Paeds Flashcards
when to refer to paediatrician - weight loss after birth
more than 10% weight loss on day 3
(community MW will weigh on day 3, 5 and 10, at day 3 check most will have lost weight, aim to regain birth weight by day 14)
normal RR
<1 - 30-40
1-2 - 25-35
2-5 - 25-30
5-12 - 10-25
> 12 - 15-20
normal HR
<1 - 110-160
1-2 - 100-150
2-5 - 95-140
5-12 - 80-120
> 12 - 60-100
adjusting for prematurity on a growth chart
separate section for premature babies until 42w
then adjustment is done on normal growth chart for the first 2 years
(prematurity = <37w)
information on a growth chart and when to refer
height, weight, and also head circumference from 0-1 years
o Failure to thrive = growth that crosses 2 centile lines
o If they cross only one centile, then refer to GP or health visitor for surveillance (could have just been due to a minor illness)
<2nd centile = underweight (overweight = 98th or above)
reasons for dips in growth charts
note that acute illness can lead to sudden weight loss and a weight centile fall, but children generally recover to their normal centile within 2-3 weeks - is a SUSTAINED drop that we are worried about
crohns coecliac cf neglect hypothyroidism GH deficiency reflux - back arching cows protein allergy
causes of short stature
primary - Down’s, turner’s, russel-silver, IUGR with fialure to catch up, osteogenesis imperfecta, achondroplasia
secondary - deprivation, neglect, malabsorptive disease, anorexia, chronic disease of any form, GH/IGF-1 deficiency, Laron syndrome (defective GH receptors), hypothyroidism, medication like steroids, cushings
if worried - continue to review and can calculate growth veloicty - growth failure is defined as height velocity <25th centile over at least 18m
investigations for poor growth
x-ray of wrist and hand - can identify bone age which has a marked delay in hypothyroidism and GH deficinecy (moderate delay in constitutional and no delay in familial short stature) fbc - anaemia in coeliac/ibd bone profile tsh in hypothyroidism karyotype for turners and others bloods for coeliac crp/esr ibd GH provocation tests using insulin/glucagon to see if gh deficiency IGF-1 measurement dex suppression test in cushings mri head for tumours skeletal survey for scoliosis
causes of failure to thrive
o Inadequate intake due to impaired suck/swallow, cleft palate
o Inadequate retention due to vomiting and GORD
o Increased nutritional requirements due to chronic illness in general
o Failure to utilise nutrients e.g. syndromic disorders
o Impaired nutrient absorption
1 year milestones
GROSS MOTOR
walks unsteadily with broad based gait, or walks with one hand held
FINE MOTOR
throws objects away
scribble with crayon
has a mature pincer grip
HEARING SPEECH ANAD LANGUAGE
uses 2-3 words with meaning
SOCIAL EMOTIONAL AND BEHAVIOURAL
uses a spoon
drinks from a cup using 2 hands
when should reflexes go
moro - 2m
palmar - 6m
rooting - 4m
asymmetric tonic neck reflex - 6m
autism vs asperger’s
autism =
abnormalities in reciprocal social interactions - failure of eye contact, facial expression, lack of relationships, inappropriate response to others emotions, dont understnat humour
speech and language disorder - delay in speaking, difficult initiating or sustaining convos, odd volume of speech, echolalia
restricted/stereotyped/repitive behaviour - rituals, routine, no imagination, unusual movements
^at least one of these must be present before age of 3 for diagnosis
asperger’s = mild social impairements but near-normal speech and language (i.e. these skills are not delayed) - more mild than autism, normal intellegence (autism ma have lower iq), more likely to live independently, diagnosis is usually made later (7 vs 3)
persistent difficulties with or differences in social communication and social interaction
restricted and repetitive patterns of behaviours, activities or interests since early childhood, to the extent that these impact negatively on day to day life
type of therapy for autism
applied behavioural analysis
red/high risk signs in a febrile child
mottled or blue no response to you if roused does not stay awake weak, high pitched or continuous cry appears ill to a healthcare professional RR >60 grunting chest in-drawing between ribs when breathing in reduced skin turgor <3m with temp >38 non-blanching rash neck stiffness bulging fontanelle seizures or fits
pattern of rash in roseola infantum and its management
fever followed later by a maculopapular rash LATER
rash starts at trunk before spreading to limbs
non-itchy
diarrhoea and cough also commonly seen
