Paeds Flashcards
What is croup?
common viral upper airway infection
affects children 6months - 3yrs
larynx inflammation causes barking cough, stridor and may have low fever
Causes of croup
parainfluenza virus is most common cause
other viral causes = influenza A and B, measles, adenovirus, resp synctial virus
bacterial causes = staphylococcus aureus, streptococcus pneumoniae, haemophilius influenzae and moraxella catarrhalis
How does croup spread?
droplet spread
outbreaks can occur in childcare settings eg school
most common in autumn
more common in males
Croup pathophysiology
following coryzal prodrome, WBCs infiltrate larynx, trachea and large bronchi, causing inflammation
- this causes oedema, results in partial airway obstruction
- when significant, airway obstruction increases work of breathing and causes stridor
Mild croup
- occasional barking cough
- no audible stridor at rest
- no or mild suprasternal and/or intercostal recession
- child happy and prepared to eat, drink and play
Moderate croup
-frequent barking cough
- easily audible stridor at rest
- suprasternal and sternal wall retraction at rest
- no or little distress or agitation
- child can be placated and is interested in its surroundings
Severe croup
- frequent barking cough
- prominent inspiratory (and occasionally expiratory) stridor at rest
- marked sternal wall retractions
- significant distress and agitation, or lethargy and restlessness
- tachycardia occurs w/ more severe obstructive symptoms and hypoxaemia
When should a child be admitted for croup?
- moderate or severe croup
- <3months of age
- known upper airway abnormalities
- uncertainty about diagnosis
Croup clinical features
coryzal prodrome which progresses over 12-48hrs to include:
- low fever <38ºC)
- hoarseness
- barking cough (worse at night)
- stridor - insidious and progressive
Features of respiratory distress
tachypnoea
cyanosis
head bobbing
nasal flaring
subcostal and intercostal recession
suprasternal and sternal recession
diaphragmatic breathing
use of accessory muscles
Croup investigations
clinical - barking cough and stridor
Croup differentials
- viral upper resp tract infection - seal like barking cough less common
- bronchiolitis - causes wheeze
- epiglottitis - absence of barking cough, muffled hot potato voice
- foreign body aspiration - history, abrupt onset during daytime
- bacterial tracheitis - school-age, reluctant to cough due to pain
Croup management
Supportive
Oral dexamethasone
Parents advised that symptoms usually resolves w/in 48hrs, and to escalate if stridor is hear or symptoms worsen
Arrange follow up
Moderate - severe croup management
supportive
oral dexamethasone
nebulised epinephrine
supplemental oxygen
advise parents
children can be discharged home after 2-4hrs of obs following epinephrine, given no stridor at rest
Croup complications
resp distress
pneumonia
pulmonary oedema
epiglottitis
bacterial tracheitis
What is bronchiolitis?
acute bronchiolar inflammation seen in infants and young children
What is the most common cause of bronchiolitis?
respiratory synctial virus (RSV) in 75-80% of cases
Bronchiolitis clinical features
coryzal symptoms (including mild fever) precede:
- dry cough
- increasing breathlessness
- wheezing, fine inspiratory crackles (not always present)
- feeding difficulties associated w/ increasing dyspnoea
Bronchiolitis investigations
immunofluorescence of nasopharyngeal secretions may show RSV
Bronchiolitis management
supportive
nasal suction
oxygen
hydration
Causes of asthma
- genetic: FH, predisposition
- environmental: allergens, air pollution, tobacco smoke
- infections: viral, bacterial
- sensitisation and atopy: eczema, food allergies
- sociodemographic: socioeconomic, urban v rural living
- lifestyle: dietary, physical activity
Asthma definition
condition characterised by variable airflow limitation and airway hyper-responsiveness in response to number of stimuli
can eventually result in permanent airway remodelling and therefore limitations in reversibility of airflow limitation
What is a HEADS assessment?
Home
Education
Activities
Drugs and alcohol
Suicidality / sex
BINDS
Birth / perinatal
Immunisation
Nutrition / feeding
Developmental
Social
Normal development gross motor milestones
Newborn = flexed arms and legs, equal movements
3 months = lifts head on tummy
6 months = chest up w/ arm support, rolls
9 months = pulls to stand
1 yr = walking
2 yrs = walks up steps
3 yrs = jumps
4 yrs = hops
5 yrs = rides bike
Normal devlopment fine motor and vision milestones
4 months = grasp an object, uses both hands
8 months = takes cube in each hand
12 months = scribbles w/ crayon
18 months = builds tower of 2 cubes
3 yrs = tower of 8 cubes
Normal development speech, language and hearing milestones
3 months = laughs and squeals
9 months = ‘dada’ ‘mama’
12 months = 1 word
2 yrs = 2 words sentences, names body parts
3 yrs = speech mainly understandable
4 yrs = knows colours, can count 5 objects
5 yrs = knows meaning of words
If they aren’t walking by … it is considered a red flag
18 months
Normal development social / self care milestones
6 weeks = smiles spontaneously
6 months = finger feeds
9 months = waves bye
12 months = uses spoon / fork
Cranial nerve exam in infants
Observe movements, scars, head shape, VP shunts etc
II = blink response to bright light, red reflex, visual fields via distraction
III,IV,VI = inspect for eye aligned in conjugate gaze, fix/follow and doll’s eye manoeuvre, pupillary response
V = suck
VII = observe face
VIII = observe behavioural response to loud noise
IX, X = assess suck and swallow w/ feeding
XI = symmetry of neck movements, head control
XII = tongue movements during feeding / sucking
Child development red flags
Gross motor - not sitting by 1yr, walk by 18m
Fine motor - hand preference before 18m
SLT - not smiling by 3m, no clear words before 18m
Social - no response to carers interaction by 8wks, not interested in playing w/ peers by 3yrs
Regression
What is a macular rash?
non-palpable rash w/ colour changes in limited areas
eg measles, rubella
What is a papular rash?
palpable rash w/ raised, solid lesions and colour changes in limited areas up to 0.5cm
eg Gianotti-Crosti, pityriasis rosea
What is a vesicular rash?
elevate lesions that are filled w/ clear fluid <0.5cm
eg chicken pox, herpes simplex, herpes zoster
What is acute epiglottitis?
inflammation of epiglottis and surrounding supraglottic structures
can lead to airway obstruction, makes management critical
Acute epiglottitis causes
- most commonly bacterial infection, haemophilus influenzae type B
- Also streptococcus pneumoniae, grp A streptococci and staphylococcus aureus
- Viral and fungal infections, and non-infectious causes (eg thermal injury) also contribute
Acute epiglottitis clinical features
- rapid onset of severe sore throat and odynophagia
- muffled voice or ‘hot potato’ voice
- stridor
- resp distress
fever
tripod or sniffing position
Acute epiglottitis investigations
clinical
can use lateral neck radiographs, blood cultures and swabs, and flexible fiberoptic laryngoscopy
Acute epiglottitis management
- airway management
- antibiotics eg third-gen cephalosporins
- supportive care - IV fluids, analgesics, antipyretics
- monitoring and follow-up
- vaccinations
What is cystic fibrosis?
life-limiting autosomal recessive disorder caused by mutations in cystic fibrosis transmembrane conductance regulator (CFTR) gene, leads to production of thick, sticky mucus that obstructs organs, primarily affecting resp and GI systems
Where is there mutation in cystic fibrosis?
