paeds level 2 conditions (pack 1) Flashcards
Birth Asphyxia/ Hypoxic Ischaemic encephalopathy (HIE):
- what is it?
- groups of causes? 5 (with example causes)
HIE = Clinical syndrome of brain injury – secondary to hypoxic ischaemic insult (2/1000 live births)
- Decreased Umbilical blood flow e.g. Cord prolapse
- Decreased placental gas exchange e.g. placental abruption
- Decreased maternal placental perfusion e.g. abruption, Accreta
- Maternal hypoxia
- Inadequate postnatal cardiopulmonary circulation
SIGNS OF Hypoxic Ischaemic encephalopathy (HIE):
- mild? 5
- moderate? 6
- severe? 10
(also rough prognosis of each)
MILD
- muscle tone increased
- tendon reflexes brief
- poor feeding
- excessive crying
- sleepiness
(typically resolves in 24hrs)
MODERATE
- lethargy
- hypotonia
- apnoeic periods
- diminshed deep tendon reflexes
- grasp, moro + sucking reflexes poor / absent
- seizures within 24hrs of birth
(full recovery 1-2 weeks is possible)
SEVERE
- hypotonia
- coma / stupor
- depressed deep tendon reflexes
- neonatal reflexes absent
- bulging fontanelle
- irregular breathing
- irregular HR and BP
- disturbed ocular motion (eg nystagmus, skewed deviation)
- pupils dilated, fixed, poorly reactive to light
- seizures (may be resistant to treatment, generalised, freq may increase in early period - with progression seizures subside)
Hypoxic Ischaemic encephalopathy (HIE):
- how to detect abnormalities intrapartum?
- test done on all babies at birth to screen for HIE?
- additional test done at birth for babies at risk of HIE?
- additional bloods which can consider?
- additional other investigations which can consider?
may be CTG abnormalities
- can also do scalp blood test
All babies get APGAR score
if risk of HIE, do cord gases after birth (pH <7.0 = encephalopathy)
additional bloods to consider - U+Es - cardiac enzymes - LFTs - coagulation screen ^basically to see how much damage done to these organs
other tests to consider
- MRI head
- echo of heart
- EEG
APGAR score
- What does it stand for? (ie what features does it look at)?
- max possible score? healthy score?
- how many minutes after birth is it done? 2
ACTIVITY (muscle tone)
- 0 = absent
- 1 = arms + legs flexed
- 2 = active movement
PULSE
- 0 = absent
- 1 = below 100 bpm
- 2 = over 100 bpm
GRIMACE (reflex irritability)
- 0 = flaccid
- 1 = some flexion of extremities / grimace
- 2 = cries on stimulation / sneezes / coughs
APPEARANCE (skin colour)
- 0 = blue or pale
- 1 = body pink, extremities blue
- 2 = completely pink
RESPIRATORY EFFORT
- 0 = absent
- 1 = slow, irregular
- 2 = vigorous cry
max score is 10
- 7-10 is normal
- 4-6 is moderately depressed
- 0-3 is severely depressed
done at:
- 1 min
- 5 mins
nb DON’T BOTHER LEARNING INS AND OUTS! JUST GET THE GIST OF THIS AND WHAT A NORMAL SCORE
Hypoxic Ischaemic encephalopathy (HIE):
- treatment with most efficacy? how long for?
- other thing to treat? 1
- important things to monitor? 3
THERAPEUTIC HYPOTHERMIA
- 33-33.5 deg for 72 hours
- followed by slow and controlled rewarming
- stops glutamine and free radicals from being released
treat seizures
MONITOR
- blood glucose
- EEG
- fluid levels (mild fluid restriction
Possible complications of HIE? 6
- death
- dyskinetic cerebral palsy
- severely reduced IQ
- epilepsy
- cortical blindness
- hearing loss
BIRTHMARKS
- definition?
- two main groups?
Coloured marks that are visible on the skin – present at birth or develop soon after birth
VASCULAR
- Often red, purple or pink
- Caused by abnormal blood vessels in or under the skin
- Often on head and neck area – mainly the face
- If affected vessels are deep, birthmark can appear blue.
PIGMENTED
- Usually brown
- Caused by clusters of pigmented cells.
NEVUS SIMPLEX
- Two other names for them?
- appearance? (incl location)
- what % of babies will have?
- prognosis?
AKA
- stork mark
- salmon patch
Flat red/ pink patches that appear on eyelids, neck or forehead at birth
- more noticeable when baby cries
50% of babies will have
- most common type of vascular birth mark
will fade within months (up to 4 years if on forehead)
INFANTILE HAEMANGIOMA
- aka?
- appearance?
- when treat? 3
- what is treatment?
- prognosis?
strawberry mark
usually not present at birth but may develop rapidly in the first month of life. They appear as erythematous, raised and multilobbed tumours
Raised red mark anywhere on body
- 5% of babies, esp girls
TREAT IF:
- grows rapidly
- interferes with feeding
- interferes with vision
treatment = systemic propranolol (or topical beta blockers)
typically increase in size until around 6-9 months then regress over next few years
- 95% resolve before age 10
PORT WINE STAIN
- appearance?
