paeds Flashcards
define colic and what advice would you give parents?
paroxysmal crying with pulling up of the legs for over 3 hours on 3+ days of the week for at least 1 week.
Reassure parents and advise them to do what they can to reduce stress e.g. enlist family/friends help
Movement (carry cot on wheels), let the baby finish the breast first (hind milk easier to digest), warm baths, burping baby, belly rubs.
What is cows milk protein intolerance?
Immune mediated allergic response to naturally occurring milk proteins whey and casein. Can be IgE-mediated, non-IgE mediated or mixed.
Describe the pathophysiology underlying CMPI
IgE mediated = Type 1 hypersensitivity - CD4+ TH2 cells stimulate B cells to produce IgE antibodies -> mast cell degranulation + cytokine release in an anaphylactic response on re-exposure to allergens after sensitisation
Non-IgE mediated = T cell activation against CMP
How does a CMPI usually present?
<3/12 in formula/mixed fed infants. Tends to be more severe and acute onset after feeding in IgE mediated.
vomiting, abdo pain ± colic, reflux, diarrhoea, pruritis, erythema, atopic eczema, lower resp tract sx (cough, SOB, wheeze), can get urticaria, angio-oedema of lips/tongue/face, anaphylaxis, severe = faltering growth
Risk factors for CMPI
atopy or a family history of atopy
Differential diagnosis for ?CMPI
allergic reaction to other food/non-food allergen
anatomical abnormality - meckels, pyloric hypertrophy, etc
chronic GI disease - reflux, coeliac, IBD, gastroenteritis
pancreatic insufficiency - hx CF?
UTI
How is ?CMPI investigated?
Usually clinical dx but may refer for RAST testing for specific IgE antibodies if faltering growth + 1 sx, 1 acute systemic or severe delayed reaction, atopy, clinical/persistent parental suspicion.
Mx of CMPI
Refer to pads if severe sx e.g. failure to thrive
Counsel parents - many will grow out of it (55% IgE by 5, non-IgE most by 3), elimination diet with re-evaluation in 6-12m(/until 9-12/12) to assess tolerance - refer parent to MAP guidelines milk ladder
Nutritional counselling and regular growth monitoring
Formula fed = trial extensively hydrolysed formula, if still symptomatic or very severe then 2nd line AA formula
Breast fed = mom eliminates cows milk from her diet
A 6 month old baby boy is brought into the GP by his mother with a rash on his bottom, O/E well-demarcated erythematous maculopapular rash with slight scaling in areas, skin folds are spared.
What is the likely diagnosis and what management would you advise?
Irritant dermatitis nappy rash
Mx - use disposable nappies as these retain less moisture, change them frequently and ideally have nappy-free periods, careful drying and use of emollient/barrier creams such as sudocream.
a 9 month old baby is brought into the GP by his father with a rash on his bottom. O/E there is an erythematous maculopapular rash affecting the bottom and inguinal folds, with papular satellite lesions, superficial pustules and scaling seen.
What is the likely diagnosis + appropriate management?
Candida dermatitis nappy rash (affects skin folds, satellite lesions)
Mx - use disposable nappies and change frequently, ideally have nappy-free periods, careful drying, use of emollients and topical imidazole, cease use of barrier creams until candida has settled.
a 1 year old is brought to the GP by her mother with a rash on her bottom. O/E there is are salmon pink patches on with scaling on the bottom and inguinal folds, you also note diffuse, yellow, greasy scales on the scalp.
What is the likely dx + appropriate mx?
Seborrheic dermatitis nappy rash (+ cradle cap)
Mx - use disposable nappies and change frequently, ideally have nappy-free periods, careful drying, use of emollients barrier creams e.g. sudocream.
Differential diagnosis for vomiting in an infant
Posseting - effortless regurgitation of milk during feeds
Physiological - as long as it is not significant or excessive (destroying carpets=?pathological)
Overfeeding - >150ml/kg/day
Gastro-oesophageal reflux or gastritis
Pyloric stenosis - projectile vomiting ~8wks
Any infection - UTI, infective gastroenteritis
Adverse food reaction e.g. CMPI
Rarer - pharyngeal pouch, obstruction (bilious vomiting), RICP, DKA
A 6month old is brought to the GP with a 9 hour history of fever. Her mother reports her to be getting worse - increasingly ‘out of it’ and drowsy, taking less feed than usual (around half), she last had a wet nappy approximately 8 hours ago. O/E she is drowsy and does not interact with you, little reaction to parents, no skin rashes, HR 165, CRT3s, RR 53, temp 39, O2 sats 94% on air.