infection should pass in a week - managed conservatively with anti-pyretics if irritable - once the fever has passed child can go back to school as that is when most contagious point has passed
cause of roseola infantum
HHV6
pattern of rash in pityraisis rosea and its management
o Herald patch - single pink or red oval patch of scaly skin appears at least 2 days before a more widespread rash
o The widespread rash does not usually involve the face
o Not painful but can be itchy
o Usually gets better without treatment in 12 weeks
o Conservative treatment involves emollients, steroid creams, antihistamines for itch
o Aetiology is not usually understood but is thought that HHV-7 may play a role
cause of slapped cheek
parvovirus b19
2 important health messages with slapped cheek
rarely can lead to aplastic crisis - usually in those seen with immunodeficiency or haemolytic anaemia
avoid pregnant ladies as can lead to hdyrops fetalis
measles pattern of rash and prodrome and management
prodrome - 3C’s = coryza, cough and conjunctivitis
starts with fever, sore eyes that are sensitive to light and grey spots inside the cheecks called Koplik’s spots
after a few days a red brown rash forms over head or neck then spreads to rest of body
- Usually improves in 7-10 days - stay away from school for at least 4 days when rash first appears
- Can use anti-pyretics, clean eyes with water, put a wet towel on warm radiator to moisten air to help with cough, warm drinks with lemon or honey
confirm with salivary swab or serum sample for measles specific immunoglobulin
complications include bronchopneumonia - return if breathing difficulties, encephalitis - return if headache, changing consciousness, or seizures (carries 15% mortality rate)
cause of scarlet fever
group a strep
treatment of scarlet fever
phenoxymethylpenicillin for 10 days
important to avoid rheumatic fever and rheumatic heart disease
scarlet fever symptoms
fever lasts 24-48 hours
pin prick rash
more in flexures
TENDER lympahdenopathy - in contrast to kawasaki which is painless
all the S’s
- Causes pink-red rash that feels like sandpaper and looks like sunburn
- Usually starts with a swollen/strawberry tongue, sore throat, headache and fever
- Starts at neck then trunk then extremities
- 7-10 days later can get desquamation - tell this to parents so they know what to expect
toxic shock syndrome symptoms, cause and management
- TSS occurs as a reaction to toxins produced by staphylococcal or group-A streptococcal (aka strep pyogenes) infections. It is suggested by fever >39, hypotension and a diffuse erythematous macular rash
- The toxin can also lead to mucositis, diarrhoea and vomiting, renal and liver impairment, and clotting abnormalities
- Management is with antibiotics. It is important to be aware that desquamation of the palms and soles will follow after around 2 weeks
Causes
- Tampons
- Female barrier contraceptives
- Cuts, burns, boils, insect bites, wounds following surgery
- Childbirth
- Nasal packing to treat a nosebleed
- Having staphylococcal infection or streptococcal infection such as throat infection, impetigo or cellulitis
phases of whooping cough/bordetella pertussis (mainly affects babies less than 6m who haavent had full vaccine 3x dose yet and teenagers where their vaccines have started to fade)
catarrhal phase - 1-2 weeks long
rhinitis, conjunctivitis, irritability, sore throat, low grade fever, dry cough (all mimic other URTI so rarely diagnosed at this stage)
paroxysmal phase - 2-8 weeks long
severe paroxysms of coughing followed by an inspiratory gasp producing the classic whoop sound (<3m the whoop is less common and apnoea is the more common feature)
the paryoxsysms are more common at night and often followed by vomiting
can be severe enough to cause cyanosis
convalescent phase - up to 3m
the cough gradually decreses in frequency and severity
notably - have no wheeze or crakes - rules out bronchiolitis and pneumonia
diagnosis of whooping cough
cough <2 weeks - per nasal swab culture for bordatella pertussis
cough >2 weeks - PCR and serology for anti-pertussis toxin IgG for <5 OR anti-pertussis toxin detection in oral fluid for 5-17
o A limitation of both serology and oral fluid testing is that a pertussis vaccine within the last year can produce a false positive
FBC will show leukocytosis
management of whooping cough
hopsital admission for <6months who is acutely unwell, or in those with significant breathing/feeding difficulties or any complications like pneumonia or sepsis
antibiotics can only be given within 3 weeks of cough onset
first line = clarithromycin <1 month, aznithromycin or clarithromycin >1 month
plus supportive care - paracetamol etc and fluids
