Paeds 1 - Cardio/Resp/GI/Infections etc Flashcards
1
Q
list some ways congenital heart disease might present
A
- antenatal diagnosis by US
- heart murmur
- cyanosis
- shock (low cardiac output)
- cardiac failure
2
Q
what are the most common left to right shunting congenital heart lesions?
A
- VSD
- PAD
- ASD
present BREATHLESS (acyanotic)
3
Q
what are the most common right to left shunting congenital heart lesions?
A
- tetralogy of fallot
- transposition of the great arteries
present BLUE (cyanotic)
4
Q
which congenital heart lesion involves common mixing of oxygenated and deoxygenated blood?
aka - breathless and blue
A
- AVSD
5
Q
give the two main causes of outflow obstruction in a well child
aka - murmur, but asymptomatic
A
pulmonary stenosis
aortic stenosis
6
Q
give the main cause of outflow obstruction in a sick neonate
aka - collapsed with shock, as opposed to well but with a murmur
A
coarctation of the aorta
7
Q
what are the features of an innoSent murmur - the 5 S’s
A
Soft Systolic aSymptomatic left Sternal edge normal heart Sounds
8
Q
explain the normal circulatory changes that occur at birth
A
with the first breath, the resistance to pulmonary blood flow falls and the volume of blood going through the lungs increases.
leads to a change in pressure making the foramen ovale close.
the ductus arteriosus (connects pulmonary artery to aorta) will usually close within first few hours/days - some babies rely on this duct to allow mixing of the blood if they have a defect, and will rapidly deteriorate once it shuts!
9
Q
when does the foramen ovale close?
A
at first breath - resistance to pulmonary blood flow falls, volume of blood going through lungs increases, change in pressure leads to closure of foramen ovale
10
Q
when does the ductus arteriosus close?
A
within first few hours/days - babies that were relying on mixing via ductus arteriosus may rapidly deteriorate once it shuts!
11
Q
what symptoms might indicate a baby is in heart failure?
A
breathlessness - especially on feeding (/exertion)
sweating
poor feeding
recurrent chest infections
12
Q
what signs might indicate a baby is in heart failure?
A
failure to thrive / faltering growth tachypnoea, tachycardia hepatomegaly cool peripheries heart murmur, gallop rhythm (third heart sound)
13
Q
give some causes of cardiac failure in a neonate
A
in neonates heart failure is usually due to obstructed systemic circulation (will be duct-dependent):
- hypoplastic left heart
- critical aortic valve stenosis
- severe coarctation of the aorta
- interruption of the aortic arch
14
Q
give some causes of cardiac failure in an infant
A
in infants heart failure is due to volume overload (‘high pulmonary blood flow’):
VSD
AVSD
large PDA
15
Q
if you suspect a neonate/infant is in cardiac failure, what investigations would be useful?
A
CXR - expect to see enlarged heart and pulmonary congestion (useful if unsure if resp v cardio issue)
ECG
Echocardiography to determine the underlying defect
16
Q
give some causes of cardiac failure in a child/adolescent (i.e. not a baby!)
A
will see R or L heart failure.
Eisenmenger syndrome (R heart failure only)
Rheumatic heart disease
Cardiomyopathy
17
Q
what causes persistent cyanosis in an otherwise well infant?
A
some kind of structural heart disease
18
Q
what might be causing cyanosis in a newborn infant with respiratory distress?
A
cardiac - the cyanotic congenital defects
resp - surfactant deficiency, meconium aspiration, pulmonary hypoplasia
persistent pulmonary hypertension of the newborn (PPHN)
infection - septicaemia from Group B strep (+ other organisms)
metabolic diseases - metabolic acidosis and shock
19
Q
what is persistent pulmonary hypertension of the newborn (PPHN)?
A
failure of the pulmonary vascular resistance to fall after birth - pressure in pulmonary vessels remains high, preventing blood flow and limiting oxygenation of the blood -> leads to cyanosis
20
Q
what investigations might you order to distinguish between causes of cyanosis/heart failure if echo is unavailable?
A
CXR + ECG
pre and post ductal sats (a difference indicates PPHN or R->L shunting)
4 limb BP (upper and lower limbs will be different in coarctation of the aorta)
21
Q
what are the two types of ASD?
A
most common = ostium secundum defect, high in atrial septum
must less common = ostium primum, occurs much lower - common in Downs
22
Q
how do you distinguish between ASD and PFO?
A
PFO only open when atrial pressure/volume raised - present in 1/3 of kids with congenital heart disease.
ASDs are large and always open (although usually asymptomatic in childhood!)
23
Q
what symptoms may be seen in ASD?
A
usually none!
might get recurrent chest infections/wheeze
in 30s onwards may get arrhythmias
24
Q
what signs will be seen in ASD?
A
ejection systolic murmur at upper left sternal edge - increased flow across pulmonary value due to L -> R shunt
fixed and widely split S2
25
CXR findings in ASD
cardiomegaly, enlarged pulmonary arteries, "pulmonary plethora" (strong pulmonary vascular markings)
26
what is the key investigation for diagnosing any structural heart defect?
ECHO
27
management of ASD
if large, consider surgery (when age 3-5y) - to prevent cardiac failure/arrythmias later in life.
secundum defects often closed transcatheter.
28
what signs/symptoms might be seen if a baby has a small VSD?
asymptomatic!
| signs - loud pansystolic murmur at lower L sternal edge, quiet pulmonary second sound (P2)
29
how would you investigate and manage a small VSD?
Ix - CXR and ECG will be normal, can be seen on echo
| Rx - none, resolves spontaneously
30
what symptoms will be seen if a baby has a large VSD?
heart failure with breathlessness and faltering growth after 1 week old
recurrent chest infections
31
what signs will be seen if a baby has a large VSD?
tachypnoea, tachycardia, enlarged liver (heart failure signs)
active precordium (excessive movement of chest wall over heart)
soft pansystolic murmur/no murmur if v large defect
apical mid-diastolic murmur
32
what CXR signs would you expect to see in a large VSD?
cardiomegaly, enlarged pulmonary arteries, pulmonary plethora/strong pulmonary vascular markings, pulmonary oedema
33
what ECG findings would occur in ASD?
RVH + incomplete RBBB
34
what ECG findings would occur in a large VSD?
biventricular hypertrophy - would occur by 2 months old
35
how would you manage a baby with a large VSD?
diuretics and ACEi for heart failure
additional feeding/calories to grow them!
medium-sized defects often spontaneously close, but if there's still a shunt at 4 years correct surgically before school starts
large defects - surgical correction at around 3-6 months.
36
what is Eisenmenger's syndrome?
obstructive pulmonary vascular disease that occurs due to significant L to R shunt - the pulmonary hypertension due to the shunt leads to permanent damage of the vessels.
this can lead to pressures equalising and the direction of blood flow shifting to R to L (reversed shunting).
it's really bad!
37
what is the ductus arteriosus and when does it normally close?
at what point would you diagnose PDA?
connects aorta to L pulmonary artery, normally closes by 4th day of life.
PDA diagnosed if not closed after 1 month of life.
38
give 3 risk factors for a PDA
preterm - although this is normal due to their prematurity
Downs
high altitude
39
how is a persistent PDA managed?
risk of pulmonary vascular disease or infective endocarditis is high - so surgical closure recommended.
usually done at 1 year. if diagnosed really early, ibuprofen may help close it without surgery, but typically surgical closure needed.