CFTR gene on chromosome 7
(F508del mutation most common)
Cystic fibrosis pathophysiology
CFTR protein regulates transport of chloride ions and bicarbonate across epithelial cell membranes
Malfunctioning results in chloride and water retention in cells
imbalance establishes sodium-rich environment outside cell, prompting sodium and water reabsorption
consequently, mucus becomes dehydrated and thickened
Cystic fibrosis resp system implications
- mucus accumulation in bronchi and bronchioles
- chronic infections
- progressive lung damage
Cystic fibrosis GI system implications
- pancreatic blockage, hindering release of digestive enzymes
- intestinal obstruction
- liver involvement / biliary duct obstruction
Cystic fibrosis reproductive system implications
Males = congenital bilateral absence of vas deferens - renders infertile
Females = thickened cervical mucus can lead to reduced fertility. Irregular menstrual cycles
Salt imbalance in cystic fibrosis
malfunctioning CFTR in sweat ducts results in diminished reabsorption of chloride, and sodium
imbalance leads to salty sweat, posing risks of dehydration and electrolyte imbalances, particularly during increased sweating
What are the 3 common causes of bronchiolitis?
RSV
rhinovirus
adenovirus
Common organisms causing respiratory infection
strep pneumoniae
haemophilus influenzae
pertussis
mycoplasma
influenza viruses
Breathlessness differentials in children
asthma
bronchiolitis
pneumonia
croup
foreign object
whooping cough
Causes of green vomit in neonates
malrotation / volvulus
duodenal atresia (double bubble)
What can cause projectile vomiting in children?
pyloric stenosis
Approach to radiology
- What is the clinical context - who/what/wh
- technically adequate?
- medical devices?
- Airway, air trapping?
- Breathing spaces - too black, too white?
- Cardiac / mediastinum
- Diaphragm / pleura
- Everything else - apices, bones, cardiac, diaphragm, edges
What do red current jelly stools usually mean?
intussusception - donut shape on scan
Causes of wheeze
asthma
bronchiolitis
viral induced wheeze
Causes of stridor
croup
foreign body aspiration
anaphylaxis
bacterial tracheitis
epiglottitis
What are the types of recession in breathing?
tracheal tug
supraclavicular
sternal
intercostal
subcostal
What is tested for on the newborn blood spot screening programme
cystic fibrosis
sickle cell
congenital hypothyroidism
phenylketonuria
MCADD (medium-chain acyl-CoA dehydrogenase deficiency)
maple syrup urine disease
isovaleric acidaemia
glutaric aciduria type 1
homocystinuria
Primary sign of CFTR dysfunction
GI tract w/ symptomatic meconium ileus, seen prior to newborn screening test
What is meconium ileus?
intestinal obstruction caused by abnormally thick and impacted first stool, causes abdominal distension, bilious green vomiting and failure to pass meconium in first few days of life
Clinical features of cystic fibrosis
chronic cough
recurrent wheeze
chronic resp infections
malabsorption in GI tract
failure to thrive
Resp manifestations of cystic fibrosis
persistent cough
wheezing and dyspnea
recurrent resp infections
nasal polyps and chronic sinusitis
GI manifestations of cystic fibrosis
meconium ileus
pancreatic insufficiency
distal intestinal obstruction syndrome
biliary cirrhosis
GORD
Endocrine manifestations of cystic fibrosis
cystic fibrosis related diabetes
growth failure
Reproductive manifestations of cystic fibrosis
male infertility
female fertility issues
Cystic fibrosis screening and diagnostic tests
newborn screening - blood spot test, measure elevated IRT lvls
sweat chloride test (>60 mmol/L)
genetic testing
Monitoring tests of cystic fibrosis
sputum culture
pulmonary function tests
chest radiography / CTs
blood tests
bone density assessments
Cystic fibrosis diagnosis
- child w/ no symptoms but a +ve screening test
- child w/ clinical features of CF, confirmed by sweat chloride or gene test results
- child w/ solely clinical features of CF, but sweat chloride or gene test normal
Cystic fibrosis management
- Airway clearance: chest physio, high-frequency chest wall oscillation, exercise
- Pharmacological: mucolytics, bronchodilators, anti-inflammatories, antibiotics, CFTR modulators
- Nutritional: pancreatic enzyme replacement therapy, fat-soluble vitamin supplementation, high energy diet
Management of cystic fibrosis complications
- Diabetes: regular screening and early intervention w/ insulin therapy and diet modification
- Liver disease: monitoring, early intervention w/ urseodeoxycholic acid
- Bone health: VitD and calcium supplementation, exercise, bisphosphonate therapy
Fertility: assisted reproductive tech
Lung transplantation
What causes the airflow obstruction of asthma?
- smooth muscle constriction: due to direct effects of contractile agonists released from inflammatory cells, accounts for rapid changes in airflow limitation
- mucous production: mucous hypersecretion and plugs
- bronchial inflammation: IgE-dependent release of mediators from mast cells, cause stimulation and contraction of smooth muscle. Results in further oedema and worsened airflow limitations
Mast cell mediators
histamine
tryptase
leukotrienes
prostaglandins
Asthma symptoms
episodes of wheezing, coughing and shortness of breath
Severe asthma exacerbation symptoms
altered mental state
maximal work of breathing accessory muscle use/recession
exhaustion
significant tachycardia
unable to talk
silent chest
Investigating suspected asthma aged 5 - 16
fractional nitric oxide
FeNO ≥ 35 ppb
If not available, measure bronchodilator reversibility w/ spirometry. Diagnose if
FEV1 increase ≥ 12% from pre-bronchodilator measurement, or
FEV1 increase ≥ 10% of predicted normal FEV
If not confirmed by these but still suspected, perform skin prick testing to house dust mite, or measure total IgE lvl and blood eosinophil count
Investigating suspected asthma in children under 5
treat w/ inhaled corticosteroids w/ regular review
attempt objective tests if still have symptoms at 5
refer to specialist resp paediatrician
What are eosinophils?
specifically involved in type 2 inflammation (key pathway in asthma), making them a targeted marker for disease activity
Release cytotoxic proteins like eosinophil peroxidase and major basic protein, which damage epithelial cells and perpetuate inflammation
Eosinophils are activated by IL-5 and other cytokines in T2 pathway, distinguishing them from neutrophils or lymphocytes
What is fractional exhaled nitric oxide?