- what to rule out? how?
- prognosis?
- treatment option?
Permanent, flat, red or purple marks
- Often on one side of body
- is a capillary malformation
Rule out Sturge-Weber syndrome: seizures, learning disorders, glaucoma, port wine mark
- DO MRI!!
Permanent, may deepen in colour over time
- is also sensitive to hormones (puberty, pregnancy, menopause)
can have multiple sessions of laser therapy to reduce appearance
- or use camouflage make up
CAFE AU LAIT SPOTS
- appearance?
- what’s normal?
- when get suspicious that could be due to an underlying condition? which condition?
Coffee coloured skin patches
One or two is normal – if >6 develop by age 5, review needed
Rule out neurofibromatosis type 1
(Growth of tumours along nerves in the skin)
MONGOLIAN BLUE SPOTS:
- appearance?
- who most commonly seen in?
- prognosis?
- what can be mistaken for?
Blue/grey or bruised looking birthmarks
- Present from birth
- Occur over lower back or buttocks
Commonly seen in darker-skinned people
May last for months – years (usually disappear by 4)
Important new baby check – may be mistaken for bruises later on
CONGENITAL MELANOCYTIC NAEVI
- appearance?
- what is there a risk of them becoming? what increases the risk?
Congenital moles
- Large, black or brown moles from birth
Fairly common
May change over time
Risk of skin cancer is low
- Risk with increased size
What are the three types of extra-cranial head injury that can occur due to trauma at birth?
- How do you tell the difference between then? (when appear, appearance and findings on palpation, cross suture lines or not)
CAPUT SUCCEDANUM
- most superficial
- localised scalp oedema
- fluid collection is greatest immediately following delivery (and will then decrease)
- soft to touch with irregular margins
- cross suture lines
CEPHALOHAEMATOMA
- rupturing of blood vessels between periosteum and bone
- firm, tender mass
- appears hours to days after birth and can increase in size for 2-3 days
- DON’T cross suture lines (even when increases in size)
SUBGALEAL HAEMORRHAGE
- damage to veins between the scalp and intracranial venous sinuses
- boggy fluid collection with ballotable fluid wave beneath the scalp + bleeding extending to above the eyes and back to the insertion of trapezius muscle
- occiptal frontal circumference will increase (potential for large blood loss - need to be monitored)
- cross suture lines
- vacuum procedure gives highest risk of this
nb these can all happen in any birth but all are more likely in instrumental delivery
CEPHALOHAEMATOMA:
- how long will it take to resolve?
- when should you do a CT head? 2
resolves over a few weeks
do CT head if:
- neurological impairment seen
- concern for skull fracture
HAEMOLYTIC DISEASE OF THE NEWBORN:
- describe the pathophysiology
- how is it prevented?
Foetus Rh positive
Mother Rh Negative
(Father usually Rh Positive)
Sensitising event makes mother produce anti bodies to Rh positive blood
On second exposure anti-Rh antibodies cross the placenta and destroy foetal RBCs
Effect seen on delivery, when baby cannot cope with haemolysis.
PREVENTION
- all mothers tested for rhesus antibodies
- rhesus -ve mothers given anti-D at 28wks and any sensitising events (eg bleeding after 24wks, miscarriage, amniocentesis etc)
HAEMOLYTIC DISEASE OF THE NEWBORN:
- antenatal presentation? (incl latin name)
- postnatal presentation?
ANTENATAL (ie on USS)
- hydrops fetalis: abnormal accumulation of fluid in two or more foetal compartments (eg ascites, pleural effusion, skin oedema)
POSTNATAL
- early jaundice (in first 24hrs)
- hepatosplenomegaly
- coagulopathy
- thrombocytopaenia
- anaemia (may be a later sign)
main groups of DDx for jaundice in first 24hrs of birth? 4
nb almost always HAEMOLYTIC cause in first 24hrs of life:
1) ABO incompatibility
2) rhesus or other isoimmunisation
3) red cell defects (eg G6PD deficiency, spherocytosis)
4) congenital infection (eg TORCH)
HAEMOLYTIC DISEASE OF THE NEWBORN:
- bloods from mother? 1
- bloods from infant? 3
MOTHER
- group and rhesus status
INFANT (can do as cord blood)
- FBC (low Hb, increased reticulocytes, low platelets)
- coombs test
- LFTs (increased bilirubin)
HAEMOLYTIC DISEASE OF THE NEWBORN:
- symptomatic management options? 2
- other management? 1
TREATMENT FOR JAUNDICE
- plot on line (make sure using correct chart for gestational age) then UV light and/or exchange transfusion
consider IV Ig as definitive treamtent
- this may not be necessary though, but monitor closely!!
PREMATURITY:
- definition?