40
what clinical features would you see in PDA?
continuous machine murmur beneath the L clavicle.
collapsing/bounding pulse (due to wide pulse pressure)
always asymptomatic - unless really severe and then you'd get heart failure
41
what features of a PDA would be seen on CXR and ECG?
both usually normal
42
how is a patent PDA (due to prematurity) managed?
oral/IV ibuprofen 10mg/kg, then 5mg/kg at 24 and 48hrs old
43
what are the four features of Tetralogy of Fallot?
1. Large VSD
2. Overriding aorta
3. Pulmonary stenosis
4. RV hypertrophy
44
how might tetralogy of fallot present?
- in first 1-2 months of life with hypoxic spells OR a murmur
- squatting on exercise in late infancy, due to hypoxic spells
- often picked up antenatally on scans
45
give the clinical signs of tetralogy of fallot
cyanosis ± clubbing (usually only in older kids)
loud and single S2
loud ejection systolic murmur maximal at lower L sternal edge
46
what would you see on a CXR in tetralogy of fallot?
```
boot shaped heart!
- RVH
- concavity on L heart border where normally the main pulmonary artery and RV outflow tract would create a convexity
- R sided aortic arch
diminished pulmonary vascular markings
```
47
how is tetralogy of fallot managed?
corrective surgery at 6 months - close the VSD, relieve RV outflow obstruction
if severe, may require shunt formation in the interim
48
what is transposition of the great arteries?
aorta connected to R ventricle, pulmonary artery connected to the L ventricle
forms two parallel circulations, one of oxygenated blood and one of deoxygenated blood
this would be incompatible with life but defects exist allowing mixing e.g. VSD, ASD etc
49
how does transposition of the great arteries present?
profound cyanosis on first day or two of life - blue, sats <95%, collapsed
presents on day 2 due to closure of the ductus arteriosus which stops/reduces the mixing of the circulations
50
what signs would you see in transposition of the great arteries?
CYANOSIS - always.
loud S2
no murmur (unless VSD/PDA causing one)
51
how is transposition of the great arteries managed?
need to improve the mixing of circulations
prostaglandin (PG) E1 infusion to reopen ductus arteriosus
emergency balloon atrial septostomy via catheter is life-saving
corrective surgery performed at a few weeks of age (you basically just cut the great arteries and swap them over)
52
what is a complete AVSD?
defect in middle of heart with single 5 leaflet valve between atria and ventricles - stretches across entire AV junction and tends to leak.
53
when would most likely see a complete AVSD?
Downs syndrome
| typically diagnosed antenatally on ultrasound.
54
how does a complete AVSD present?
antenatally on US
| cyanotic at birth, or heart failure at 2-3 weeks
55
how is a complete AVSD managed?
diuretics/ACEis for heart failure
| surgery at 3-6 months
56
what is tricuspid atresia?
defect where only the L ventricle works - R is small and non functioning.
there's 'common mixing' of oxygenated/deoxygenated blood in the L atrium
57
how does tricuspid atresia present?
with cyanosis in newborn period, after the ductus arteriosus closes
58
how is tricuspid atresia managed?
surgically - palliative as there is no completely corrective surgical option
59
what are the two main causes of outflow obstruction in a well child?
aortic stenosis, pulmonary stenosis
60
what is aortic stenosis (paediatric) and how does it present?
partly fused aortic valve leaflets.
| presents with asymptomatic ejection systolic murmur at upper R sternal edge that radiates to neck
61
how is aortic stenosis managed?
if surgery needed - balloon valvotomy, possibly valve replacement in long term
before surgery/if no surgery needed, advise to avoid strenuous exercise
62
what is pulmonary stenosis and how does it present?
partly fused pulmonary valve leaflets.
| presents with asymptomatic ejection systolic murmur at upper R sternal edge
63
how is pulmonary stenosis managed?
surgery - transvenous balloon dilatation or pulmonary valvotomy
64
what are the three main causes of outflow obstruction in a sick infant?
coarctation of the aorta
interruption of the aortic arch
hypoplastic left heart syndrome
65
what is the general presentation of an infant unwell due to obstructive lesions?
really sick with heart failure and shock in neonatal period, unless lesion was diagnosed antenatally
66
what are the general principles of managing a neonate unwell due to obstructive lesions?
ABC resuscitation is key!
early prostaglandins
refer for early surgical intervention
67
what is coarctation of the aorta?
arterial duct tissue encircling the aorta just at the point of insertion of the ductus arteriosus - when this shuts, the aorta also constricts causing severe obstruction of LV outflow
68
what are the clinical features of coarctation of the aorta?
normal exam on day 1.
then acute circulatory collapse on day 2 (after ductus closes!)
really sick baby, severe heart failure, absent femorals, severe metabolic acidosis.
69
how is coarctation of the aorta managed?
once diagnosed, give a prostaglandin infusion to maintain ductal patency and transfer to cardiac centre for surgery ASAP
70
what is interruption of the aortic arch?
there's no connection between proximal aorta and aorta distal to the ductus arteriosus - cardiac output relies on R to L shunt via duct.
normally a VSD as well.
71
how does interruption of the aortic arch present?
shock as a neonate.
| associated with DiGeorge syndrome (22q 11.2)
72
how is interruption of the aortic arch managed?
complete correction in first days of life
73
what is hypoplastic left heart syndrome and how is it managed?
complete underdevelopment of entire L side of heart, detected at antenatal US.
surgery called Norwood procedure + further 2 surgeries.
74
what is the only common paediatric cardiac arrhythmia?
| can you name any others?
supraventricular tachycardia
others - congenital complete heart block, long QT syndrome
75
what is supraventricular tachycardia and how does it present in children?
HR >220bpm, often up to 300bpm
| typically asymptomatic, but infants may have heart failure - ensure an echo is done to rule out structure defects.
76
what would you see on an ECG of a child with a supraventricular tachycardia?
narrow complex tachycardia - P waves discernible after QRS complex.
77
how is an acute episode of supraventricular tachycardia managed?
to restore sinus rhythm:
- vagal stimulation - ice cold compress to face, carotid sinus massage
- IV adenosine bolus - safe and effective
DC cardioversion only if the above fail.
78
what is rheumatic fever?
abnormal immune response to a preceding group A beta-haemolytic strep infection
v rare in developed world!
79
what are the clinical features of rheumatic fever?
polyarthritis, fever and malaise 2-6 weeks after pharyngeal infection.
arthritis is fleeting - lasts less than a week in individual joints (tends to affect knees and ankles)
50% of patients have pancarditis:
- pericarditis - friction rub and pericardial effusion
- endocarditis - murmurs
- myocarditis - heart failure
erythema marginatum (pink macules on trunk and limbs) = uncommon, painless, early
Modified Duckett Jones criteria used to diangose
80
how is rheumatic fever managed?
bed rest and aspirin (suppresses fever and arthritis).
monthly IM ben pen is prophylactic
81
what is the main potential complication of rheumatic fever?
number one cause of valvular disease world wide! usually mitral valve - scarring and fibrosis.
82
when might you suspect infective endocarditis?
```
children with congenital heart disease are at risk, but suspect in anyone with:
sustained fever
malaise
raised ESR
unexplained anaemia or haematuria
```
any kid with fever and significant cardiac murmur - think IE
83
what are the clinical features of infective endocarditis?