How would this child be stratified and what should the management plan be?
Amber - ‘out of it’ apathy, not responding to social clues, no smile, drowsy; RR>50, O2 <95, HR>160, CRT>3s, poor UO and half feeding.
Mx - need to ensure they are seen face to face, no known dx = refer to paeds for further assessment, otherwise may be able to safety-net - verbal and/or written info on warning symptoms, how to access further healthcare, follow up appt and liaise with other HCP (e.g. out of hours providers to ensure direct assessment if needed).
A 1yr old is brought to the GP with a 9 hour history of fever. Her mother reports her to be getting worse - increasingly drowsy and tearful, taking less feed than usual (around half), she last had a wet nappy approximately 8 hours ago. O/E she is pale and appears ill, is crying weakly, and shows subcostal recession and moderate chest wall indrawing. HS 1+2+0, abdo SANT, chest crackles heard L base. HR 165, CRT3s, RR 61, temp 39, O2 sats 94% on air.
How would this child be stratified and what should the management plan be?
Red - pale, weak cry, appears ill to HCP, tachypnoea, moderate chest indrawing
mx - urgent referral to paeds specialist to be seen within 2h.
How would you manage a severely unwell child with no obvious source of fever?
Sepsis 6 + urine ± LP
Urine dip for UTI (>3m; younger clean catch MC&S)
FBC, U&Es, blood culture, CRP, VBG
CXR
LP if clinically indicated
Fluids - bolus 20ml/kg if lactate >2
Abx - 0-1m = cefotaxime + amoxicillin + gentamicin, 1-3m = ceftriaxone + amoxicillin, >3m = ceftriaxone
When and in whom would you expect to see an intraventricular haemorrhage?
Within first 72h of life, pre-mature neonate with very low birthweight (<1.5kg)
How are IVHs usually diagnosed? Clinical sx and Ix
Often asymptomatic but may see seizures, cerebral irritability, bulging fontanelle, hydrocephalus due to clot obstructing CSF outflow.
Premature <32/40 = cranial US on day 4-7 to assess; >32 weeks if clinically indicated.
How are IVHs managed and what complications may arise?
Mx - supportive care, hydrocephalus may require shunt insertion
Complications - learning disability, cerebral palsy, hydrocephalus. May recover completely.
What is neonatal apnoea and what causes it? How is it prevented and managed?
Failure to make respiratory effort for over 20 seconds, or less than 20 seconds with accompanying bradycardia
Causes - prematurity, infection, hypothermia, aspiration, congenital heart disease. Prevent with maternal IM corticosteroids.
Mx - physical stimulation and IV caffeine
What is retinopathy of prematurity?
Incomplete maturation of the retina in-utero usually seen in <32/40, vascularisation of the retina begins centrally spreading outwards and is driven by hypoxia. Baby born early means O2 drives abnormal BV development - friable and grow outside the plane of the retina = liable to bleed into the eye which can cause retinal scarring, detachment and blindness. This is exacerbated by O2 supplementation.
How is retinopathy of prematurity picked up/diagnosed and managed?
babies born before 32 weeks gestation or with very low birthweight (<1.5kg) are screened for it.
- Born =<27/40 = screen at 30-31 weeks gestational age
- Born >27wks = screen 4-5 weeks of age
Screen at least every 2 weeks by ophtho until sufficient vascularisation of retina, rx diode laser therapy
Define neonatal sepsis
Serious bacterial or viral blood infection in first 28d of life, it can be classed EONS (in first 72h of life) or LONS (onset between 3 and 28d of life)
Which are the most likely causative organisms in early onset neonatal sepsis?
Group B streptococcus and E.Coli, coagulase negative staph, H.Influenzae, listeria
Risk factors for early onset neonatal sepsis
Mother - known carrier of GBS (prev baby with GBS sepsis, prenatal test), UTI, intrapartum pyrexia 38+, ROM 18+hrs, evidence of maternal chorioamnionitis
What are the most likely causative organisms in LONS and list risk factors for this
gram + organisms - mainly coagulase negative staphylococci, also s.aureus; E.Coli, pseudomonas, klebsiella.
Central line and catheters, congenital malformations, severe illness, immunodeficiency, poor cord care.