- at what gestation are most problems seen though?
- If an infant is born prematurely, what full history should be taken?
- risk factors for prematurity? 11 (as identified in the hx)
- what percentage of premature births are idiopathic? (ie have no risk factors)
birth before 37 wks gestation (8%)
most problems seen in infants born <32 wks (2%)
TAKE FULL OBSTETRIC Hx
RISK FACTORS:
- young maternal age
- previous premature birth
- cervical incompetence
- multiple pregnancies
- gestational HTN / pre-eclampsia
- antepartum haemorrhage
- congenital infection (TORCH)
- certain medications during pregnancy
- maternal smoking
- maternal alcohol
- domestic violence
40% have no known risk factors
COMPLICATIONS ASSOCIATED WITH PREMATURITY:
- CNS? 4
- metabolic? 4
- blood? 2
- cardiovascular? 2
- respiratory? 3
- GI? 5
- other? 2
- later? 4
CNS
- intraventricular haemorrhage (bleeding into ventricular system, can lead to cerebral palsy)
- periventricular leukomalacia (white matter surrounding ventricle deprived of blood and oxygen -> softening)
- cerebral palsy
- retinopathy of prematurity (ROP)
(also higher risk of HIE during delivery)
METABOLIC
- hypoglycaemia
- electrolyte imbalance
- hypocalcaemia (poor renal function)
- osteopenia of prematurity (w risk of fractures)
BLOOD
- anaemia of prematurity
- neonatal jaundice
CARDIOVASCULAR
- hypotension
- patent ductus arteriosus
RESPIRATORY
- surfactant deficiency -> resp distress syndrome (RDS)
- recurrent apnoea
- chronic lung disease (broncho-pulmonary dysplasia)
GI (incl nutriution)
- inability to suck (lack of reflex)
- poor milk tolerance
- Necrotising enterocolitis (NEC)
- Gastro-oesophageal reflux
- inguinal hernia
OTHER
- hypothermia (poor temp regulation)
- immunocompromised (increased risk of infection)
LATER
- increased risk of adverse neurodevelopment
- behavioural problems
- sudden infant death syndrome (SIDS)
- non-accidental injury (stress of long-term complications)
How to antenatally prevent resp distress syndrome?
at what gestation is this given?
IM corticosteroids to mother
- 2 doses, 12-24 hrs apart
give if <34 weeks gestation
Management of preterm birth:
- where to deliver?
- who present at birth?
- cord clamping?
- how to keep warm if small?
- what resp support can be provided if needed? 3
delivery in centre with preterm facilities
<28 weeks, senior paediatrician present at birth
Delay cord clamping for 1 min where possible
to prevent heat loss: can put in polytheme bag at birth to prevent evaporative loss of fluid and heat
- ie if really preterm, do this before drying them
- also warm them
RESP SUPPORT OPTIONS
- PEEP
- intubation
- surfactant replacement therapy (through endotracheal tube)
PRETERM INFANTS
- how to manage poor thermoregulation?
- how to minimise risk of infection? 2
- how to manage hypoglycaemia?
- how to feed? (which also reduces risk of NEC)
- how to manage patent ductus arteriosus?
- how to manage retinopathy of prematurity?
- put baby in incubator
- minimal handling of baby
- low threshold for starting broad spec abx
- start feeding as soon as possible, can also add glucose to milk
- get mother to express breast milk and (norm) feed through nasogastric tube (breast milk reduces risk of NEC)
can give NSAIDs (eg iboprofen) to close PDA
- check no duct-dependant heart disease first though
all premature babies are screened for ROP
- if have, treat with laser treatment to the extra blood vessels
RESPIRATORY DISTRESS IN THE NEWBORN:
- what RR?
- other signs? 5
- aside
tachypnea, RR = >66
- intercostal recession
- subcostal recession
- grunting (endogenous PEEP)
- nasal flaring
- cyanosis
RESP DISTRESS SYNDROME:
- what other risk factors? 5 (aside from prematurity)
- Imaging? 1 (incl findings)
- what things to monitor? 2
OTHER RISK FACTORS
- caesarian section
- hypothermia
- meconium aspiration
- maternal diabetes
- family Hx
CXR
- ground glass appearance in all lung fields
- generalised atelectasis = a complete or partial collapse of a lung or a lobe
- air bronchograms
- reduced lung volume
MONITOR
- spo2
- blood gasses
RESPIRATORY DISTRESS SYNDROME
- management? 5 (1 treatment, 3 supportive, 1 prevention)
- prognosis?
- how long does condition normally take to resolve?
- most common complication?
nb also antenatal steroids if poss
1) sufficient oxygen + supporting respiration
- CPAP
- intubation
2) surfactant replacement therapy down endotracheal tube
3) abx - penicillin and gentamicin
- until congenital pneumonia excluded (can mimic or co-exist with RDS)
4) IV fluids
5) NG tube feeding (mothers expressed milk if poss)
generally good prognosis (mortality is 5-10%)
norm resolves over 3-7 days as surfactant production increases
most common complication = bronchopulmonary dysplasia (require O2 at home)
What are the two different types of IUGR?
causes of each?
which tends to have better prognosis?