```
fever
malaise
anaemia/pallor
splinter haemorrhages
clubbing
neurological signs from cerebral infarct/CNS abscess
haematuria - glomerulonephritis
arthritis
```
84
how is infective endocarditis diagnosed?
combo of clinical and lab:
- blood cultures - take 3+ within first 24h in hospital
- echo to confirm presence of vegetations
- raised ESR (useful for monitoring treatment)
strep viridans (alpha haemolytic strep) is most common cause
85
how is infective endocarditis treated?
high dose penicillin and an aminoglycoside - 6 weeks IV
86
list some factors increasing risk of respiratory infections in babies/kids
- parental smoking (esp maternal)
- low SE status (large family, overcrowded, damp housing)
- poor nutrition
- underlying lung disease (bronchopulmonary dysplasia, CF, asthma)
- Male
- congenital heart disease
- immunodeficiency
87
what are the different most common causes of a wheezy child, by age group?
0 - 12m = bronchiolitis
12m - 3y = viral induced wheeze
3y+ = asthma (probably)
88
give the common URTIs in kids
common cold (coryza)
sore throat (pharyngitis, tonsillitis)
acute otitis media
sinusitis (relatively uncommon)
89
what complications can URTIs cause in kids?
- difficulty feeding in infants (blocked nose obstructs breathing during feed)
- febrile convulsions
- acute asthma exacerbations
90
what are the 'coryzal' symptoms?
clear/mucopurulent nasal discharge and nasal blockage
91
what viruses typically cause coryzal symptoms
rhinoviruses, coronaviruses, RSV
92
what is the clinical picture of pharyngitis and what typically causes it?
inflamed pharynx and soft palate, enlarged and tender lymph nodes.
usually viral - adenoviruses, enteroviruses, rhinoviruses.
older child - might by group A beta haemolytic strep
93
what is tonsillitis?
a form of pharyngitis with inflamed tonsils +/- purulent exudate
94
what are the usual causative organisms in tonsillitis? how do you distinguish between viral and bacterial?
typically viral (rhinovirus, coronavirus, parainfluenza etc)
might see EBV (infectious mononucleosis), group A beta haemolytic strep
hard to distinguish clinically - more severe systemic symptoms in bacterial (headache, apathy etc)
95
what treatment is often given for bacterial tonsillitis?
penicillin
erythromycin if allergic to penicillin
avoid amoxicillin as can cause a rash if it's EBV
96
when might you admit a patient for tonsillitis?
if difficulty swallowing - give IV fluids and analgesia
97
what is acute otitis media and who gets it?
middle ear infection
| most common at 6-12 months age due to their short, horizontal Eustachian tubes
98
what are the clinical features of acute otitis media?
pain in ear and fever - examine tympanic membranes of any kid with fever!
99
what would the tympanic membranes look like in a kid with acute otitis media?
bright red and bulging, loss of normal light reflection.
might see acute perforation - pus in external canal.
recurrent otitis media --> scarring of tympanic membrane
100
give some common causative organisms of acute otitis media
RSV, rhinovirus, pneumococcus, H. influenza, Moraxella catarrhalis
101
how would you manage acute otitis media?
pain - regular paracetamol/ibuprofen
amoxicillin can shorten duration - prescribe, ask parent only to use if still unwell after 2-3 days
102
what is glue ear and how does it present?
recurrent ear infections that have led to otitis media with effusion (OME)
often asymptomatic, may have reduced hearing - usually in a 2-7yo kid
103
what would you see down the otoscope if a child has glue ear/OME?
eardrum dull and retracted, visible fluid level
104
what Ix might ENT perform in glue ear and what would you see?
tympanometry - flat trace
105
how is glue ear managed?
generally resolves spontaneously
| Grommet insertion if conductive hearing loss impacting speech development/school
106
what type of hearing loss is seen in glue ear?
conductive
107
what is the clinical picture of sinusitis in a child?
concurrent viral URTI, possibly a secondary bacterial infection - pain/swelling/tenderness over cheek
108
how might you manage a child with sinusitis?
abx if you suspect bacterial cause.
| analgesia, topical decongestants
109
what are the characteristic features of a laryngeal/tracheal infection? what is the major risk with these?
stridor, hoarseness, barking cough, dyspnoea (variable degree)
risk of airway obstruction!!! DO NOT EXAMINE THE THROAT
110
what is stridor?
rasping sound, predominantly on inspiration
111
how do you assess degree of airway obstruction in a child with suspected croup/laryngeal or tracheal infection?
degree of chest retraction (none/only on crying/at rest)
degree of stridor (none/only on crying/at rest/biphasic)
DON'T EXAMINE THE THROAT
112
describe the basic acute management of upper airways obstruction in a child
1. DO NOT EXAMINE THE THROAT
2. observe for signs of hypoxia or deterioration
3. consider oral dexamethasone or budesonide nebs before adrenaline
4. if severe, use adrenaline nebs (bleep anaesthetist in case you have to intubate)
113
what's the fancy name for croup?
laryngeotracheobronchitis
114
explain the pathology of croup
mucosal inflammation and increased secretions affect the airway - subglottic area oedema is the dangerous bit that can obstruct
115
what are the causative organisms of croup?
95% viral (parainfluenza most common, or human metapneumovirus, RSV, influenza)
116
who gets croup and when?
kids age 6m - 6y (peak @ 2y).
| typically in autumn and spring.
117
how does croup present?
barking cough, hoarseness, harsh stridor - all worse at night.
preceded by fever and coryza.
118
how do you manage a kid with croup presenting with mild obstruction, no stridor, plus chest recession?
home care, with close observation by parent - supportive care as it's self-limiting
119
how do you manage a kid with serious croup - stridor etc
ITU, oral dexamethasone (squirt into mouth with syringe), nebulised budesonide (adrenaline nebs if gets v bad), possible need to intubate.
supportive care - protecting airway - as it's self-limiting
120
what is bacterial tracheitis?
similar to croup, but bacterial - very rare but dangerous!
| Staph. aureus
121
how does bacterial tracheitis present?
similar to croup but with high fever - child appears toxic, with rapidly progressing airways obstruction and thick secretions
122
how do you treat bacterial tracheitis?
IV abx ± intubation ± ventilation
123
what is epiglottitis?
an emergency! caused by Hib (suspect if not up to date with imms).
swelling of epiglottis and surrounding tissues, with septicaemia.
typically age 1-6y, but can affect any age.
124
how does acute epiglottitis present?
high fever in an unwell child. intensely painful throat - prevents child speaking and swallowing (drooling saliva). soft inspiratory stridor.
child sits immobile, upright and with open mouth to optimise airway.
minimal/no cough - contrast to croup etc
125
how do you manage a child with suspected acute epiglottitis?
DON'T lie them down or examine the throat!!
admit to ITU - intubate under GA, then do blood cultures and start IV abx (3-5 days e.g. cefuroxime).
remove tracheal tube at 24 hours.
rifampicin prophylaxis to close contacts.
126
what organism causes whooping cough?
Bordatella pertussis
127
describe the clinical presentation of whooping cough
1 week of coryzal symptoms (catarrhal phase).
then characteristic paroxymal cough followed by inspiratory whoop (paroxysmal phase - lasts 3-6 weeks).
worse at night. might cough until vomit, or get epistaxis/subconjunctival haemorrhage.
symptoms gradually reduce after 3-6 weeks but can persist for months (convalescent phase).
128
what would you do to confirm a case of whooping cough?
culture/PCR of per-nasal swab
also will see marked lymphocytosis on blood film.