lvl of nitric oxide produced by airway epithelial cells in response to eosinohpilic inflammation (hallmark of asthma)
pt exhales steadily into device, measured conc in parts per billion
What is IgE?
plays central role in allergic asthma by mediating hypersensitivity reactions through binding to high-affinity IgE receptors on mast cells and basophils
Upon allergen exposure, cross-linking of bound IgE triggers release of inflammatory mediators (histamine, leukotrines), leading to airway inflammation, bronchoconstriction and asthma symptoms
Give an example of anti-IgE therapy
omalizumab
Asthma differentials
Viral induced wheeze (<3)
bronchiolitis
protracted bacterial bronchitis
inhaled foreign body
cystic fibrosis
structural airway abnormality
Asthma management aged 5-16 (check if this has changed)
- Short-acting beta agonist
- SABA + low-dose inhaled corticosteroid
- SABA + low-dose ICS + leukotriene receptor antagonist (LTRA)
- SABA + ICS + LABA
- SABA + switch ICS/LABA for maintenance and reliever therapy (MART)
- SABA + paeds moderate-dose ICS MART
- SABA + either: increasse ICS, trial of additional drug, or seek advice
Asthma management <5yrs
- Short-acting beta agonist
- SABA + 8wk trial of paed moderate dose ICS (start on low-dose and work up if symptoms resolved)
- SABA + low-dose ICS + leukotriene receptor antagonist (LTRA)
- stop LTRA and refer to specialist
What is maintenance and reliever therapy (MART)?
form of combined ICS and LABA treatment in a single inhaler, used for both daily maintenance therapy and relief of symptoms as required
What are the features of poorly controlled asthma?
3+ days per wk w/ symptoms or 3+ days per week requiring use of bronchodilator for symptomatic relief or 1+ night per wk awakening due to asthma symptoms
What is otitis media?
common infection of middle ear , may be bacterial or viral in nature
found mainly in <4s
often self resolve and no lasting effects
Microbial pathogens that cause otitis media
Bacterial:
streptococcus pneumoniae
haemophilus influenzae
moraxella catarrhalis
Viral:
respiratory syncytial virsu
influenza virus
rhinoviruses
Risk factors of otitis media
eustachian tube dysfunction
age - children more at risk
immunodeficiency
allergies
tobacco smoke exposure
bottle feeding
daycare attendance
What are the eustachian tubes?
allow ventilation and drainage of middle ear
any dysfunction can lead to -ve middle ear pressure, fluid accumulation and subsequent infection
Conditions affecting ciliary motility
cystic fibrosis
primary ciliary dsykinesia
Kartagener’s syndrome
Otitis media pathophysiology
occurs 2ndary to oedema and narrowing of eustachian tube
Oedematous eustachian tube prevents middle ear from draining, predisposing it to bacteria colonisation
low pressure in middle ear can cause earache
rupture of TM will resolve pressure differential and relieve pain
Why are children predisposed to otitis media?
eustachian tubes are narrower and more prone to blockage
tubes are more horizontal, inhibiting drainage (this is why pinna is pulled down for paed exam)
children have less developed immune systems, more prone to upper resp tract infections, common cause of tube oedema
Acute v chronic otitis media
Can be w/ effusion
Chronic has a build up of fluid behind an intact TM, must be present for >3 months
Chronic suppurative = discharge present >2wks, persistent ear discharge through perforated tympanic membrane
Symptoms of otitis media
Otalgia (ear ache)
fever (around 50%)
hearing loss
recent viral URTI symptoms
ear discharge
Possible otoscopy findings in otitis media
bulging tympanic membrane - loss of light reflex
opacification or erythema of TM
perforation w/ purulent otorrhoea
decreased mobility if using pneumatic otoscope
Otitis media investigations
clinical examination
tympanometry - change outer ear pressure, play sound and analyse reflected sound waves degree of reflection
Otitis media diagnosis
- acute onset of symptoms: otalgia or ear tugging
- presence of middle ear effusion: bulging or TM, otorrhoea or decreased mobility of pneumatic otoscopy
- inflammation of TM
Otitis media differentials
impacted cerumen
otitis externa
foreign body
cholesteatoma
bullous myringitis
mastoiditis
labyrinthitis
conditions causing referred pain
Otitis media v otitis externa
otitis externa has erythematous ear canal +/- exudate
ensure visualisation of TM to exclude perforated OM or other signs of concurrent OM
Otitis media management
most cases resolve w/out antibiotics, manage pain w/ analgesia
Abx = amoxicillin, erythromycin or clarithromycin
if abx don’t resolve, consider alternative diagnosis, referral
management to prevent recurrence = avoid passive smoking, avoid flat or supine feeding
What grps should be given abx for otitis media?
children <2 w/ bilateral OM
children <3 months w/ temp over 38
Om w/ ear discharge
those systemically unwell
those at high risk of complication
Otitis media complications
chronic OM
tympanic membrane perforation
hearing loss
mastoiditis
bacterial meningitis
extradural or subdural abscess
labrinthitis
facial paralysis
What is otitis externa?
Swimmer’s ear
inflammatory condition affecting exernal auditory canal and pinna
acute <6wks or chronic
Otitis externa risk factors
water exposure
high humidity
trauma to auditory canal
narrow ear canals
immunosuppression
Causes of otitis externa
- Infection: Bacterial = staph aureus, pseudomonas aeruginosa
Fungal = aspergillus species and candida albicans - Seborrhoeic dermatitis
- Contact dermatitis
Symptoms of otitis externa
ear pain
ear itch
ear discharge
Otitis externa otoscopy findings
view may be limited secondary to discharge, debris or swelling
red, swollen or eczematous canal
Otitis externa management
topical abx or combined topical abx w/ steroid
if tympanic membrane is perforated = aminoglycosides not used
debris = remove
if canal is extensively swollen then ear wick sometimes used
2nd line: consider contact dermatitis 2nd to neomycin
oral abx if infection spreads
taking swab inside canal
empirical use of antifungal agent
Otitis externa complications
malignant otitis externa more common in elderly diabetics - extension of infection into bony ear canal and soft tissues deep to bony canal
IV abx may be required
What is glue ear?