parents should be advised that despite antibiotic treatment the cough may take 3 months to resolve
The child should avoid nursery or school until they have had the cough for 21 days or 48 hours after starting abx
exclusion of school for whooping cough
they should avoid school until they have had the cough for 21 days or 48 hours after commencing antibiotics
treatment of tetanus
tetanus immunoglobulin
fluid requirement based on weights - maintenance fluids
first 10kg = 100ml/kg/day
second 10kg = 50ml/kg/day
subsequent kg = 20ml/kg/day
used for day 5 onwards
rate = roughly this figure /24
use bags of 500ml rather than 1L as this gives better control
generally 0.9% NaCl with 5% glucose +/- 10mml potassium chloride
fluid resuscitation
20mlkg bolus over less than 10 minuttes
for neonates - 10-20ml/kg over 10 minutes (under 28 days)
seek expert advice (e.g. paediatric intensive care team) if 40-60ml/kg or more is needed as part of the initial fluid resuscitation
o Consider inotropes e.g. adrenaline
o Consider endotracheal intubation and ventilatory support
hypoglycaemia management in children
o In conscious child give oral glucose drink or gel e.g. 1 slice of bread or a banana
o In non-conscious
• 1U of glucagon if no IV access
• bolus of 2ml/kg 10% IV glucose if IV access
o In all
• Followed by continuous infusion of salt solution with 5-10% glucose (60ml/kg/day) e.g. 0.9% saline and 5% glucose
WETFLAG
The purpose of WETFLAG is to work out (quickly) appropriate weight based drugs and equipment for the child you are looking after
weight energy - 4 joules/kg tube fluids - 20ml/kg bolus lorazepam adrenaline glucose - 2ml/kg dextrose solution 10% (bolus needed in a hypo)
chest compressions ratio in cardiac arrest in a child
first give 5 rescue breaths (before even checking a pulse)
then 15:2
1-8 years - use heel of one hand over lower third of sternum
less than this - two thumbs over lower third of sternum or tips of two fingers
most causes of cardiac arrest = hypoxia
innocent murmurs
STILLS MURMUR mid-systolic murmur buzzing quality left lower sternal edge softens on standing - best heard supine PULMONARY FLOW MURMUR systolic murmur best heard at upper left sternal edge disappears with valsavas softens on standing - best heard supine VENOUS HUM supraclavicular continous murmur best heard standing NECK MURMUR innocent murmur/bruit in neck are common - best heard above clavicle PERIPHERAL PULMONARY STENOSIS upper left sternal border radiates to axilla
when to refer a murmur
loud
pansystolic
diastolic
continuous, unless a venous hum
NB heart murmurs in neonates are much more likely to indicate structural heart disease and should prompt specialist assessment. Less than 1% of newborns have a heart murmur but more than 50% of those with a murmur have structural heart disease
causes of ejection systolic murmurs in children
PATAT
pulmonar stenosis aortic stenosis tetrology of fallot ASD - a split double - split S2 truncus arteriosus
pan systolic murmurs in children
VSD - very systolic - pan systolic
mitral regurgitation
partial AVSD
continuous murmurs in children
venous hum
PDA
co-arctation
complications of kawasaki disease
coronary artery aneurysm
coronary thrombosis
MI
dysarrthymias
symptoms of kawasaki disease
fever >38.5 degrees present for at least 5 days with 4/5 of the following
CRASH
congestion of conjunctivae
rash - polymorphous rash
lymphAdenopathy
strawberry tongue (or general redness to mucus membranes)
hands and feet - oedema and/or erythema and periungual desquamation
investigatinos for kawasaki
diagnosis is clinical
- FBC - leukocytosis and neutrophilia
- CRP and ESR will be raised
- Platelets may be raised to start with but will decrease throughout second and third weeks of illness
- LFTs may be slightly deranged - albumin may be low (negative acute phase reactant)
- Urinalysis may show sterile pyuria +/- proteinuria
- ECG may show conduction abnormalities due to carditis
- Echo to assess for aneurysms - at onset, then 6-8 weeks then 12 months
management of kawasaki
usually cared for as inpatients and put on bed rest due to risk of myocardial events
high dose IV immunoglobulin (2g/kg as a single infusion over 10-12 hours - but may require a second dose if fever not resolving by 36 hrs later)
aspirin until fever resolves - how much is given depends on symptoms - but usually given high-dose aspirin until fever subsides, then may be prescribed low-dose until 6-8 weeks after the start of their symptoms when their next echo is due (NB has association with Reye syndrome –> rapidly progressive encephalopathy (vomiting, confusion, seizures, LOC))
refractor cases - steroids, anti-TNF, plasma exchange…