SYMMETRICAL GROWTH RESTRICTION
= head circum and weight equally reduced
= EARLY insult
- genetic
- foetal abnormality
- congenital viral infection (eg TORCH)
- early foetal malnutrition
- early teratogen exposure
ASYMMETRICAL GROWTH RESTRICTION
= head circum significantly higher on centiles than weight
= LATE insult
- tend to have better prognosis (ie less likely to have developmental delay etc)
- late foetal malnutrition
- pre-eclampsia
- smoking
Potential complications for IUGR:
- immediate? 4
- late? 2
- hypoglycaemia
- hypothermia
- polycythaemia
- bone marrow / hepatic compromise (thrombocytopenia, neutropenia, coagulopathy)
LATE
- poor post-natal growth
- neurodevelopment impairments
TALIPES:
- also known as?
- what is the deformity seen? (describe it)
- two different types? how to tell difference? which needs treatment?
- when is it normally picked up / examined for?
aka neonatal club foot (talipes equinovarus)
- nb bilateral in 50% of cases
inversion + adduction of forefoot
- plantarflexion deformity
TWO TYPES
= postural: CAN be passively everted and dorsiflexed through full range of motion (not concerning)
= structural: can NOT be passively everted and dorsiflexed through full range of motion (needs treatment)
- newborn exam OR 6/8 week exam
STRUCTURAL TALIPES:
- two management options?
Ponseti Method – foot manipulated over 6 weeks, held in long leg plaster cast. Gradual correction
Operation if Ponseti doesn’t work – from 2 years old
CHICKEN POX:
- virus it’s caused by?
- first sign / symptom?
- other symptoms?
- appearance and distribution of rash?
varicella zoster virus (VZV)
FIRST SIGN = fever (about 2 days before rash)
other symptoms:
- ITCHY RASH
- headache
- anorexia
- signs of URTI (sore throat, coryza, cough)
RASH:
- predominantly starts on torso (also perineum + scalp) then may go over whole body
- lesions evolve: red macules, papules, VESICLES, pustules then crusting/scabs (will have lesions at different stages)
CHICKEN POX:
- how is it spread?
- incubation period?
- when most infective?
- when tell parents that children can go back to school?
- how diagnosed?
spread by respiratory droplets or direct contact with lesion
incubation of 10-21 days (norm 14 days)
most infective 4 days before the rash to 5 days after rash first appeared (ie norm when lesions are all crusted over)
should be excluded from school and then can go back when all lesions have crusted over
diagnosed clinically (based on appearance and distribution of rash) - though can do test of vesicular fluid for virus - but very rarely done!
CHICKEN POX:
- most common complication? 1
- rarer, more serious complications? 4
most common complication is secondary bacterial infected of lesions (eg impetigo)
RARE COMPLICATIONS
- conjunctival lesions
- encephalitis (presents as ataxia about a week after rash appears, good prognosis)
- pneumonia (esp in infants)
- necrotising fascitis
CHICKEN POX:
- who is most at risk if infected? 3
- what give them as prophylaxis if have contact? 1
- what give them if they get infected? 1
- pregnant women
- infants under 1 year
- immunocompromised children
Varicella Zoster Immunoglobulins – prophylaxis following contact e.g. when pregnant or on chemo (or give to newborn if antenatal exposure)
Aciclovir if get infected (also use for anyone else who gets complications)
MANAGEMENT OF UNCOMPLICATED CHICKEN POX:
- advice to parents?
- options to try to reduce itching? 2
- option if distressing fever?
- who to give antivirals to? 4
cut children’s nails (to prevent itching + scarring)
to reduce itching
- calamine lotion
- chlorphenamine (if >1 year)
antipyretics if child is distressed by the fever
GIVE ANTIVIRALS (acyclovir)
- immunosuppressed
- pregnant
- infants <1 year
- get any complications
INFECTIVE CONJUNCTIVITIS:
- key features? 3
- how to tell difference between bacterial and viral?
- main differential for infective conjunctivitis?
- sore
- red eyes
- discharge
BACTERIAL:
- purulent discharge
- Eyes may be ‘stuck together’ in the morning
VIRAL:
- Serous discharge
- Recent URTI
- Preauricular lymph nodes
main differential = allergic conjunctivitis (ie norm w hayfever)
MANAGEMENT OF CONJUNCTIVITIS:
- viral?
- bacterial? (incl name of abx)
- advice given to parents? 1
- school exclusion needed?
viral if norm self-limiting within 1-2 wks
bacterial
= chloramphenicol drops OR ointment multiple times a day
ADVICE
- don’t share towels while have symptoms
- school exclusion not necessary
(also don’t wear contact lenses while have symptoms)
NEONATAL CONJUNCTIVITIS:
- likely cause if <48hrs after birth? management?