129
how do you treat whooping cough?
erythromycin - give to close contacts as well.
imms - decrease risk of getting it but also reduce severity if you do get infected.
130
what age group gets bronchiolitis and when?
90% are aged 1-9 months.
bonfire night -> valentines day
131
what is the usual causative organism of bronchiolitis? can you list some others?
RSV - 80%
human metapneumovirus, parainfluenza virus, rhinovirus, adenovirus, influenza
132
what are the clinical features of bronchiolitis?
coryzal symptoms preceding a dry cough and increased work of breathing/breathlessness.
feeding difficulties with increased dyspnoea = admit.
133
what would you find on examination of an infant with bronchiolitis?
```
sharp, dry cough
tachypnoea
subcostal and intercostal recession
hyperinflation of chest - prominent sternum, liver displaced downwards.
fine end-inspiratory crackles.
high-pitched wheezes - expiratory > inspiratory.
tachycardia
cyanosis/pallor
```
134
what investigations would you perform for an infant with suspected bronchiolitis?
PCR of nasopharyngeal aspirate to assess for respiratory viruses.
don't bother with CXR - but it would show hyperinflation of lungs (due to small airway obstruction), air trapping and focal atelectasias.
pulse oximetry.
135
how would you manage an infant with bronchiolitis?
humidified O2 via nasal cannulae if pulse ox indicates needed.
IV fluids if needed.
most recover within two weeks - some babies will get recurrent episodes.
136
what prophylaxis can you offer high-risk prem babies for bronchiolitis?
monoclonal antibodies to RSV (palivizumab) via monthly IM injection
137
what are the common causative organisms of pneumonia in a newborn?
group B strep, gran -ve enterococci
138
what are the common causative organisms of pneumonia in an infant/toddler?
RSV, strep pneumoniae, H influenzae
139
what are the common causative organisms of pneumonia in a child over 5?
M. pneumoniae, strep pneumoniae
at any age - always consider TB.
140
what are the clinical features of pneumonia in a child?
fever and difficulty breathing
often preceded by an URTI
cough, poor feeding, generally 'unwell' child.
if there's localised chest/abdo pain => pleural irritation => bacterial
141
what would you expect to see on examination of a child with a pneumonia?
tachypnoea
also - nasal flaring, chest indrawing, possibly end-inspiratory coarse crackles over infected area.
142
how would you investigate a suspected pneumonia in a child?
CXR can confirm diagnosis.
NPA can detect viral causes.
143
how do you manage a child with pneumonia?
normally home management - admit if sats <93% with severe tachypnoea, difficulty breathing and feeding.
supportive care - O2, analgesia, IV fluids.
oral amoxicillin (IV for newborns/young infants)
144
what is viral-induced wheeze?
commonly diagnosed in "chesty" kids when they're too young for it to be asthma - kids have got small airways that are more likely to narrow and obstruct in response to viruses/other triggers
can split into episodic viral wheeze - kid gets wheezy when they have an URTI but symptom free in between episodes. non-atopic.
and multi-trigger wheeze - wheeze triggered by smoke, exercise, cold air etc - more associated with future asthma. associated with atopy.
145
how do you manage episodic viral wheeze?
symptomatic treatment - SABA (salbutamol) or anticholinergic with a spacer.
next step = leukotriene receptor agonist (montelukast) or intermitted inhaled corticosteroids or both
146
how do you manage a child with multi-trigger wheeze?
trial inhaled corticosteroids or montelukast for 4-8 weeks.
147
briefly describe the pathophysiology of asthma
combo of triggers, atopy and genetic predisposition --> bronchial inflammation --> bronchial hyperresponsiveness --> airway narrowing --> symptoms
148
what are the clinical features of asthma?
polyphonic wheeze.
symptoms worse at night and first thing in the morning.
symptoms appear with triggers - but may have some interval symptoms.
personal/family hx of atopy
positive response to asthma Rx
149
what investigations might be performed if you suspect a child has asthma?
peak expiratory flow!! - peak flow diaries usually used, helps identify diurnal variation and triggers.
may also do skin prick testing for specific allergens
150
a child has been diagnosed as asthmatic - what initial treatment would the GP prescribe?
PRN salbutamol (SABA) - if using 3+ times per week, add an inhaled corticosteroid (ICS) e.g. beclometasone as a regular preventer
151
a child has been using their ICS preventer inhaler for several weeks now but still uses salbutamol about 6 times a week - what is the next step?
consider montelukast (leukotriene receptor antagonist).
if older, add a LABA (salmeterol, formeterol)
152
an asthmatic child comes to the doctor as they're still using their salbutamol 5 times a week - they're using a beclomethasone regular preventer and salmeterol - they've noticed some improvement since the salmeterol.
next step?
raise dose of ICS (beclomethasone).
as long as responding to LABA, keep that on.
if you hadn't already added, montelukast could be trialled now.
need to refer for asthma specialist.
153
an asthmatic child has been referred to your clinic as they're using their salbutamol inhaler 8 times a week despite being on the max appropriate doses of PRN salbutamol, regular preventer (ICS, beclomethasone) and montelukast
next step?
oral steroids, on lowest feasible dose.
154
what are the key principles behind moving patients up/down the asthma treatment guidelines?
move up if using PRN inhaler 3+ times per week.
| if asthma well-controlled, always try to step down to see if they can remain symptomless on less treatment.
155
describe the management of an acute asthma attack
OSHITME:
```
Oxygen - 15L 100% nonrebreathe
Salbutamol nebs
Hydrocortisone IV
Ipratropium
Theophylline
Magnesium sulphate
Escalate, consider ITU
```
give oral pred 3-5 days after acute attack
156
what is the most common reason a child hasn't seen an improvement in their asthma symptoms after starting a new inhaler?
they're not using it right! always check inhaler technique
157
list some possible causes of recurrent cough in a child
```
recurrent resp infections
post-specific resp infection e.g. pertussis
asthma
CF
recurrent aspiration ± GORD
persistent endobronchial infection
inhaled foreign body
active/passive smoking
TB
```
158
what is the mode of inheritance/genetic mutation for cystic fibrosis?
autosomal recessive
mutation in the cystic fibrosis transmembrane conductance regulator gene (CFTR) on chromosome 7 - codes for a cyclic AMP-regulated sodium/chloride channel
159
describe how CF affects the airways
reduction in airway surface liquid layer leads to impaired ciliary function and retention of mucopurulent secretions.
also get chronic infection with pseudomonas aeruginosa
160
what pathogens commonly affects CF patients
*pseudomonas aeruginosa*
| also see chronic staph aureus or H influenzae infections
161
how does CF affect the digestive tract?
intestines - thick viscous meconium produced, leads to meconium ileus
pancreas - ducts become blocked, leads to pancreatic enzyme deficiency and malabsorption
162
how are most CF cases identified in the UK?
the Guthrie (heel prick test)
163
what diseases does the Guthrie/heel prick test assess for?