Clinical presentation of neonatal sepsis
respiratory distress most common - grunting, nasal flaring, tachypnoea/apnoea
seizures
sx of shock - tachycardia, low UO, low BP, resp distress
jaundice
feed intolerance inc vomiting
abdo distension
labile temperature, abnormal HR, poor O2 sats
How would you manage a neonate with ?sepsis
A-E assessment and initiate sepsis 6 bundle
- Bloods - culture, blood gas, CRP, FBC
- LP, ?urine MC&S, ?CXR
- Fluid - bolus 10-20ml/kg, maint 120-150ml/kg day 5-28
- Abx
- EONS - IV benzylpenicillin + gentamicin
- LONS - IV flucloxacillin + gentamicin
- ?meningitis - IV cefotaxime + amoxicillin
Causes of neonatal seizures
Metabolic - hypoglycaemia (r/o immed), hypo/hyper-natraemia, hypocalcaemia, hypomagnesaemia HIE Infection - meningitis, encephalitis Kernicterus Inborn error of metabolism Intracranial haemorrhage/infarction Structural CNS lesion Neonatal withdrawal from maternal drugs/substance Idiopathic
How may neonatal seizures present?
Subtle signs - blinking, chewing, eye deviation, lip smacking, staring, cycling/boxing, apnoea
Repetitive jerking, stiffening and posturing limbs/trunk
EEG can confirm
How would you manage neonatal seizure?
A-E assessment
Rule out hypoglycaemia
Blood - FBC, U&Es, Ca, Mg, VBG; ?culture/metabolic screen/LP
Arrange EEG; if poss Cerebral Function Analysis Monitor
Rx seizures if prolonged (>3mins or 4+ in hour) IV phenobarbitol
What is hypoxic-ischaemic encephalopathy?
Clinical syndrome of brain injury in neonates due to prolonged or severe hypoxia during birth causing ischaemic brain damage. Severe = CP, death
Causes of HIE
Maternal shock, intrapartum haemorrhage, amniotic fluid embolism, prolapsed or nuchal cord
How might HIE present?
Antenatal - foetal distress on CTG (abnormal HR + contraction patterns), RFM, cramps, PV bleed
Postnatal - cord blood gas acidosis, low Apgar score at 5 and 10mins, seizures, difficulty feeding, breathing problems, hypotonia, organ damage/failure, abnormal level of conscious (up or down)
How is HIE managed?
in NICU, resuscitation, supportive care (ventilation, circulatory support, rx acidosis and seizures), therapeutic hypothermia if moderate/severe.
Define neglect
Persistent failure to meet Childs basic physical /psychological needs that is likely to result in serious impairment of Childs health and development
Define child abuse
Deliberate infliction of harm to a child or failure to prevent harm, may be physical/sexual/emotional/bullying/online abuse
How old should a child be when they first smile?
6 weeks
How old should a child be when they have no head lag on pulling to sit?
3 months
At what age would you expect a child to be able to sit?
6 months - pull self to sitting, sit with a straight back when held
7-8 months - sit without support
How old should a child be when they can pull themself to standing?
9 months
How old should a child be when they start crawling?
9 months
How old should a child be when they start cruising and then walking unsupported and at what age would you refer to a specialist if this has not yet happened?
cruising 12 months
13-15 months, refer at 18
By what age should a child be able to hop on one leg?
4 years old
Describe the social interaction you may see in normal childhood development
6 weeks - first smile 3 months - laughs, enjoys friendly handling 6 months - not shy 9 months - shy but can play basic games like peek a boo or pat a cake 12 months - waves bye bye 18 months - plays alone 2y - plays near but not with others 4y - plays with other children
Describe the speech development and milestones you would expect to see in a normal child
6 months - 2 syllables
9 months - ‘mama’ ‘dada’ understands no
12 months - knows and responds to own name
12-15 months - knows 2-6 words (refer at 18months)
2 yrs - combines two words
3y - 3-5 word sentences, what and who questions
4y - why, when and how questions
At what age would you expect a child to be able to build a tower of 3 blocks?
18 months
At what age would you expect a child to be able to copy a circle?
3y
Who receives a BCG vaccine and when do they receive it?
at risk of TB (e.g. family case in last 6 months) get it at birth
Childhood vaccine schedule
2 months - 6 in 1 + oral rotavirus + MenB
3 months - 6 in 1 + oral rotavirus + PCV
4 months - 6 in 1 + MenB
12-13months - HiB/MenC + MMR + MenB + PCV
2-8 - annual flu vaccine
3-4 - MMR + pre-school booster (dip/tet/whoop/polio)
12-13 - HPV vaccine
13-18 - MenACWY + dip/tet/polio booster
What is in the 6 in 1 vaccine and when is it given?