- likely cause if day 3-4 after birth? management?
- likely cause if >7 days after birth? management?
GONORRHOEA
= within 48hrs of birth
- purulent discharge + swelling of eyelids
- treat w cephalosporin
NEONATAL CONJUNCTIVITIS
= day 3-4
- simple cleaning normally sufficient
CHLAMYDIA
= suspect if after day 7
- diagnosis with monoclonal antibody text
- treat w abx
nb gonorrhoea and chlamydia are vertical transmission
ALLERGIC CONJUNCTIVITIS:
- features? 5
- 1st line management?
- Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis)
- Itch is prominent
- eyelids may also be swollen
- May be a history of atopy
- May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)
1ST LINE
= topical or systemic antihistamines
Common food allergies? 8
which tend to grow out of?
TEND TO GROW OUT OF:
- cow’s milk protein
- soya
- eggs
- wheat
TEND TO HAVE FOR LIFE:
- fish
- shellfish
- peanuts
- tree nuts
Possible symptoms of a food allergy:
- most serious presentation?
- other possible symptoms / presentations? 8
ANAPHYLAXIS
- dysphagia
- Diarrhoea +/- blood or mucus
- Vomiting
- Abdominal pain
- Failure of growth/ weight loss
- Eczema
- Erythematous rash – esp. peri-orbital
- Asthma symptoms
nb always think of cow’s milk protein allergy if weaning infant starts getting rash or blood in stools and doesn’t seem acutely unwell
Food allergy:
- two possible ways of testing for it? 2
- if these are negative but allergy still suspected, what investigation to do?
- skin prick test
- blood test for IgE specific to that allergen
if negative: can do controlled exposure in hospital
Food allergy:
- dietary advice?
- what give for emergencies? how to describe how to give to parents?
- medication to give if mild reaction?
AVOID FOOD ALLERGIC TO!
give epipen (one for home and one for school nursery)
teach how to use:
- remove blue cap then hold with a fist around and stab into thigh (don’t put thumb over end)
- ‘orange to the thigh, blue to the sky’
- hear a click
- hold in for 5 secs then remove
can give antihistamines if mild reaction
GLANDULAR FEVER:
- other name for it?
- most common virus that causes it?
- which age group most common in?
infectious mononucleosis
- ‘mono’ in the US
90% is ebstein-barr virus (EBV)
- rarer causes: CMV, HHV-6
most common in teenagers and young adults
GLANDULAR FEVER:
- three classical features?
- other possible features? 6 (3 symptoms, 3 clinical signs)
- describe the typical course of the disease?
1) SORE THROAT
2) LYMPHADENOPATHY
3) FEVER
nb lymphadenopathy may be present in the anterior and posterior triangles of the neck
- tend to be firm and non-tender
OTHER POSSIBLE FEATURES:
- malaise
- anorexia
- headache
- palatal petechiae
- splenomegaly (50%, may rarely lead to rupture)
- hepatitis (transient rise in ALT)
PRESENTATION IS VERY VARIABLE
- may be gradual with malaise, anorexia + low-grade fever for 1-2 weeks
- may begin abruptly with high fever and headache
what is the main DDx for glandular fever?
How is the pattern of lymphadenopathy differ between these two conditions?
other rarer, but more serious, DDx? 2
TONSILITIS
- typically only upper anterior chain are enlarged
glandular fever
- may be present in anterior and posterior triangles of neck
other DDx
- hodgkins lymphoma
- other haem or solid tumours
GLANDULAR FEVER:
- two investigations to order if suspect?
- when to order?
- findings on these?
FBC
- increased lymphocytes and monocytes
- may be thrombocytopenia
- may get a haemolytic anaemia
MONOSPOT
- test for antibody to the virus
- takes 1-2 weeks to become positive
order both in 2ND WEEK of illness (may get false negatives if ordered before this)
GLANDULAR FEVER:
- non-pharm management advice? 3
- medication for symptomatic management?
- what medication to avoid? why?
- what else to avoid? why? for how long?
- how long norm take symptoms to resolve?
- rest during early stages
- drink plenty of fluid
- avoid alcohol
- simple analgesia for aches + pains
AVOID ampicillin or amoxycillin when glandular fever suspected
- will cause a maculopapular rash in 99% of pts with glandular fever (may be misdiagnosed as an allergy)
AVOID contact sports for 8 weeks
- to reduce risk of splenic rupture
Symptoms typically resolve after 2-4 weeks
KAWASAKI DISEASE:
- pathophysiology?
- age group normally affected?
- systemic vasculitis of unknown aetiology
- affects children under age of 5 years
KAWASAKI DISEASE:
- What are the 6 diagnostic criteria? (how many do you need to diagnose?)