```
galactosemia
CF
branched chain ketonuria
MCADD
phenylketonuria
sickle-cell
congenital hypothyroidism
```
164
describe the clinical features of CF
chronic infections (pseudomonas/staph aureus/H influenzae) due to viscous mucus in small airways --> leads to damage of bronchial wall, bronchiectasis and abscess formation --> persistent loose cough, producing purulent sputum
90% will have pancreatic exocrine insufficiency as well
165
describe how pancreatic exocrine insufficiency affects people with CF
present in 90%
deficient in lipase, amylase and proteases
leads to maldigestion and malabsorption
leads to failure to thrive, passing of frequent large pale and offensive stools (steatorrhoea)
166
what test is used to diagnose pancreatic exocrine insufficiency in people with CF
low faecal elastase
167
how might neonates present with CF?
meconium ileus - intestinal obstruction - vomiting, abdo distension etc
168
what diagnostic tests are used in CF?
the Guthrie
genetic testing for CTFR mutations
SWEAT TEST - salty sweat! raised Na+
169
what are the basic principles of managing a CF patient?
involve MDT, involve patient when they're old enough, isolate from other CF patients (prevents pseudomonas spread).
aim is to prevent progression of lung disease and maintain nutrition/growth
170
how do manage CF, from a respiratory perspective?
PHYSIO - exercises to be done at least twice a day, helps to clear secretions.
regular lung function tests.
prophylactic oral abx (fluclox) and rescue abx as required.
hypertonic saline/nebulised DNAse may help.
end stage = bilateral lung transplant.
171
how do you manage CF from a nutritional perspective?
oral enteric coated pancreatic replacement therapy.
high kcal diet (150% of RDAs)
fat soluble vitamin supplements.
screen for impaired glucose tolerance once they reach adolescence.
172
how does periorbital cellulitis present?
fever with erythema, tenderness and oedema of eyelid - usually unilateral.
might follow local trauma or spread from a paranasal sinus infection.
173
how do you manage a child with periorbital cellulitis?
always need referring to hospital, JIC it's orbital.
prompt IV abx to prevent progressing to orbit (would then have proptosis, painful/limited occular movement, reduced visual acuity)
174
what is strabismus/squint?
when one eye is misaligned in relation to another
| affect 2-3% of children in UK
175
what is the most common type of childhood squint?
Congenital/infantile squint - most commonly an esotropia (convergent squint).
develops within the first six months of life and is usually idiopathic in a child with otherwise normal health.
176
why do squints develop?
because there is lack of coordination which prevents the gaze of both eyes being directed at the same point in space
177
give some causes of a squint
Idiopathic.
Refractive errors, especially hypermetropia.
Other causes of poor visual acuity in one or both eyes - incl congenital cataract and retinoblastoma.
Neurodevelopmental conditions and syndromes.
cranial nerve palsies, brain lesions and muscle diseases - rare in kids.
178
how might a squint be managed?
Glasses to correct any refractive error.
Occlusion therapy to treat amblyopia (lazy eye - eye patch)
Surgery (or in some cases injection of botulinum toxin) to correct misalignment of eyes.
treatment basically helps correct or reduce squint. in some, normal vision can be restored.
179
what's the difference between regurgitation and posseting?
posseting is the return of small amounts of milk with burps/wind
regurgitation is larger more frequent loss
both are 'non-forceful' return of milk (differs from vomiting)
posseting is normal, regurg might mean GORD
180
what would bile-stained vomit in a child indicate?
intestinal obstruction
181
what might haematemesis in a vomiting child indicate?
oesophagitis, peptic ulcer, oral/nasal bleeding
| teenagers - mallory-weiss tears (drinking/bulimia)
182
what might projectile vomiting in first few weeks of life indicate?
pyloric stenosis
183
what might abdo distension in a vomiting child indicate?
obstruction - including strangulated inguinal hernia
184
what might blood in the stool of a vomiting child indicate?
intussusception, gastroenteritis (salmonella/campylobacter)
185
what might failure to thrive in a vomiting child indicate?
reflux, coeliac disease, other chronic GI conditions
186
define gastro-oesophageal reflux - what causes it? why is it common in infants?
the involuntary passage of gastric contents into the oesophagus
due to inappropriate relaxation of the lower oesophageal sphincter (LOS) due to functional immaturity
common as infants have a fluid diet, are horizontal most of the time, and have a short intra-abdominal oesophagus
187
what's the usual prognosis of GORD in an infant? when might you be more worried?
usually resolves by 12 months of age - they then have an upright posture, matured LOS and more solid diet!
worry if - failure to thrive (due to severe vomiting), oesophagitis, aspiration
188
what investigations would you do if you suspected GORD in an infant?
usually none - clinical diagnosis
COULD do - 24h oesophageal pH monitoring, endoscopy with oesophageal biopsies
189
how would you manage GORD in an infant? give answers for mild vs more significant
mild - reassure, add thickener (E.g. carobel), hold upright after feeds
significant - ranitidine (H2 receptor blocker) or gaviscon (omeprazole, PPI)
if no response - consider cow's milk protein allergy
190
what is pyloric stenosis and how does it typically present?
hypertrophy of pyloric muscle causing gastric outlet obstruction
presents at 2-7 weeks old, boys > girls
191
what are the clinical features of pyloric stenosis?
vomiting that increases in frequency and forcefulness over time, becoming projectile in nature.
initially hungry after vomits, but might become dehydrated and lose interest in feeds.
will see weight loss if delayed presentation.
192
how would you go about diagnosing pyloric stenosis?
give a test feed of milk, will calm them to allow examination
might see visible gastric peristalsis across abdomen.
olive sized mass in RUQ - pyloric mass.
USS if in doubt.
193
how would you treat a baby with pyloric stenosis?
IV fluids - rehydrate, correct electrolyte disturbance.
pylomyotomy - open/laparoscopic - division of hypertrophied muscle down to mucosa.
194
what are the symptoms of acute appendicitis in a child?
anorexia, vomiting, abdo pain (central and colicky then localised to RIF
v. uncommon if <3 yrs
195
what are the signs of acute appendicitis in a child?
low grade fever
abdo pain aggravated by movement
persistent tenderness with guarding of RIF (McBurney's point)
196
what is intussusception and what age group does it usually affect?
invagination of proximal bowel into a distal segment - usually ileum passing into caecum through the ileocaecal valve
3 months - 2 years
197
what are the possible complications of intussusception?
stretching and constriction of mesentery, resulting in venous obstruction --> engorgement and bleeding from bowel mucosa --> fluid loss, bowel perf, peritonitis, gut necrosis
need prompt diagnosis, immediate fluid resus and urgent reduction!!
198
how does intussusception present?
paroxysmal severe colicky pain and pallor - during pain episodes, baby becomes pale and draws up legs
refuse feeds, may vomit (might be bile stained depending on site of intussusception)
sausage shaped mass in abdomen
redcurrant jelly stool - blood stained mucus
abdo distension and shock
199
how would you manage an infant with an intussusception?
immediate IV fluid resus
XR abdo / USS (more useful than XR)
interventional radiology - rectal air insufflation
25% will require surgery - if air insufflation unsuccessful or signs of peritonitis
200
what is Meckel's diverticulum and how does it present?
small bulge in the small intestine present from birth - remnant of the omphalomesenteric duct - contains ectopic gastric mucosa or pancreatic tissue.
mostly asymptomatic - might have severe rectal bleeding (somewhere between bright red and malaena)
201
how is Meckel's diverticulum diagnosed and treated?
shows up on Technetium scan - technetium picks up gastric mucosa so shows up as spot on the scan.
treatment is surgical resection
202
what happens in malrotation of the bowel?
during rotation of small bowel, if the mesentery isn't fixed at the duodenojejunal flexure or in the ileocaecal region then the rotation goes wrong - end up with a shorter base and predisposition to volvulus
203
how does a child with malrotation of the bowel present? how should they be managed?
obstruction with bilious vomiting, usually in first few days of life.
needs urgent surgery + pass an NG tube
204
what is abdominal migraine?
bit of a vague 'diagnosis' of recurrent abdo pain - might be associated with headaches.
midline abdo pain w/vomiting and facial pallor + personal/family hx of migraine.