otitis media w/ effusion
fluid accumulation in middle ear
usually self-limiting and resolves w/in few months
Glue ear risk factors
age
seasonality (winter and early spring)
atopy (asthma, eczema, allergic rhinitis)
craniofacial abnormalities (cleft palate, Down syndrome)
Underlying causes of glue ear
Eustachian tube dysfunction leading to -ve pressure in middle ear, promoting transudation of fluid from surrounding tissues. Contributing factors =
infections
passive smoking
bottle feeding
Glue ear pathophysiology
- Eustachian tube dysfunction causes retraction of tympanic membrane and pooling of secretions in middle ear
- Inflammatory processes - increased mucus production by goblet cells and hypertrophy of mucosal glands in middle ear. Overproduction outpaces drainage capacity, leading to accumulation
- Osmotic gradient - fluid contains high concs of glycoproteins and ions, draws water into middle ear from surrounding tissues
- Biofilm formation by bacteria on mucosal surface in chronic cases, can resist abx treatment and host immune responses, contributing to persistence or reccurence
- Viscous fluid-filled middle ear - glue ear. Dampens vibrations of tympanic membrane and ossicles
Glue ear typical presentation
child between 2-5 presents w/ hearing difficulties
child not responding to sounds or instructions as expected
may also exhibit speech and language delay due to impaired auditory input
Clinical features of glue ear
hearing loss
tinnitus
speech and language delay
behavioural changes
balance problems
Glue ear otoscopic exam
dull or retracted tympanic membrane w/ limited mobility on pneumatic otoscopy
visible bubbles or air-fluid lvl behind tympanic membrane indicating middle ear effusion
Glue ear differentials
acute otitis media
chronic suppurative otitis media
eustachian tube dysfunction
Glue ear management
majority resolve spontaneously w/in 3 months
encourage autoinflation (valsalva manoeuvre or politerisation)
surgery intervention:
myringotomy and grommet insertion
adenoidectomy
tympanostomy and balloon dilation
What is myringotomy and grommet insertion?
myringotomy = small incision in tympanic membrane
grommet = ventilation tube inserted into middle ear to equalise pressure and facilitate drainage of accumulated fluid
grommets typically fall out spontaneously after 6-12 months, during which time they must be monitored for complications eg otorrhoea, tympanic membrane perforation or scarring
Glue ear complications
hearing loss
speech and language delay
tympanic membrane atrophy or retraction
bacterial superinfection
mastoiditis
meningitis
What is periorbital cellulitis?
eyelid and skin infection in front of orbital septum where inflammation and infection remains confined to soft tissue layers superficial to orbital septum
What is orbital cellulitis?
post-septal infection involving orbit’s soft tissues posterior to orbital septum
can cause optic nerve compression leading to vision loss
muscles of orbit affected, usually due to bacterial sinusitis
life-threatening
Risk factors of periorbital and orbital cellulitis
age <5
sinusitis
trauma
lack of Hib infection
boys
Underlying causes of periorbital and orbital cellulitis
staphylococcus aureus (MRSA)
streptococcus pneumoniae
haemophilus influenzae type B
bacteroides species
fungal cause can occur in immunocompromised or following trauma w/ soil or plants
Periorbital and orbital cellulitis pathophysiology
- Initial infection typically occurs in adjacent structures (eg paranasal sinus)
- Bacteria invades through direct extension or by haematogenous spread
- Once inside tissue, bacteria releases endotoxins that trigger inflammatory response, results in increased vasc permeability leading to oedema and erythema, neutrophil recruited which phagocytose pathogens and release proteolytic enzymes causing further tissue damage
- If not treated promptly, disease progresses and extends posteriorly to orbital fat and ocular muscles
Periorbital cellulitis classification
Primary = direct inoculation or extension from local facial or eyelid infections
Secondary = 2nd to sinusitis, particularly from ethmoid sinuses
Periorbital and orbital cellulitis severity classification
grp 1 inflammatory oedema
grp 2 orbital cellulitis
grp 3 subperiosteal abscess
grp 4 orbital abscess
grp 5 cavernous sinus thrpmbosis
Periorbital and orbital cellulitis presentation
unilateral eyelid erythema, oedema and tenderness
systemic - fever, malaise
ocular pain, impaired vision and restricted eye movement
proptosis in orbital cellulitis
Periorbital and orbital cellulitis investigations
CT sinus and orbits w/ contrast
MRI
bloods
Periorbital and orbital cellulitis differentials
allergic reaction
dacryocystitis - lacrimal sac infection
blepharitis - eyelid inflammation
Periorbital and orbital cellulitis management
abx - empiric IV after getting cultures (cefotaxime / clindamycin)
surgical intervention
close monitoring
prevent by ensuring up to date immunisations against strep pneumoniae and hemophilus influenzae tybe b
Periorbital and orbital cellulitis complications
subperiosteal abscess
cavernous sinus thrombosis
optic neuritis
meningitis
brain abscess
epidural abscess
sepsis
toxic shock syndrome
What is an atrial septal defect?
abnormal opening in atrial septum, allowing blood flow from left to right atria due to higher pressure in left
Atrial septal defect pathophysiology
oxygenated blood shunted from left to right, increasing pulmonary blood flow
augmented vol load on RHS leads to dilation of both atrium and ventricle
over time, vol overload can cause R vent hypertrophy due to increased workload, can also cause elevated pulmonary artery pressures
Increased pulmonary circulation causes enhanced venous return to LHS, potentially enlarging LA and LV
systemic cardiac output may be reduced despite overall increased cardiac work as portion of oxygenated blood recirculates
Consequences of chronically elevated pulmonary pressures
vasc changes w/in lungs, including medial hypertrophy and intimal proliferation w/in small pulmonary arteries
changes further exacerbate pulmonary HTN and can lead to Eisenmenger syndrome: reversal of shunt direction occurs due to significantly elevated right-sided pressures
Atrial septal defect classification
Ostium secundum ASD: most common (70%), central part of septum
Ostium primum ASD: endocardial cushion defect, abnormalities of AV valves
Sinus venosus ASD: near entry point of superior or inferior vena cava
Coronary sinus ASD: rare, unroofing of coronary sinus
Size of atrial septal defect
from small = <5mm to large = >15mm
Atrial septal defect investigations
echo - TTE (transthoracic) and TEE (transesophageal)
chest x-ray
EEG
cardiac MRI or CT
Atrial septal defect management
Evaluate w/ echo
Decision-making to close
Treat w/ percutaneous device closure, surgical repair or medical management
Post-procedure = recommend dual antiplatelet therapy for 6 months to prevent thrombus formation on device
Atrial septal defect complications
pulmonary HTN
RSHF
atrial arrhythmias
stroke
migraine w/ aura
pulmonary arteriovenous malformations
mitral valve prolapse
What are the types of viral induced wheeze?
episodic wheeze - symptom of viral URTI and symptom free in between events
multiple trigger wheeze - URTI and other factors trigger wheeze
Symptomatic treatment of viral induced wheeze
SABA inhaler via spacer 4hrly up to 10 puffs
LTRA and ICS via spacer
for multiple trigger wheeze = trial ICS or LTRA for 4-8wks
What is pneumonia?