1) high grade FEVER which lasts >5 DAYS
- nb fever is characteristically resistant to antipyretics
2) bilateral CONJUNCTIVITIS
- non-purulent
3) inflamed + red mouth, CRACKED LIPS, red pharynx
- also STRAWBERRY TONGUE
4) polymorphous RASH
5) changes to extremities: HAND/FOOT palm/soles reddening, oedema and later desquamation (ie PEELING)
6) cervical LYMPHADENOPATHY
“Think:
- fever, nodes, rash
- eyes, mouth, hands/feet”
need at least 5 of the 6 criteria to diagnose kawasaki
nb kawasaki is a clinical diagnosis, there’s no specific diagnostic test
KAWASAKI DISEASE:
- what is the main two DDx? 2
main DDx
- scarlet fever
- atypical infection (eg if someone has a sore throat and persistant fever not responding to 1st line abx then maybe try macrolides)
KAWASAKI DISEASE
- medications for management? 2
- when do you need to treat by?
- most important complication?
- investigation used to screen for this complication?
MANAGEMENT:
- high dose aspirin
- IV immunoglobulins
treat within 10 days of start of fever! - ie treat fast!
complication = CORONARY ARTERY ANEURYSMS
- screen for with echo
nb this is the most common cause of acquired heart disease in the UK
MEASLES:
- describe the course of the disease (incl symptoms, what first symptoms to occur, where does rash start and spread, features of rash)
- also incubation period and when infective from
incubation = 7-14 days (average 10 days)
infective from prodrome until 4 days after rash starts
1st) PRODROME (about 3 days)
- fever
- miserable
- cough
- coryza
- conjunctivitis
^”all the C’s”
2nd) KOPLIK SPOTS
- white spots (‘grain of salt’) on buccal mucosa
- nb doesn’t occur in any other condition
3rd) RASH (about day 4)
- starts BEHIND EARS
- then spreads to face + trunk
- discrete maculopapular rash, becoming blotchy and confluent
MEASLES:
- mainstay of management? 2
- investigation you can do?
- who may need admission to hospital? 2
- what should you do whenever you see someone with measles?
- school exclusion required?
- what should contacts do?
- fluids
- antipyretics
can test for IgM antibodies within a few days of rash onset
may need admission:
- pregnant women
- immunosuppressed
NOTIFY PUBLIC HEALT
- exclude from school (?how long for**)
- unvaccinated contacts should get urgent MMR vaccine
MEASLES:
- age group most common in?
- who at increased risk? 1
- most common complication?
- most common cause of death?
- other possible complications?
pre school + young children
increased risk if have Vit A deficiency
most common
= OTITIS MEDIA
most common cause of death
= PNEUMONIA
OTHER COMPLICATIONS:
- encephalitis: typically 1-2 wks following onset of illness
- subacute sclerosing panencephalitis: very rare, may present 5-10 years after illness
- febrile convulsions
- keratoconjunctivitis, corneal ulceration
- diarrhoea
- increased incidence of appendicitis
- myocarditis
PERIORBITAL CELLULITIS:
- also known as?
- what is it?
- which age group most common in?
aka preseptal cellulitis
an infection of the soft tissues anterior to the orbital septum - this includes the eyelids, skin and subcutaneous tissue of the face, but not the contents of the orbit
- nb this is in contrast to orbital cellulitis, which is an infection of the soft tissues behind the orbital septum, and is a much more serious infection
most common in children under 5
- 80% of patients are under 10
- median age of presentation is 21 months
PERIORBITAL CELLULITIS:
- common causes / mechanisms of infection?
- common causative organisms? 4
MECHANISMS OF SPREAD:
= sinus or respiratory infection
= cut, scratch, or foreign object in or near the eye
- bite from an insect or animal
- skin infection, such as impetigo
- stye (eyelid bumps) or swelling of the gland that makes tears
CAUSATIVE ORGANISMS:
- Staph. aureus
- Staph. epidermidis
- streptococci
- anaerobic bacteria
nb is more common in winter dt increased prevelence of resp pathogens
PERIORBITAL CELLULITIS:
- local symptoms?
- main systemic symptom?
- findings on examination?
- what examination should be performed?
- what signs should NOT be found, but should be examined/tested for? 6 (what would they indicate)
red, swollen, painful eye
- acute onset
- fever
O/E
- erythema and oedema of the eyelids, which can spread onto the surrounding skin
- partial or complete ptosis of the eye due to swelling
PERFORM CRANIAL NERVE EXAM (just ones that affect eye)
SIGNS INDICATIVE OF ORBITAL CELLULITIS:
- pain on eye movement
- restriction of eye movements
- proptosis
- chemosis (oedema of conjunctiva)
- visual disturbance
- RAPD (ie fail swinging light test)
PERIORBITAL CELLULITIS:
- main two differentials?
- how to differentiate between?
ORBITAL CELLULITIS
- do neuro exam: will have painful and reduced eye movement, proptosis, visual disturbance and RAPD
- can do imaging to differentiate if not sure
ALLERGIC REACTION
- more likely to be bilateral
- ask about other allergy symptoms (incl PMH + FH)
- ask about any new exposures etc
PERIORBITAL CELLULITIS:
- bloods? 2
- other bedside investigation?