205
what are the 3 'symptom constellations' (?) you might see in a child with recurrent abdo pain lasting at least 3 months?
IBS - by far most common
peptic ulcer/functional dypepsia
abdominal migraine
206
what are some characteristic symptoms of IBS in a child?
abdo pain worse before/relieved by defecation
explosive, loose or mucus-y stools
bloating
feeling of incomplete defecation (tenesmus)
constipation - that might alternate with normal/loose stools
207
explain how you'd differentiate between peptic ulcer and functional dypepsia in a child
do a 13C breath test to check for h pylori
treat with PPI + h pylori eradication if indicated
failure to respond to this = upper GI endoscopy
if that's normal = functional dyspepsia
208
what is the most common cause of gastroenteritis in children? name a couple of others
rotavirus
adenovirus, norovirus, bacterial (much less common)
209
name some bacterial causes of gastroenteritis in children
```
Campylobacter jejuni
Shigella
Salmonella
Cholera
E. Coli
```
210
how would a child with gastroenteritis due to camylobacter typically present?
severe abdo pain + diarrhoea
211
how would a child with gastroenteritis due to shigella or salmonellae typically present?
dysentery type picture - blood and pus in stool, pain, tenesmus
212
how would a child with gastroenteritis due to cholera or E coli typically present?
profuse and rapidly dehydrating diarrhoea
213
what is the concern with a child with gastroenteritis?
dehydration --> shock
214
what factors increase a child with gastroenteritis's risk of dehydration?
- infant, especially if <6 months or low birthweight (greater insensible fluid loss + greater basal fluid requirements
- 6+ diarrhoeal stools in prev 24h
- vomited 3+ in prev 24h
- unable to tolerate (or not been offered) extra fluids
- evidence of malnutrition
215
list the components of a dehydration assessment in a child
- general appearance
- level of consciousness
- skin colour - pale, mottled
- pale extremities
- sunken eyes
- dry mucous membranes
- tachycardia, tachypnoea, low BP
- peripheral pulses
- cap refill time (should be < 3s)
- skin turgor
- sunken fontanelle
216
what investigations might be done for a child with gastroenteritis?
if septic, blood/mucus in stool or immunocompromised - do a stool culture.
might check U&Es and glucose
if start abx - should do blood cultures first
217
how would you manage a child with gastroenteritis?
- encourage oral fluids
- dioralyte - little and often
- consider NG dioralyte if refusing orally
- if shocked give fluid resus
- IV fluids - replace deficit, plus maintenance
- gradually introduce usual foods after recovery
- don't return to school/childcare for 48h, encourage handwashing
- anti-diarrhoeals and abx rarely used
218
briefly describe the pathology of coeliac disease
immune system overreacts to the gliadin bit of gluten - causes damage to the villi of the proximal small intestine - increased cell loss from villous tips, eventually end up with a flattened mucosa
219
describe the classical presentation of coeliac disease in a child
8-24 months - after weaning onto wheat-containing foods.
Failure to thrive, abnormal stools, buttock wasting and general irritability.
but - children are more likely to present less acutely, later in childhood
220
how is coeliac disease diagnosed?
serology for IgA tissue transglutaminase antibodies + endomysial antibodies
small intestinal biopsy - increased intraepithelial lymphocytes and villous atrophy, plus crypt hypertrophy
plus - symptoms go away when you withdraw gluten, and they catch up on growth!
221
how is coeliac disease managed?
gluten free diet - involve dietician
| monitor growth
222
how does Crohn's disease present in a child?
- growth failure, delayed puberty
- general ill health - fever, lethargy, weight loss
- random signs - oral lesions, perianal skin tags, uveitis, arthralgia, erythema nodosum
- classical stuff - abdo pain, diarroea, weight loss
223
what might you find on blood tests of a child with Crohn's disease?
raised ESR and CRP
iron-deficient anaemia
low albumin
224
how does Crohn's affect the bowel?
usually the distal ileum and proximal colon
initial areas of acutely inflamed, thickened bowel - then you get strictures and fistulas between loops of bowel and skin/other organs
225
how is Crohn's definitively diagnosed?
endoscopy + biopsy - shows non-caseating epitheliod cell granuloma
226
how would you induce and maintain remission from Crohn's disease in an infant?
nutritional therapy - whole protein modular feeds (polymeric diet) for 6-8 weeks
systemic steroids if that doesn't work.
to maintain remission - immunosuppressants (azathioprine, methotrexate)
227
describe the characteristic presentation of ulcerative colitis?
- rectal bleeding, diarrhoea, colicky pain
- may get weight loss/growth failure
- erythema nodosum, arthritis
228
how would you diagnose UC in a child?
endoscopy and biopsy - after excluding infectious causes
you would see continuous colitis from rectum, extending proximally - mucosal inflammation, crypt damage and ulceration
229
describe the management of UC in children
induction and maintenance of remission with aminosalicylates (mesalazine), topical steroids.
if more severe - azathioprine, systemic steroids.
really severe - colectomy with ileostomy or ileorectal pouch.
230
define constipation
decreased frequency or increased pain on defecation
231
list some causes of constipation in babies that should be considered
Hirschprung's disease, anorectal abnormalities, hypothyroidism, hypercalcaemia
also - dehydration, decreased oral intake, anal fissure (causes pain)
in older children, could be an issue with toilet training / stress
232
what would you find on the abdominal examination of a constipated child?
hard palpable mass, often in a well child
233
what might happen if a child has long-standing constipation?
rectum becomes over-distended, lose feeling of need to defecate - may have involuntary soiling as contractions of full rectum inhibit internal sphincter (overflow, may be diarrhoeal)
234
describe the management of a child with constipation
- reassure and explain
- evacuate overloaded rectum - use Movicol (macrogol laxative, contains polyethylene glycol and electrolytes) - escalating dose until impaction resolves and then maintenance
- add stimulant laxative if needed (e.g. sodium picosulphate)
- ensure sufficient fluids, high fibre diet and encourage child to sit on toilet after meals (physiological gastrocolic reflux)
- star charts!
235
what is hirschsprung's disease?
congenital abnormality involving abnormal innervation of large bowel - absence of parasympathetic ganglion cells in rectum (may extend to colon).
results in constantly constricted colon - functional obstruction at birth.
236
how does Hirschsprung's disease present?
failure to pass meconium within 24h of birth - abdo distension and bile-stained vomiting develops
237
how is Hirschsprung's disease diagnosed and treated?
rectal biopsy - absence of ganglion cells in mesenteric plexus, plus presence of acetylcholinesterase-positive nerve trunks
treatment - surgery - affected sections of bowel removed and ends are anastomosed.
238
what is infantile colic?
baby has recurrent episodes of inconsolable crying + drawing up of legs - usually from around 2 weeks old -> 4 months.
no treatment or anything - just differentiate from cow's milk protein allergy and GORD - movement can help soothe.
