
necrosis of mucosa
perforation
peritonitis
sepsis
death
167
Q

What causes chicken pox?

A

varicella zoster virus

168
Q

Describe the transmission, incubation and infectious period of chicken pox

A

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

169
Q

What are the risk factors for developing severe chicken pox

A

immunocompromised
steroids
older age
malignancy

170
Q

What are the features of chicken pox

A

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.

171
Q

Give some differentials for chicken pox

A

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.
172
Q

What is the management of chicken pox

A

if otherwise healthy: supportive management

if immunocompromosied: oral/IV aciclovir

> 14y - oral aciclovir if present within 24 hrs of onset

173
Q

What are the potenital complications of chicken pox

A

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

174
Q

Which people should people with infectious chicken pox avoid?

A

immunocompromised
neonates
pregnant women