LRT infection and lung parenchyma infection which leads to consolidation
Pneumonia epidemiology
highest incidence in infants
viral cause more common in young infants
bacterial more common in older children
viral disease more common in winter
Pneumonia causes
Neonates = grp B strep, E.coli, Klebsiella, Staph aureus
Infants = strep pneumoniae, chlamydia
School age = strep pneumoniae, staph aureus, grp A strep, mycoplasma pneumoniae
Pneumonia clinical presentation
usually precede URTI
fever
SOB
lethargy
signs of resp distress
On examination - dullness, crackles, decreased breath sounds, bronchial breathing
wheeze and hyperinflation more typical of viral infection
Pneumonia investigations
mainly clinical
CXR - fluid in lungs (associated w/ staph)
Pneumonia treatment
manage at home w/ analgesia
if admitted, oxygen therapy and IV fluids
Abx:
neonates = broad spec IVAbx
infants = amoxicillin / co-amox
over 5s = amox / erythromycin
Pneumonia complications
risk of parapneumonic collapse and empyema, follow up at 4-6wks w/ fluid sample
What is strabismus?
misalignment of the eyes
when not aligned, images on retina will not match and pt experiences double vision
Strabismus pathophysiology
on childhood, eyes haven’t fully established connections w/ brain, brain copes by reducing signal from less dominant eyes
results in one dominant eyes and one eye which will be ignored
when left untreated, lazy eye becomes more and more disconnected from brain and problem worsens (abmblyopia)
Esotropia v Exotropia
Esotropia = inward position squint - affected eye deviates towards nose
Exotropia = outward position squint - affected eye deviated towards ear
What is a concomitant squint?
differences in control of extra ocular muscles
Hypertropia v hypotropia
hypertropia = upward moving affected eye
hypotropia = downward moving affected eye
Causes of squint
idiopathic
hydrocephalus
cerebral palsy
space occupying lesion eg retinoblastoma
trauma
Squint investigations
eye movements and inspection
fundoscopy
visual acuity
Hrischberg’s test = shine torch from 1m away, when pt looks at light, observe reflection of light source on their cornea (should be central and symmetrical)
Cover test = cover one eye and ask pt to focus on object, move cover to other eye and watch movement of other eye and observe any exo/esotropia
Squint management
treatment must start before 8yrs
occlusive patch - cover good eye and force weak eye to develop
atropine drops in good eye - causes blurred vision and force weak eye to develop
Atrial septal defect causes
maternal smoking in 1st trimester
FH of CHD
maternal diabetes
maternal rubella
Atrial septal defect clinical presentation
tachypnoea
poor weight gain
recurrent chest infections
soft, systolic ejection murmur heard in 2nd intercostal space
wide, fixed split S2 sound
What is ventricular septal defect?
most common heart defect
opening in interventricular septum, causes left to right shunting, leading to increased pulmonary blood flow and right ventricular volume overload
Ventricular septal defect causes
Genetic = chromosomal disorders eg Down, Edwards, Patau, DiGeorge
Environmental = prenatal exposure to teratogens, maternal illness, advanced maternal age, premature birth
Ventricular septal defect pathophysiology
left-to-right shunt due to higher pressures in LV, oxygenated blood from LV pushed into RV instead of being ejected into systemic circulation via aorta
increases pulmonary blood flow, vol overload on both RS chambers
can cause hypertrophy and dilation of chambers
Moderate v severe ventricular septal defect
moderate = enlarged atria and ventricles, leads to pulmonary HTN and congestive HF
severe = severe pulmonary HTN and early onset HF
Ventricular septal defect clinical presentation
can be symptomless
pansystolic murmur at lower left sternal border
poor feeding
tachypnoea
dyspnoea
failure to thrive
Ventricular septal defect investigations
Echo - TTE, TOE
cardiac MRI
x-ray showing cardiomegaly
Ventricular septal defect differentials
atrial septal defect
patent ductus arteriosus
pulmonary stenosis
Ventricular septal defect management
diuretics - pulmonary congestion
ACE inhibitors to reduce systemic pressure
interventional cardiac catheterisation
surgical repair
Ventricular septal defect
Eisenmenger syndrome
heart failure
endocarditis
pulmonary HTN
aortic regurgitation
arrhythmias
stroke
What is tetralogy of fallot?
most common cyanotic congenital heart disease
overriding aorta
large VSD
pulmonary stenosis
R.vent hypertrophy
Tetralogy of Fallot causes
more common in males
rubella
increased age of mother (>40)
Tetralogy of Fallot pathophysiology
decreased r. vent flow
dilated and displaced aorta
Mild = asymptomatic but as heart grows, develops cyanosis aged 1-3
Moderate = cyanosis and resp distress in first few months of life
Extreme = often detected on antenatal scan, present w/ cyanosis in first few hrs of life
Tetralogy of Fallot presentation
irritability
cyanosis
clubbing
poor feeding
poor weight gain
ejection systolic murmur in pulmonary region (from pulmonary stenosis)
tet spells
Tetralogy of Fallot investigations
CXR - boot shaped heart
MRI / cardiac catheter
echo
Tetralogy of Fallot treatment
prostaglandin infusion PGE1 to maintain ductus arteriosus
beta blockers
morphine to reduce resp drive
surgical - repair under bypass 3months - 4yrs but needs ICU post op
Tetralogy of Fallot complications
pulmonary regurgitation
lifelong follow up
What is transposition of the great arteries?
aorta rises from right ventricle and pulmonary artery from left ventricle
Transposition of great arteries risk factors
more common in males
mum > 40
rubella
maternal diabetes
alcohol consumption
Transposition of great arteries pathophysiology
deoxygenated blood delivered systemically
mixing needs to be possible to sustain life - patent foramen ovale, VSD or patent ductus arteriosus must be present alongside
Presentation of transposition of great arteries
cyanosis in first 24hrs of life
R vent heave
loud S2 heart sound
systolic murmur if VSD present
sometimes PD / VSD can make symptoms however w/in a few wks they will develop resp distress, poor feeding etc
Transposition of great arteries diagnosis
low SATS
echo
CXR - egg on a string due to narrowed mediastinum and cardiomegaly
metabolic acidosis
Transposition of great arteries treatment
PGE1 infusion to ensure PDA and mixing of blood
surgical correction before 4wks
What is truncus arteriosus?
heart defect where only one large blood vessel comes out of heart instead of the two separate aorta and pulmonary artery
VSD usually present
blood mixes, heart has to pump harder, leads to HF
What is a patent ductus arteriosus?
persistent connection between aorta and pulmonary artery
normal in utero but usually closes w/in first 10-15 mins of life
causes left to right shunt
Patent ductus arteriosus risk factors
female
prematurity
Patent ductus arteriosus presentation
resp distress
apnoea
tachypnoea
tachycardia
continuous machinery murmur at left sternal edge
Patent ductus arteriosus diagnosis
echo
ECG / CXR
Patent ductus arteriosus management
cardiac catheterisation to close around 1yrs or sooner
in premature infants = indomethacin or ibuprofren - inhibits prostaglandin and stimulates closure
What is rheumatic fever?