- imaging to do if suspect orbital cellulitis? 1
- FBC (raised inflam markers)
- CRP
swab discharge from eye
if suspect orbital cellulitis
= contrast CT of head
PERIORBITAL CELLULITIS:
- where should it be managed?
- oral or IV abx? which abx?
- other medication to give?
- main complication to look out for?
All cases should be referred into hospital for assessment
Oral antibiotics are frequently sufficient - usually co-amoxiclav
Children may require admission for observation
give analgesia / anti-pyretics
Monitor for signs of orbital cellulitis
- also, rarely, meningitis
BRAIN TUMOURS IN CHILDREN:
- concerning characteristics of a headache?
- other symptoms / signs of raised ICP?
- other symptoms / signs? 3
CONCERNING HEADACHE
- worse on coughing / sneezing
- worse in the morning
- present on walking
- recent onset, worsening or persistent
- any associated neuro and/or focal symptoms
SIGNS OF RAISED ICP
- headache
- vomiting
- seizures
- new-onset squint
- blurred vision
OTHER SYMPTOMS
- new-onset ataxia, clumsiness
- incoordination
- nystagmus
nb brain tumours can often be in cerebellum, hence ataxic etc symptoms
BRAIN TUMOUR PRESENTATION BY AGE:
- symptoms/signs at any age? 5
- in young children? 1
- in older children? 3
ANY AGE
- abnormal eye movements
- fits / seizures
- behavioural change (lethargy under 5)
- abnormal balance / walking / coordination
- persistent / recurren t vomiting
YOUNG CHILDREN
- abnormal head position such as: wry neck, head tilt or stiff neck
OLDER CHILDREN:
- persistent / recurrent headache
- blurred or double vision
- delayed or arrested puberty
nb can also get symptoms similar to a stroke but with more insidious onset (eg weakness or loss of sensation down one side of arm
nb if on spinal cord can also present with symptoms of spinal cord compression
nb can also have endocrine effects
Differential diagnosis of raised ICP in children/adolescents:
- infective? 3
- non-infective? 4
- brain abscess
- meningitis
- encephalitis
- brain tumour
- seizures / post-ictal
- trauma (incl non-accidental injury)
- idiopathic intracranial hypertension (esp teenagers)
Child with symptoms suggestive of raised ICP:
- bedside investigation? 1
- 1st line imaging? 1
ophthalmoscope to look for papilloedema
CT head
Commonest type of brain tumour in children?
- two common subtypes of these? which better prognosis?
GLIOMAS = most common
- either astrocytomas or medulloblastomas
- astrocytomas have best survival rates
nb in children most brain tumours are primary (whereas in adults, most are mets)
Which clotting factors are deficient in:
- Haemophilia A?
- Haemophilia B?
what is the inheritance of both conditions?
what proportion have no family history? (ie de novo mutations)
Haemophilia A = factor 8
- VIII
Haemophilia B = factor 9
- IX
- aka christmas disease
both are X-linked recessive
1/3rd have no FHx
nb carrier females are rarely symptomatic
nb haemophilia A is 5x more common than haemophilia B (B is less serious)
HAEMOPHILIA:
- common presentations? 2
- excessive bruising / joint swelling as child learns to crawl / walk (haemarthrosis, haematomas)
- prolonged bleeding following circumcision, tooth eruption
nb rare to present in neonates - the more severe the disease is, the earlier it is likely to present
Differential diagnoses for haemophilia? (ie easy bleeding/bruising) 3
- von willebrand disease
- platelet disorder
- non-accidental injury (look at pattern of bruises etc)
Haemophilia:
- which clotting test will be prolonged?
- other blood tests to do? 2
- imaging to consider? 2
APTT (activated partial thromboplastin time) is prolonged
- nb bleeding time, thrombin time and prothrombin time will all be normal
- FBC
- factor 8 and factor 9 assay
consider doing:
- head + neck CT/MRI (if injury)
- abdominal / joint USS (if injury / bruising / swelling)
HAEMOPHILIA:
- which class of medication should people with haemophilia avoid?
- what activities should children avoid?
- which medication used for management? how often given?
- additional medication that can be used in haemophilia A? (how does it work?)
avoid NSAIDs (they interfere with platelets)
avoid contact sports (but can do other sports)
give IV injections of of factor concentrate (either 8 or 9)
- most families manage this at home
- portacaths are useful
- frequency of injection depends on severity of disease and what doing (eg have more before surgery/dental procedures)
Desmopressin may allow mild haemophilia A to be managed without use of blood products – stimulates endogenous release of factor 8 and Von Willebrand factor
- nb this doesn’t work for haemophilia B
nb there is a huge range of disease from mild (who rarely bleed and only need only need prophylaxis for surgery) and severe disease who have spontaneous bleeds and need constant prophylactic factor concentrate
- always ask pts how often take factors, how bad symptoms are etc
HENOCH- SCHONLEIN PURPURA:
- also known as?