2/3/4 months; dip/tet/whoop/polio/HiB/HBV
In what scenario should vaccinations be delayed?
acute febrile illness/intercurrent infection
Features of trisomy 21?
Short stature
Hypotonia
Face = upslanting palpebral fissures, epicanthic folds, brush field spots, round/flat face, small low-set ears, protruding tongue
Flat occiput
Single palmar crease
Sandle-gap deformity
Duodenal atresia, Hirschsprung’s disease, congenital heart defect
What complications might you see of T21?
learning difficulties, repeated respiratory infections ± hearing impairment from glue ear, congenital heart defect (endocardial cushion defect, VSD, TOF, PDA)
ALL, hypothyroidism, early onset Alzheimers, cataracts, subfertility
How would you expect croup to present and what is the causative organism?
Stridor - caused by laryngeal oedema, inflammation and secretions
Cough - barking cough commonly worse at night
Fever and coryzal sx
Parainfluenza viruses
How is croup graded and what does this mean for management?
Mild - occasional cough, no stridor or sternal recession
Moderate - frequent cough, stridor and sternal recession at rest
Severe - frequent cough, stridor and sternal recession at rest WITH agitation/lethargy
Mild - stat dose PO dexamethasone, safety net usually self-limiting and will resolve within 48h but can last up to 1 week, fluids and paracetamol/ibuprofen, seek medical advice if cough worsens and stridor/recession.
Moderate/severe - admit for observation to prevent resp failure, stat PO dexamethasone, highflown O2/neb adrenaline if required.
How would you expect epiglottitis to present?
Rapid onset, continuous stridor, significant pyrexia and generally unwell (T>39), drooling/pooling of saliva with muffled voice no cough. Used to be disease of childhood but HiB vaccination now (2m/3m/4m/12m) means more commonly presenting in adults.
How do you manage acute epiglottitis?
As soon as it is suspected call anaesthetist and ENT. Do not examine throat, keep child with mom and do not approach/intervene as any upset can cause airway obstruction due to increased oedema/inflammation.
Most common causative organisms of bronchiolitis?
RSV, more rarely mycoplasma/adenovirus/parainfluenza
How does bronchiolitis typically present?
coryza, dry cough, breathlessness, wheeze, fine crackles, poor feeding
What signs/symptoms would make you admit patient with suspected bronchiolitis?
Respiratory distress (grunting, severe recessions, RR>70), hypoxia, feeding 50% usual amount.
How is bronchiolitis managed?
Supportive - oxygen if required and NG tube if poor feeding.
What is the causative organism of whooping cough?
Bordetella pertussis
How does whooping cough present? How would you investigate it?
2-3 days of coryza, then paroxysmal coughing (usually worse at night or after feeds, may vomit after, lasts for 10-14 WEEKS) ± inspiratory whooping (forced inspiration against closed glottis), in infants may have episodes of apnoea
Nasal swab PCR, may see lymphocytosis on FBC
How is whooping cough managed?
Notifiable disease
Admit infants under 6 months old, anyone with severe breathing difficulties or a significant complication
Onset of cough <21d ago = PO clarithromycin
Exclusion from school until 48h of abx or 21 days from sx onset if not using abx
Offer prophylactic abx to household members who have been contacts in last 21d who are not fully vaccinated.
Describe the pathophysiology of cystic fibrosis
Characterised by an autosomal recessive mutation on chromosome 7 affecting the CFTR gene which codes cAMP-regulated Na/Cl channels. This causes exocrine secretions to become more viscous, which may manifest clinically as recurrent chest infections, pancreatic insufficiency, malabsorption, meconium ileus etc.
How may cystic fibrosis present?
Screened on neonatal blood spot screening (Guthrie testing) day 5-9.
May present as neonate with meconium ileus
Later - recurrent pneumonias, failure to thrive, steatorrhoea, slow growth
What test is used to diagnose CF? Is it always correct?
Sweat test - abnormally high sweat chloride. false positives - glycogen storage disease, malnutrition, diabetes insipidus, hypo(para)thyroidism, G6PD, adrenal insufficency. false negatives - skin oedema
How is CF managed?
Counselling for patient and family - direct to online resources and support groups; genetic counselling
MDT very important! inc transition paeds to adult services
Chest physio at least twice a day to dislodge mucus (teach parents how to do it), postural drainage.