develops following immunological reaction to recent (2-6wks ago) streptococcus pyogenes infection
can affect multiple organ systems eg heart, joints, skin and CNS
Rheumatic fever pathogenesis
- streptococcus pyogenes infection -> activation of innate immune system leading to antigen presentation to T cells
- B and T cells produce IgG and IgM antibodies and CD4+ T cells activated
- cross-reactive immune response (T2 hypersensitivity), mediated by molecular mimicry
- CW of streptococcus pyogenes includes M protein, virulence factor that’s highly antigenic, antibodies against M protein cross-react w/ myosin and arteries smooth muscle
- response leads to features of rheumatic fever
What are Aschoff bodies?
small granulomatous lesions found in heart muscle in rheumatic fever
Rheumatic fever diagnosis
evidence of recent streptococcal infection and either 2 major criteria or 1 major w/ 2 minor
Major:
- erythema marginatum (non-pruritic erythematous macules or annular lesions w/ clear centres and well-defined margins on trunk and proximal extremities)
- Sydenham’s chorea (involuntary movements, muscular weakness and emotional disturbance)
- polyarthritis
- carditis and valvulitis
- subcutaneous nodules
Minor:
- raised ESR or CRP
- pyrexia
- arthralgia
-prolonged PR interval
Rheumatic fever management
Abx - penicillin, erythromycin
anti-inflammatory therapy - aspirin or NSAIDs, corticosteroids
diuretics, ACE inhibitors, beta blockers for HF
anticonvulsants for Sydenham chorea
What is the most common cause of vomiting in infancy?
GORD
GORD risk factors
preterm delivery
neurological disorders
Clinical features of GORD
typically develops before 8wks
vomiting / regurgitation following feeds
GORD diagnosis
24-hr pH monitoring or pH impedence studies
GORD management
advise 30 degree head up position during feeding
infants should sleep on back as per guidelines
ensure infant not overfed, consider smaller and more frequent feeds
trial of thickened formula
trial of alginate therapy (gaviscon)
PPI not recommended in infants and children as isolated symptom
prokinetic agents only used w/ specialist advice
When should a PPI be considered for GORD in infants and children?
if there is:
unexplained feeding difficulties
distressed behaviour
faltering growth
GORD complications
distress
failure to thrive
aspiration
frequent otitis media
in older children dental erosion may occur
What percentage of children have a cow’s milk protein intolerance/allergy? When does it present?
around 3-6% of all children
presents in first 3 months
Cow’s milk protein intolerance / allergy classification
immediate (IgE mediated), seen w/in 2hrs of ingestion - CMPA
delayed (non-IgE mediated), up to 48hrs after ingestion - CMPI
Clinical features of cow’s milk protein intolerance / allergy
diarrhoea
vomiting
abdo pain
faltering growth
constipation
eczema, rash
asthma-like symptoms
What other symptoms and conditions can cow’s milk protein intolerance be associated with?
iron deficiency anaemia due to GI blood loss
behavioural changes eg irritability
sleep disturbance
Cow’s milk protein intolerance / allergy investigations
dietary elimination (2-6wks) and reintroduction
skin prick test
specific IgE testing
Cow’s milk protein intolerance / allergy differentials
lactose intolerance
GORD
eosinophilic oesophagitis
Cow’s milk protein intolerance / allergy management if formula-fed
mild-moderate symptoms = extensive hydrolysed formula (eHF) milk
severe CMPA = amino-acid based formula
around 10% infants also intolerant to soya
Cow’s milk protein intolerance / allergy if breast fed
continue breast-feeding
eliminate cow’s milk protein from maternal diet, consider prescribing calcium supplements to mother
use eHF milk when breastfeeding stops, until 12 months of age and at least for 6months
What is infantile colic?
paroxysms of persistent and uncontrollable crying in an otherwise healthy infant
affects approx 15-20% of infants, more frequent in first 6wks of life
Causes of colic
faulty feeding techniques
infrequent burping
stressful pregnancy and birth
possible GI origin based on gut biomes
tobacco smoke and nicotine exposure
Clinical features of colic
Colic cry = louder, higher, screaming, more piercing/grating
unable to consoled, clear beginning and end with no explanation
facial flushing
tense abdomen
drawing legs up to abdomen
clenched fist
back arching
circumoral pallor
What is the Wessel criteria?
defines infantile colic:
- unexplained crying or fussiness (otherwise healthy, other causes ruled out)
- resolves by 3months
- lasts >3hrs a day
- occurs >3 days per week
- persists for >3 weeks
What red flags should be absent in infantile colic?
fever
diarrhoea, vomiting, abdo distension
reduced conscious state
signs of trauma
poor feeding
poor weight gain and growth
signs of developmental delay
Infantile colic differentials
normal crying
intussesception
cow’s milk protein allergy
GORD
lactose overload / intolerance
UTI
Infantile colic management
caregiver education and support
appropriate feeding techniques
dietary changes
What is the most common cause of non-bilious vomiting in children?
pyloric stenosis
Risk factors of pyloric stenosis
male
firstborn
FH of pyloric stenosis
maternal smoking
bottle feeding
preterm birth
ethnicity - caucasian and hispanic
erythromycin
Clinical features of pyloric stenosis
projectile non-bilious vomiting - follows a feed, child hungry and irritable after episode
haematemesis in around 10%
weight loss / inadequate gain
dehydration
stool changes
firm, non-tender 1-2cm mass in URQ of abdo
visible peristalsis
Signs of dehydration in infants
sunken fontanelles
sunken eyes
dry mucous membranes
poor skin turgor
decreased tearing
lethargy
tachycardia
prolonged CRT
decreased urine output
Excess vomiting leads to…
severe hypochloraemic, hypokalaemic dehydration
w/ metabolic alkalosis
What is pyloric stenosis?
result of hypertrophy of pylorus muscles of stomach leading to gastric outlet obstruction
infant well at birth then present w/ vomiting from 2-8wks
Pyloric stenosis classical triad
palpable pyloric mass
visible peristalsis
non-bilious, forceful projectile vomiting
Investigations of pyloric stenosis
classical triad
assessment of degree of dehydration
weight and height tracked
blood gas
‘target sign’ on US, pyloric thickness >3mm and length >15-17mm
Pyloric stenosis differentials
intestinal malrotation and volvulus
duodenal atresia
necrotising enterocolitis
tracheoesophgeal fistula
meconium ileus
Hirschprung
GORD
Pyloric stenosis management
correct metabolic imbalances - NaCl
fluid bolus for hypovolemia
NG tube and aspiration of stomach
Ramstedt’s pyloromyotomy
Pyloric stenosis complications
dehydration
weight loss
electrolyte disturbance
from surgery: anaesthetic risk, persistent vomiting if incomplete, mucosal perforation, infection, foveolar cell hyperplasia
Dysphagia vs GORD
dysphagia may be due to anatomical abnormalities, neuro disorders or functional issues
GORD characterised by frequent regurgitation associated w/ complications like poor weight gain, distress or resp symptoms
What is Hirschsprungs disease?