- what is it? (ie pathophysiology)
- age group most common in?
- what does it normally follow?
- what condition does it overlap with?
aka IgA vasculitis
HSP is an IgA-mediated small vessel vasculitis
most common aged 2-10 years
normally follows an infection (eg an URTI)
There is a degree of overlap with IgA nephropathy (Berger’s disease)
HENOCH- SCHONLEIN PURPURA:
- which four organ systems does/can it affect? how does it affect each?
- which feature is most responsible for morbidity / mortality?
1) SKIN
- begins as a maculopapular, red rash which gradually becomes a palpable purpuric rash (w localised oedema)
- BUM, ANKLES, EXTENSOR surfaces
2) GUT
- colicky abdo pain (can be mistaken for an acute abdomen)
+/- diarrhoea / vomiting (common)
+/- haematemesis / meleana (less common)
- intussception (may occur)
- perforation (very rare)
3) JOINTS (60%)
- arthralgia of of medium-sized joints
- may progress to an obvious arthritis with red, swollen, tender joints
4) KIDNEYS (50%)
- haematuria is common (concerning if accompanied by proteinuria)
- if severe, can cause acute nephritic or nephrotic syndrome (AKI or CKD follow in a minority)
- renal complications are responsible for majority of morbidity + mortality
nb renal injury is caused by deposition of IgA immune complexes
HENOCH- SCHONLEIN PURPURA:
- bedside investigation? 1
- bloods? 2
- additional investigation if suspect renal involvement?
- additional investigation if suspect abdo complication?
- urine dipstick
- FBC (nb pa
- U+E (for renal function)
do USS with biopsy if suspect renal involvement
do relevant abdo investigations, eg USS if suspect intussusception
nb also do obs to rule out more serious causes of purpuric rash
HENOCH- SCHONLEIN PURPURA:
- medication for symptomatic management?
- investigations to repeat to screen for complications? 2
- how long does it normally take to resolve?
- recurrence rate?
simple analgesia for arthritis
- can use nsaids only if no kidney involvement
repeat for a few weeks at home to screen for renal complications:
- dipstick for blood + protein
- BP
self-limiting, normally resolves in 1-3 weeks
around 1/3rds of patients relapse
LEUKAEMIA:
- commonest type in children?
- what cells are these?
- which age group normally affect?
- what genetic condition increases likelihood of getting it?
acute lymphoblastic leukaemia (ALL)
Malignant proliferation of pre-B or T-cell lymphoid precursors in the bone marrow
nb ALL accounts for 85% of all leukaemias in childhood and 25% of all cancers in childhood
peak incidence ages 2-5 years
- affects boys slightly more than girls
increased likelihood in pts with Downs
nb also get AML but rarer, is more common n adults
PRESENTATION OF LEUKAEMIA
- three groups of symptoms which logically follow on from the three cells affected by bone marrow failure?
- additional symptoms? 4
- what is the normal timescale for progression of symptoms?
thrombocytopenia -> BRUISING, PETECHIAE
anaemia -> LETHARGY, PALLOR
neutropenia -> frequent or severe INFECTIONS
OTHER SYMPTOMS
- bone pain (secondary to bone marrow infiltration)
^ may present as a limp - hepatosplenomegaly
- lymphadenopathy
- fever
may also see testicular swelling in boys
nb can also get AML in kids but is rarer (the lymphadenopathy tends to be less prominent than in ALL)
What are poor prognostic features for ALL? 5
- age < 2 years or > 10 years
- WBC > 20 * 109/l at diagnosis
- T or B cell surface markers
- non-Caucasian
- male sex
LYMPHADENOPATHY:
- size and features of lymph nodes which make malignancy more likely?
- location of lymph nodes which make malignancy more likely?
- additional symptoms which make malignancy more likely?
MALIGNANCY UNLIKELY
- smooth, mobile, <2cm
- cervical or small inguinal
- well child (or signs of URTI / otitis media etc)
MALIGNANCY LIKELY
- hard, craggy, tethered, >2cm
- more widespread distribution
- bruising, pallor, fever, hepatosplenomegaly
LEUKAEMIA
- initial bloods if suspect? 2
- key investigation? 1
- FBC
- LFTs
bone marrow biopsy
MANAGEMENT OF ALL:
- mainstay of management? for how long?
- additional prophylactic treatment?
- overall survival rates?
chemotherapy (to remove blast cells from circulation
- then intermittent cycles of chemo for 2 years
intrathecal methotrexate +/- cranial irradiation to prevent spread to CNS
nb may also need steroids
80% at 5 years (rare to relapse after that)
MANAGEMENT OF AML:
- mainstay of management?
- management option that may be needed?
- overall survival rates?
intensive myeloablative chemo
relapse is common
bone marrow transplant offers best chance of cure
overall survival is about 60%