follow-up is very important for cardiac review e.g. echo - CV disease is a severe complication of Kawasaki disease- which most commonly presents as coronary artery aneurysms and can lead to arrythmias, MI and ultimately HF
cyanotic (right to left shunt) is due to all the Ts plus what else
pulmonary atresia
hypoplastic left heart
presentation of TOF
3 categories
mild-pink TOF - has mild pulmonary stenosis/RVF and usually asymptomatic, presents by 1-3 years
moderate-severe - cyanotic TOF - presents in first few weeks of life with cyanosis and respiratory distress - may have recurrent chest infections and failure to thrive
extreme - further divided into TOF w pulmonary atresia or absent pulmonary valves - presents in first few hrs of life
clubbing
low o2 sats
murmur - ejectinon systolic
hypoxic/tet spells - restless, cyanosed and can cause LOC (CO2 accumulates which stimulates fast deep respirations which worsens shunt - may be precipitated by dehydration, anaemia or prolonged crying - all cause tachycardia and reduced systemic vascular resistance which will worsen shunt and deoxygenation)
investigations for TOF
- ECG (RVH)
- CXR - boot shaped heart and reduced pulmonary vascular marking due to decreased blood flow
- Echocardiography - gold standard to diagnose
- Cardiac MRI pre- and post-operatively can be done - more so in tertiary centres
- Karyotyping if genetic syndromes suspected
management of TOF
MEDICAL
o Squatting - parents may observe infants squatting or keeping knees to their chest - this helps them improve venous return therefore increasing systemic resistance
o PG infusion to keep PDA open in more severe-extreme forms - must be started urgently following delivery
o BB - propranolol is commonly used in tet spells and prophylaxis in severe disease (decreases HR thus improved venous return so improved right ventricular outflow)
o Morphine - reduces respiratory drive therefore reduces the abnormal breathing that form tet spells
o Saline 0.9% bolus can be used in tet spells to increase pulmonary blood flow through right ventricular outflow tract
SURGERY
o Definitive treatment is with closure of the VSD and relief of the RVOT with placement of a graft between the right ventricle and pulmonary artery from 4 months onwards (or removal of muscle causing the obstruction)
FOLLOW-UP
o Due to risk of long-term complications, will require regular ECG, echo and in cases of exercise intolerance = cardiopulmonary exercise testing
in furture - may need pulmonary valve replacement due to pulmonary regurgitation as a result of TOF surgery
egg on a string vs boot shaped heart
boot shaped in TOF
egg on a string in transposition of great arteries
management of transposition of great arteries
prostaglandin to increase patency of ductus arteriosus
in some it may be necessary to do an early balloon atrial septostomy to reopen foramen ovale
eventually will require an arterial switch operation - usually done before the age of 4 weeks
management of VSD
Medical
o Increase calorie intake
o Diuretics like furosemide to relieve pulmonary congestion
o ACEi to reduce afterload - allows more blood through the aortic valve and less through the VSD
o Digoxin
Surgery
o Surgical repair may not be required for a small muscular VSD, as this will close on its own as the heart grows
o Large VSDs will require medical management up to the point of surgical repair at 3 – 4 months, this can be trans-catheter repair or open surgery
Long-term
o There is an increased risk of endocarditis so advised to maintain good dental hygiene
management of ASD
Conservative
o If <5mm should close within 12 months of birth
o In adults, if patient is presenting with no signs of right heart failure and a small defect, then monitor every 2 – 3 years with echocardiogram
Medical
o In children with HF, diuretics, ACEi, digoxin, higher calorie intake may be needed
Surgical repair - >1cm
o Via cardiac catheterisation or open
o This is usually performed at about 3 – 5 years’ old (complete AVSDs between 3-6m)
what does congenital diaphragmatic result in
pulmonary hypertension and pulmonary hypoplasia
because abdominal organs migrate up into chest cavity
usually diagnosed on us scans
can present soon after bith with cyanosis, tachypnoea, tachycardia, asymmetry of chest wall, absent breath sounds, bowel sounds over chest wall
investigations for coeliac disease
- Before testing, confirm that the person has eaten gluten-containing foods at least twice every day over the previous 6 weeks
- FIRST send-off serology (before any biopsy)
o Use IgA tTG and total IgA as first line. IgA EMA can be used if IgA tTG is unavailable.