High calorie high fat diet, pancreatic enzyme and vitamin supplementation
Minimise contact with other CF patients (cross infection with pseudomonas, burkholderia)
Heart and lung transplant
How would asthma present in a child?
Episodes of wheeze, breathlessness, chest tightness or cough with diurnal variability, but minimal symptoms between attacks. Recorded observation of wheeze by HCP. Hx of atopy. Ideally a recorded PEF/FEV1 which is significantly lower during symptomatic periods. Lack of sx suggestive of other dx.
Describe the pathophysiology of asthma
Dendritic cells present allergens to TH2+ T cells which are then activated and stimulate the humeral immune system to produce cytokines which promote inflammation and bronchoconstriction, with increased proliferation of mast cells, eosinophils and dendritic cells.
Risk factors for childhood asthma
Atopy, family hx of atopy, low birth weight, prematurity, parental smoking
Important factors to elucidate in ?asthma hx
Cough/wheeze/SOB/chest tightness Sx frequency Sx severity Any identifiable triggers Age of onset How is this affecting the child in terms of school attendance, ability to take part in hobbies, sleep? Have they had to attend hospital for it? Any treatments tried? PMH - other allergies, prev viruses/eczema/hayfever FHx atopy
What investigations might you perform for ?asthma?
Often a clinical dx but can perform as baseline tests
SPIROMETRY - baseline FEV1/FVC, and if unsure of dx can perform baseline spirometry and trial with bronchodilators to check for improvement
Baseline CXR, PEFR
Exhaled NO
Can do exercise testing or skin prick testing to identify specific allergens but not to identify asthma itself.
Describe the management of asthma in children
Stepwise treatment step up/down until at the minimum intervention which controls symptoms. At each step ensure compliance and correct spacer technique, ensure written asthma management plan
1) Short acting B2 agonist (salbutamol)
2) + Low dose ICS as regular preventer (beclometasone; can jump straight to this step if sx 3+ times a week or at night)
3) + Leukotriene receptor antagonist
4) Switch LTRA to LABA if not effective
5) SABA + Maintenance + Reliever Therapy (low ICS)
6) SABA + MART (moderate dose ICS)
7) SABA + MART (high dose ICS)/additional drug such as theophylline
Define a severe asthma attack
O2 <92 PEF 33-50% best or predicted too breathless to talk/feed HR >125 if 6+, >140 if 1-5 RR >30 if 6+, >40 if 1-5 use of accessory neck muscles
Define a life threatening asthma attack
O2 <92 PEF <33% best or predicted Silent chest Poor respiratory effort Agitation Altered consciousness Cyanosis
How would you manage an acute asthma attack
High flow O2
Salbutamol (mild/mod = spacer, severe = nebuliser) ± nebuliser ipratroprium bromide
PO prednisolone 3/7
2nd line = consult specialist for ?IV salbutamol, add MgSO4
Causes of diarrhoea in children
Acute = can be early sign of sepsis so beware! Usually gastroenteritis due to rotavirus infection, initial fever and vomiting, biggest risk is dehydration which requires oral rehydration therapy.
Chronic
- breastfed infant - normal for their stools to be liquid
- CMPI
- toddler diarrhoea - undigested food
- coeliac disease
- post gastroenteritis lactose intolerance
describe pathophysiology of coeliac disease?
T-cell mediated immune reaction to gluten causing small intestine epithelial cell destruction and villous atrophy.
How would you expect a child with coeliac disease to present?
Usually 9-24 months
Malabsorption - failure to thrive, weightloss, loose stools, steatorrhoea, abdo pain/distension, anorexia, muscle waste. Miserable child with behavioural changes.
Could present with extra-intestinal symptoms - dermatitis herpetiformis, osteoporosis, delayed puberty, short stature, IDA, arthritis.
How would you investigate ?coeliac disease
serology - total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG)
ttg only weakly positive then IgA endomysial abtibodies (EMA)
Positive serology = endoscopic duodenal bx
How would you mx coeliac disease?
gluten free diet
diet supplements if malabsorption e.g. iron
annual f/u for sx, development, growth, long term complications
How does GORD differ from gastro-oesophageal reflux?
reflux is the passage of gastric contents into the oesophagus, which is normal in infants if asymptomatic
GORD is the symptoms and complications which arise as a result of reflux
Risk factors for GORD
prematurity, parental hx heartburn/acid reflux, obesity, hiatus hernia, hx congenital diaphragmatic hernia/oesophageal atresia (whether repaired or not), neurodisability e.g. CP