239
define failure to thrive
poor weight gain in infancy - falling across centile lines
240
what can cause failure to thrive?
global main cause is poverty.
feeding technique can be an issue - check latching, teat of bottles etc. be on look out for evidence of maltreatment, NAI etc.
also - organic causes - coeliac, cow's milk protein allergy, etc etc etc
241
what is the anatomical cause of inguinal hernias in babies/children?
patent processus vaginalis (passage which ushers the descending testicle into the scrotum)
242
If a baby presents with a bulge lateral to pubic tubercle during crying, what is the likely cause and how should it be managed?
inguinal hernia - repair promptly - six/two rule:
< 6 weeks = operate within 2 days
< 6 months = within 2 weeks
< 6 years = within 2 months
243
what is "toddler's diarrhoea" and what causes it?
most common cause of persistent loose stools in a well and thriving preschool child - maturational delay in intestinal motility causes intermittent explosive loose stools (often with undigested vegetables in it - grim) - thought to be to do with dodgy diet - aim for high in fat (whole milk), normal (not high) fibre, not loads of fruit juice
244
what is cow's milk protein allergy?
usually transient intolerance to cow's milk in babies - colic symptoms, GORD, diarrhoea (±blood/mucus), failure to thrive
245
how do you manage a child with suspected cow's milk protein allergy?
if exclusively breastfed - get mum to cut out cow's milk
| if bottle - hypoallergenic formula (hydrolysed or amino acid)
246
what causes Kwashiorkor, how does it present and how would you manage it?
low intake of PROTEIN and essential amino acids - malnutrition
signs - poor growth, diarrhoea, apathy, anorexia, oedema, skin/hair depigmentation, distended abdomen.
Rx - gradually increasing high-protein diet + vitamins
247
what is marasmus and how does it present and how would you manage?
lack of CALORIES + discrepancy between height and weight. associated with HIV.
signs - distended abdomen, diarrhoea, constipation, infection, low albumin.
parenteral nutrition to rehydrate and restore renal function. then balanced diet with vitamins.
head circumference and stature may remain poor.
248
what is biliary atresia/how does it present?
rare but serious. apparently healthy babies with jaundice, yellow urine and pale stools - either destruction/absence of extrahepatic biliary tree.
persistent jaundice from day 2 after birth, predominantly conjugated hyperbilirubinaemia.
spleen palpable in week 3 or 4.
249
how is biliary atresia managed?
surgery - OK prognosis with early referral but late presentation means will need liver transplant by 1 year old.
refer all term babies jaundiced beyond 2 weeks!
US can be helpful for diagnosis.
250
what are the two main (rare but treatable) causes of persistent obstructive neonatal jaundice?
biliary atresia and choledochal cyst
251
choledochal cysts - what are they, symptoms, management
congenital cysts on the bile duct - cause neonatal obstructive jaundice persisting for >14 days, enlarged liver.
Rx - surgical excision
252
what is meningitis?
inflammation of the meninges covering the brain.
raised WCC in CSF.
usually viral but can be bacterial.
253
what is bacterial meningitis?
bacterial infection of meninges following bacteraemia.
damage caused due to host response instead of organism itself --> inflammation mediators, activated leukocytes, endothelial damage --> raised ICP, cerebral oedema, reduced cerebral blood flow
254
give some causes of bacterial meningitis
pathogens carried in nasal passages, invade meninges via bloodstream.
over 50% are meningococcal - Group B most common variety, vaccinated in childhood imms (MenB).
neonates - 3 months:
Group B strep, E coli, listeria monocytogenes
1 month - 6 yrs:
neisseria meningitidis
streptococcus pneumoniae - quite rare
haemophilus influenzae type B - rare due to HiB vaccine.
> 6 yrs:
N. meningitidis, Strep pneumonia
255
give some causes of viral meningitis, how does it present compared to bacterial and how is it diagnosed?
enteroviruses, EBV, adenovrisues, mumps
usually less severe than bacterial.
confirmed by PCR of CSF (there's also specific changes to sugar/protein levels in CSF I think?)
256
what are the clinical features of meningitis?
can be non-specific - irritability, poor feeding, vomiting, fever, drowsiness.
purpuric rash (non-blanching - glass test) if meningococcal sepitcaemia - bad news!
bulging fontanelle in infants
neck stiffness and photophobia in older kids
seizures - be careful diagnosing febrile convulsions.
257
what investigations should be performed if you suspect a child has meningitis?
LP - examine CSF, PCR, MC&S
blood cultures and PCR before start abx
throat/nasal swabs
NB - LP contraidicated if signs of raised ICP, coagulopathy or sepsis
258
how would you manage a child with bacterial meningitis?
cefotaxime or ceftriaxone.
if in community and child has purpuric rash - give IM benzylpenicillin and transfer urgently to hospital
give prophylactic rifampicin (or ciprofloxacin/ceftriaxone) to contacts - eliminates nasopharyngeal carriage
259
give some complications/sequelae of meningitis
sensorineural deafness, subdural effusion, cerebral oedema, local vasculitis, cerebral infarcts (seizures), hydrocephalus, cerebral abscess
260
what pathogens typically cause periorbital cellulitis?
staph aureus, group A strep
| H. influenzae if young/unimmunised
261
describe the transmission of chicken pox
```
Varicella Zoster (VZV) infection - highly infectious vis droplet transmission, direct contact or contact with soiled materials.
average incubation period = 14 days.
infectious from 2 days pre rash --> all lesions encrusted.
```
262
what are the clinical features of chicken pox?
preceded by short period of coryza, then itchy vesicular rash - starts on head and trunk then spreads out over 3-5 days.
in immunocompromised kids can get a secondary staph infection of vesicles.
263
how is chicken pox diagnosed?
clinical diagnosis.
| can isolate virus from vesicular fluid if needed but don't normally bother.
264
how is chicken pox managed?
usually symptomatic.
if immunocompromised - IV acyclovir or varicella zoster Ig (this is also given to new babies if mum has VZ or herpes in 7 days before/after birth, plus any exposed premature babies).
might also use valcyclovir in adolescents/adults - disease is much more severe than if they'd contracted in childhood.
265
describe the transmission of glandular fever/infectious mononucleosis
Epstein-Barr Virus.
droplet transmission or directly via saliva (kissing disease).
most people asymptomatically infected in childhood. symptomatic infection is most common in adolescents.
incubation period 30-50 days
266
what are the clinical features of glandular fever?
fever, malaise, pharyngitis, cervical lymphadenopathy.
| might see petechiae on palate, sparse maculopapular rash.
267
how is glandular fever diagnosed and managed?
clinical diagnosis usually
heterophil antibody test (Monospot test) - NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm.
management is symptomatic.
268
what is Kawasaki's disease? why is it important?
uncommon systemic vasculitis occurring in kids age 6m - 4 yrs.
important because they are at high risk of developing coronary artery aneurysms afterwards - early recognition is important.
269
what are the clinical features of Kawasaki's disease?
prolonged fever and rash is the general gist.
Fever >5 days, plus 4 of 5 out of:
- conjunctival infection
- mucous membrane changes - pharyngeal injection, red dry cracked lips, strawberry tongue
- cervical lymphadenopathy
- rash
- extremities - red and oedematous, then peeling
270
how would you manage a child with Kawasaki's?
single dose of IVIG plus high dose aspirin, continued at low dose for 6-8 weeks.
refer for echocardiography monitoring - coronary artery aneurysm formation, usually occurs in first 4-6 weeks of illness - repeat echos at intervals throughout next year.