nerve cells of myenteric plexus are absent in distal bowel and rectum, specifically parasympathetic ganglionic cells resulting in lack of peristalsis
Hirschsprungs disease risk factors
90% present in neonatal period
average = 2 days old
males
Down’s syndrome
Hirschsprungs disease pathophysiology
most common = short segment, disease confined to rectosigmoid part of colon
ganglion cells of submucosal plexus not present
failure of peristalsis and bowel movements causing obstruction
can lead to bacterial build up and enterocolitis and sepsis
Hirschsprungs disease presentation
failure to pass meconium (w/in 48 hrs of birth)
abdo distension
bilious vomiting
palpable faecal mass in LL abdo
empty rectal vault
Hirschsprungs disease investigations
rectal suction biopsy - test for ganglionic cells in anyone who has:
- delayed meconium passage
- constipation in first few wks
- chronic abdo distension
- +ve FH
- faltering growth
contrast enema
Hirschsprungs disease management
IV Abx
bowel decompression
NG tube
surgery - Swenson, Soave, Dunhamel pull through surgery
What is intussusception?
one piece of bowel telescopes inside another, leading to ischaemia and bowel obstruction
most common in distal ileum at ileocecal junction
most common cause of obstruction in neonates
Intussusception risk factors
3months - 3yrs
CF
Meckel’s diverticulum
HSP
rotavirus vaccine >23 wks
Intussusception presentation
colic abdo pain
pallor
sausage shaped mass palpable in RUQ
redcurrant jelly stools
abdo distension
shock
peritonitis (guarding, rigidity, pyrexia)
Intussusception investigations
USS - target shaped mass
abdo x-ray - distended small bowel, absence of gas in large bowel
Intussusception treatment
med emergency
IV fluids
air enema using US to stretch bowel walls and reduce, if unsuccessful, surgery to manually repair
Abx (gentamicin) if perforated or peritonitis
What is necrotising enterocolitis?
acute inflammatory disease affecting preterm neonates leading to bowel necrosis and multi system organ failure
most common surgical emergency in neonates
Necrotising enterocolitis causes
low birth weight (1500g)
in first 2 wks of life
prematurity
Abx therapy >10 days
genetic
Necrotising enterocolitis presentation
new feed intolerance
vomiting and bile
fresh blood in stools
abdo distension
reduced bowel sounds
palpable abdo mass
visible intestinal loops
sepsis
Necrotising enterocolitis investigations
bloods - thrombocytopenia, neutropenia
cultures
blood gas - acidotic
USS - air in portal system, ascites, perforation
XR - Rigler’s sign
What is seen on an x-ray in necrotising enterocolitis?
Rigler’s - both signs of bowel are visible due to gas in peritoneal cavity
dilated bowel loops
distended bowel
thickened bowel wall
air outlining falciform ligament
Necrotising enterocolitis management
nil by mouth
bowel decompression by NG tube
IV cefotaxime
surgery to remove necrotic bowel
What is Meckel’s diverticulum?
congenital diverticulum of small intestine containing ileal, gastric and pancreatic mucosa, pouch-like structure forms as remnant of the vitelline duct
2cm from ileocecal valve
occurs in 2% of population
What supplies Meckel’s diverticulum?
ompthalomesenteric artery
Meckel’s diverticulum presentation
abdo pain
rectal bleeding in children 1-2yrs
obstruction due to intussusception and volvulus
at risk of peptic ulceration
Meckel’s diverticulum management
removal if symptomatic - resection
what is biliary atresia?
obstruction of biliary tree due to sclerosis of bile duct, reducing blood flow
Biliary atresia risk factors
female
neonatal cholestasis 2-8wks
associated w/ CMV
congenital malformations
Biliary atresia presentation
jaundice post 2 wks
dark urine
pale stolls
apetite disturbance
hepatosplenomegaly
abnormal growth
duodenal atresia - presents in first 24hrs of life, more common in trisomy 21
Biliary atresia pathophysiology
T1 = common duct is obliterated
T2 = atresia of cystic duct in porta hepatis
T3 = most common, atresia of right and left ducts at lvl of porta hepatis
Biliary atresia investigations
serum bilirubin - high conjugated bilirubin
raised LFTs
alpha 1 antitrypsin - rule out
sweat test - rule out CF
USS - structural abnormalities
Biliary atresia management
surgical dissection of abnormalities - Kasai procedure
Abx
Biliary atresia complications
cirrhosis
Hepatocellular carcinoma
progressive liver disease
Neonatal jaundice pathophysiology
breakdown of in-utero Hb
immature liver can’t break down high bilirubin concentrations
Physiological v pathological v prolonged neonatal jaundice
pathological = onset <24hrs
physiological = starts 2-3 days, peak at day 5, usually resolves by 14 days
prolonged = >14 days in term infants, 21 days in preterm
Neonatal prolonged jaundice causes
biliary atresia
hypothyroidism
breast milk jaundice (resolves 1.5-4 months)
UTI / infection
Pathological neonatal jaundice causes
G6PD deficiency
spherocytosis
Physiological jaundice causes
prematurity
small for dates
previous sibling w/ neonatal jaundice
Neonatal jaundice presentation
yellow colour
drowsiness
signs of infection
Neonatal jaundice investigations
TCB (transcutaneous bilirubin) - used over 35 wks gestation, non-invasive
serum bilirubin
total and conjugated bilirubin
Coombs test
infection screen
Neonatal jaundice management
treatment threshold graphs for specific gestation
phototherapy for above threshold
below threshold have lvls monitored and rechecked w/in 24hrs
repeat bilirubin 4-6 hrs after commencing phototherapy and 6-12 hrly once lvls stabilise
stop phototherapy once over 50umol/L of treatment line
recheck 12-18hrs after stopping
If severe = exchange transfusion
Complications of neonatal jaundiace
Kernicterus - bilirubin induced encephalopathy and irreversible neurological damage
> 360umol/L
What is an exchange transfusion?
used in severe jaundice cases (rise of >8.5umol/L/hour) , and signs of kernicterus
exchange of blood w/ donated plasma to decrease lvl of circulating bilirubin
via umbilical artery or vein
Causes of organic failure to thrive
GI - GORD, IBD, CMPA
metabolic - coeliac, CF
thyroid disorders
chronic - congenital heart disease
infections - HIV, TB
Causes of non-organic failure to thrive
behavioural issues
family dynamics
usually attributed to inadequate caloric intake
What is failure to thrive?
condition of insufficient weight gain or inappropriate growth in infants and children
manifestation of underlying medical or psychosocial issues
Secondary causes of constipation
Hirschsprung’s disease
CF
hypothyroidism
spinal cord lesions
sexual abuse
intestinal obstruction
cows milk intolerance
Constipation clinical presentation
<3 stools a wk
hard stools that are difficult to pass
rabbit dropping stools
straining and painful passage of stools
abdo pain
overflow soiling caused by faecal impaction
palpable hard stools in abdomen
Constipation management
correct any reversible contributors eg high fibre diet, good hydration
movicol - laxative
disimpaction regimen may be needed w/ high dose laxative at first, followed by half disimpaction dose as maintenance
What’s the most common cause of UTIs in children?