271
what causes primary immunodeficiency? when should you consider it?
uncommon - X linked or autosomal recessive disorders e.g. SCID.
consider if they have SPUR infections - Severe, Prolonged, Unusual or Recurrent
272
how would you investigate and manage a child with a possible primary immunodeficiency?
start investigations with FBC and serum Igs
| management involves antibiotic prophylaxis, Ig replacement therapies, bone marrow transplants, gene therapy (SCID)
273
give some causes of secondary immunodeficiency
drugs - cytotoxic agents (e.g. chemo), steroids
| another disease - intercurrent infection, malignancy, HIV, nephrotic syndrome
274
what causes measles?
infection with a single-stranded RNA virus (Morbillivirus)
not vaccinating kids!
highly infectious, transmitted by droplet spread, incubation period 10 days.
275
describe the clinical features of measles
fever, cough, coryza and conjunctivitis - then Koplik's spots (white lesions) on buccal mucosa (pathognomic, but only present in some cases).
3 or 4 days later - erythematous maculopapular rash which becomes blotchy and confluent.
276
how would you manage a child with measles?
diagnosis confirmed by specific IgM in serum samples taken 3 days after rash appeared - notifiable.
symptomatic treatment.
need to be off school for a week after appearance of the rash.
277
what are some complications that might occur in a child with measles?
acute - febrile convulsions, otitis media, tracheobronchitis, pneumonia.
rarely - severe encephalitis. 40% of these will have neurological sequelae.
278
what is rubella?
aka German measles.
infection with rubivirus.
MMR vaccine!
mild childhood disease, only important re. maternal infection and congenital rubella
279
what are the clinical features of childhood rubella (i.e. not congenital)?
often subclinical.
incubation period of 14-21 days, low grade fever, then pink-red maculopapular rash - starts on face and spreads over whole body - but only lasts a couple of days.
280
how would you diagnose and treat childhood rubella?
clinical diagnosis.
can detect rubella IgM in saliva if necessary.
supportive treatment.
MMR vaccine! live attenuated vaccine.
281
what is congenital rubella?
occurs when mother is infected with rubella during pregnancy - extend of foetal damage is determined by its gestational age at onset - in first 8-10 weeks risk is hight, beyond 18 weeks risk is minimal.
282
what features might a baby affected by congenital rubella have?
deafness, congenital heart disease, cataracts.
hearing impairment is the main thing really - sensorineural deafness.
also - growth retardation, heaptosplenomegaly, retinopathy, glaucoma.
283
how would you manage a pregnant woman with exposure to rubella?
test for antirubella IgG and IgM - vaccinate after delivery.
| can offer termination if highly likely woman is infected in first 8-10 weeks.
284
what is erythema infectiosum?
slapped cheek disease.
infection with parvovirus B19 - DNA virus.
transmitted via respiratory secretions, from mother to fetus or by contaminated blood products.
285
what are the clinical features of slapped cheek disease/erythema infectiosum? how is it diagnosed/managed?
often asymptomatic.
fever, then a week later red appearance on face, progresses to symmetrical lacy rash on extremities and trunk.
Dx - clinical
Rx - supportive
286
what is staphylococcal scalded skin syndrome? how is it treated?
life-threatening, toxin mediated manifestation of localised skin infection.
epidermolytic toxins produced by bacteria cause blistering (disruption to epidermal granular cell layer) - appearance of scalding.
Rx - IV flucloxacillin and pay attention to fluid balance
287
what is scarlet fever?
occurs in kids with streptococcal pharyngitis - organism (group A strep) produces a toxin which causes characteristic rash - widespread, erythematous rash starting on trunk that becomes puncatet and desquamates after 7-10 days.
288
what are the clinical features of scarlet fever?
- tonsillitis
- strawberry tongue
- palatal petechiae
- fever
- rash - widespread, erythematous, starts on trunk, becomes punctate and desquamates after 7-10 days
289
how do you diagnose and treat scarlet fever?
clinical diagnosis - can isolate streptococcus from a throat swab if needed
Rx - penicillin or erythromycin.
290
how does TB present in kids?
kids <4 y more at risk of disseminated disease e.g. TB meningitis, bone TB etc.
main symptoms of active TB included prolonged cough, weight loss, anorexia, fever
291
how is TB tested for?
Mantoux test.
culture is ideal but hard to get from kids - early morning gastric washings.
on XR - consolidation, hilar/mediastinal lymphadenopathy
292
how is TB treated?
```
6 months of 4 drugs - RIPE
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
```
last two just for first two months.
BCG given to immigrants from countries with high incidence, contacts of TB, babies in certain parts of country with high TB.
293
what are the four common nematodes affecting children?
- enterobius vermicularis - threadworm
- ascaris lumbricoides - roundworm
- ancylostoma duodenale - hookworm
- toxocara canis
294
how does threadworm present? how do you diagnose/treat?
v common in preschool - faecal oral transmission. eggs laid in perianal area at night, causes scratching, eggs then carried under fingernails to the mouth - autoinfection.
present with perianal pruritus and vulvovaginitis.
diagnosis - apply sellotape to perianal region in morning and look for eggs on it with magnifying glass.
Rx - two doses of piperazine two weeks apart, or single dose of mebendazole for kids >2 years.
295
describe the transmission of polio?
enterovirus with three antigenic types.
faecal-oral transmission, incubation period of 7-21 days.
exists only in a few countries now - vaccination working towards eradication woo!
296
what are the clinical features of polio infection?
90% asymptomatic.
some have minor illness - fever, malaise, headache.
some have CNS involvement / paralytic polio - virus attacks anterior horn cells of spinal cord leading to paralysis.
notifiable disease.
297
how is HIV transmitted to children? how is it diagnosed?
vertical transmission - intrauterine, intrapartum or via breastfeeding.
if current treatment given, vertical transmission occurs in < 1%.
newborns to HIV-infected mothers will have circulating maternal HIV abs until 15-18 months - so can't diagnose based on antibodies till after this.
at < 18 months - HIV viral cultures (gold standard but not available widely) or PCR for viral genome.
298
describe the clinical manifestation of HIV in kids?
incubation period from infection to disease is shorter in perinatally affected kids than for adults - but treatment has reduced mortality and hospital admissions.
they get lots of infections, lymphadenopathy, hepatosplenomegaly, failure to thrive/wasting, encephalopathy, severe bacterial infections and weird opportunistic infections etc etc
299
how is paediatric HIV managed/prevented?
antiretroviral treatment once symptomatic/low CD4 count.
lots of psychological treatment for child, mum and rest of family.
prevention - zidovudine given during pregnancy and delivery, then to neonate in first weeks, reduces risk of vertical transmission. birth via C section recommended unless maternal viral load is low.
300
what is hand, foot and mouth disease and what is the most common viral cause?
disease beginning with fever, irritability, malaise, then you get rash on palms/soles of feet and around mouth.
Coxsackie A16 - transmitted by nasopharyngeal secretions.
symptomatic treatment only.
301
what are the features of a life-threatening asthma attack?
```
92 33 CHEST
sats < 92%
PEFR < 33% predicted
Cyanosis
Hypotension
Exhaustion - "reduced/poor respiratory effort"
Silent chest
Tachypnoea
```
also altered consciousness, agitation
302
what are the features of a severe asthma attack?
SpO2 < 92%
PEFR 33-50% predicted
Too breathless to talk or feed / can't complete full sentences (once at talking age!)
Heart rate > 140/min if age 2-5y, >125 if >5yrs
Respiratory rate > 40/min (2-5y), >30 (>5y)
Use of accessory neck muscles
303
what rash might you see on the shins in association with streptococcal infections?
erythema nodosum - tender, erythematous, nodular lesions