Escherichia coli (80%)
others include klebsiella pneumonia, proteus mirabilis, enterococcus spp, staphyloccocus saprophyticus
Features of a LUTI (cystitis)
dysuria
frequency
urgency
haematuria
suprapubic pain or tenderness
foul-smelling urine
enuresis
Features of an UUTI (pyelonephritis)
fever
flank pain or costovertebral angle tenderness
abdo pain
nausea and vomiting
lethargy or irritability
poor feeding or failure to thrive
UTI management
<3 months = refer
>3 months, UUTI = consider admission, oral abx (cephalosporin or co-amox x7-10days)
>3 months, LUTI = oral abx x3days (trimethoprim, nitrofurantoin, cephalosporin or co-amox)
abx prophylaxis not given after first UTI but should be considered w/ recurrent UTIs
What is Down’s syndrome?
genetic disorder
extra copy of chromosome 21, 3 copies total
1/700 live births
Down’s syndrome risk factor
increase risk w/ increasing maternal age
30 yrs = 1/1000
35 yrs = 1/300
40yrs = 1/100
What is the most common mode of Down’s syndrome?
nondisjunction = 94%
Robertsonian translocation = 5%
mosaicism = 1%
What is mosaicism?
presence of 2 genetically different populations of cells in the body
Down’s syndrome clinical features
hypotonia
small head w/ flat back
short neck
short stature
flattened face and nose
low set ears
single palmar crease
prominent epicanthic folds
upward sloping palpebral fissures
Complications of Down’s syndrome
cardiac = endocardial cushion, vent septal defect, secundum atrial septal defect, tetralogy of fallot
subfertility
learning difficulties
short stature
repeated resp infections
acute lymphoblastic leukaemia
hypothyroidism
Alzheimer’s
atlantoaxial instability
vision and hearing problems
Screening for Down’s syndrome
combined test - 11-14wks, US looking at thickness on back of neck (thickened) and beta-HCG (raised) and PAPPA (reduced)
if women book later in pregnancy either triple or quadruple test offered between 15-20wks
Triple and quadruple Down’s syndrome test
triple = 14-20wks, beta-HCG (raised), AFP (low), serum oestriol (low)
quadruple = triple + inhibin-A (high)
Down’s syndrome management
MDT approach
regular screening of complications - echo, thyroid checks, eye checks and audiometry
What is epilepsy?
umbrella term for tendency to have seizures which are transient episodes of abnormal electrical activity in the brain
What are the types of seizures?
generalised tonic-clonic
focal
absence
myoclonic
tonic / atonic
What are generalised tonic-clonic seizures?
loss of consciousness w/ tonic (rigidity) and clonic (rhythmic jerking)
phase w/ possible tongue biting, incontinence, groaning and irregular breathing
postictal period - confused, drowsy and irritable
Generalised tonic-clonic seizure management
sodium valproate
lamotrigine
carbamezapine
What are focal seizures?
begin in temporal lobes and affects speech, memory and emotions
can present w/ hallucinations, memory flashbacks and deja vu
Focal seizure management
lamotrigine
levetiracetam
What is an absence seizure?
most common in children, become blank and stare into space then abruptly return to normal
unaware of surroundings during
10-20 secs
Absence seizures management
stop with age
ethosuximide
What are myoclonic seizures?
sudden brief muscle contractions where person remains awake
often part of juvenile myoclonic epilepsy
Myoclonic seizure management
sodium valproate
levetiracetam
What are tonic/atonic seizures?
sudden tension/stiffness affecting body
Tonic / atonic seizure management
sodium valproate
lamotrigine
Epilepsy investigations
full history
EEG after second simple tonic-clonic seizure
MRI brain
blood electrolytes, glucose, cultures and LP considered
Management of acute seizures
recovery position if possible
soft under head
remove obstacles
make note of start and end time
call ambulance if >5mins
Sodium valproate side effect
teratogenic
liver damage
hair loss
temors
Carbamezapine side effects
agranulocytosis
aplastic anaemia
Ethosuximide side effects
night tremors
rashes
N & V
Lamotrigine side effects
DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms)
leukopenia
What is status epilepticus?
med emergency
seizure >5 mins or 2 or more seizures w/out regaining consciousness
management = secure airway, high conc o2, assess cardiac and resp function
IV lorazepam, repeat after 10mins
buccal and rectal available in community
What are febrile convulsions?
seizure + high fever 6months - 5yrs
simple = generalised tonic clonic, <15mins, once during febrile illness
complex = focal, >15mins or multiple times during same illness
Febrile convulsions investigations
rule out other causes eg epilepsy, syncopal episode, trauma, space-occupying lesions and neurological infection
Febrile convulsions management
identify and manage infection
control fever w/ simple analgesia
parental education
(prognosis slightly higher for epilepsy in future)
What is eczema?
atopic dermatitis
common chronic inflammatory skin disorder characterised by pruritus and xerosis
Eczema pathophysiology
defects in normal continuity of skin barrier
provides entrance for irritants, microbes and allergens that create immune response, leads to inflammation
Eczema clinical presentation
usually in infancy
dry, red, itchy skin w/ sore patches over flexor surfaces (elbows, knees) and face and neck
often episodic w/ flares
Eczema management
Maintenance = emolients eg E45, diprobase, use often, after washing and before bed to create artificial barrier over skin
Flare ups = thicker emolients eg cetraben ointment or topical steroids eg hydrocortisone and betnovate (beclomethasone), help keep moisture locked overnight
specialist treatment = topical tacrolimus, oral corticosteroids and methotrexate
What is eczema hepeticum?
viral skin infection in pts w/ eczema caused by herpes simplex virus or varicella zoster virus
Eczema herpticum presentation
widespread, painful, vesicular rash w/ systemic symptoms
lymphadenopathy
Eczema herpeticum management
viral swabs of vesicles, treatment usually started based on clinical appearance
Aciclovir - oral or IV
Eczema herpeticum complications
life-threatening in immunocompromised
bacterial superinfection - Abx