(If IgA is deficient, this will cause a false-negative result so test for IgG tTG, IgG EMA or IgG DGP (deamidated gliadin peptide) instead) - FBC - IDA is a common presentation - could also do vitamin B12 and folate
- Small bowel – 2 biopsies of the bulb and at least 4 of the distal duodenum - will show presence of intra-epithelial lymphocytes, villous atrophy and crypt hyperplasia
- Skin biopsy
o In any patient with skin lesions suggestive of dermatitis herpetiformis
management of coeliac disease
gluten-free diet - consists of most dairy products, fruit and veg, meat and fish, potatoes, rice, gluten-free flours
vitamin replacement if deficient
consider annual blood testing
o Coeliac serology
o FBC and ferritin
o TFTs – to screen for autoimmune thyroiditis
o LFTs – to screen for autoimmune hepatitis
o Vitamin D, B12, red cell folate and serum calcium
o Electrolytes – for Addison’s
patients with coeliac disease often have functional hyposplenism - making it important they receive the pneumococcal vaccine and yearly influenza vaccines
what is infantile colic and how can it be treated
crying with no apparent cause in a healthy baby with drawing up of the knees
usually resolves by 4 months
may be due to sensitiesed pathways in the gut viscera
simethicone may help but has not been proven to give a wide benefit - is an anti-flatulent
what is hirschprungs disease
absence of parasympathetic ganglion cells in the myenteric and submucosal plexus of the rectum causing a functional obstruction
mesenteric adenitis vs appendicitis
mesenteric lymphadenitis = associated with a viral infection leading to inflammation of mesenteric lymph nodes
no loss of appetite and has a high-grade pyrexia around 39 whereas appendicitis is usually low grade around 38
also has more diffuse abdominal pain because there is no peritonism
also normally normal WCC and CRP in mesenteric adenitis
(usually no treatment needed - maybe abx if bacterial cause)
score to see how useful it is they have appendicitis
paediatric appendicitis score
investigations for food allergy
skin prick - swollen red bump will form if allergic
RAST testing to look for specific IgE antibodies
or ELISA - widely replaced RAST
in severe cases when allergen cannot be found - start a full elimination diet in which only have hypoallergenic foods for 1-2 weeks e.g. lamb, rice, water followed by retintroduction of food
lactose intolerance in children
often post-viral gastroenteritis e.g. rotavirus
most cases are short lasting - 4-6 weeks
management of cows protein allergy
o In exclusively breast-fed infants, this is achieved by a maternal exclusion diet to these proteins
o In formula fed infants feed with a hydrolysed formula (short peptides)
o If symptoms severe, or unresponsive to hydrolysed formula, then an elemental (amino acid) formula may be required
o After weaning, introduce a cow’s milk protein free diet (supplement with oral calcium if required)
o Consider a cow’s milk protein challenge after 6–12mths
follow-up after anaphylaxis
observe for 6-12 hours from onset of symptoms depending on response to emergency treatment - is due to possibility of a biphasic reaction
ofter referral to specialty allergy clinical - skin prick tests to identify allergen
inform person that a blood sample may be required at follow-up allergy clinic to establish what mast cell tryptase is at baseline
suggest a medicalert bracelt
offer an adnrelaine injector - 0.15mg in children, 0.3mg in adults
adrenaline IM dose in anaphylaxis in children and how much can be given
- 5mg >12
- 3mg in 6-12
- 15mg in <6
assess response after 5 minutes and repeat at 5 minute intervals until adequate response - people needing lots of repeat doses may need IV adrenaline - requires ICU physician help
when to measure mast cell tryptase in anaphylaxis
one as soon as possible after emergency treatment starts
second ideally within 1-2 hours, no later than 4
(should also monitor patient with pulse oximetry, BP and ECG)
management of GORD
thickened milk feeds in those that are formula fed
ensure not overfed - 150ml/kg/day max
small frequent meals
avoid food before sleep
gaviscon (alginate therapy) immediately after feeds
if no response after 2 weeks can try gastric acid reducing drugs like ranitidien or omeprazole
or prokinetic drugs like domperidone
surgery - fundoplication
what VBG will pyloric stensosi cause
hypochloraemic, hypokalaemia metabolic alkalosis (vomiting up Hcl and potassium)
surgery for pyloric stensosi
ramstedt pyloromyotomy
general investigations for diarrhoea
stool - microscopy, fat globules and faecal eslastase (low in pancreatitis), culture, pH (low in carb malasorption), fecal occlut blood (colitis)
bloods - FBC, UE, raised eosinophils in food hypersenstivity or parasties, raised CRP and ESR in inflammation, RAST in food allergy
AXR or US for NEC
hydrogen breath test for lactose malabsorption of H pylori
sweat test/genetics in CF
biopsy for coeliac and IBD
rectal biopsy in hirschprungs
investigations for gastroenteritis
- Consider stool microbiology if
o the child has recently been abroad or
o the diarrhoea has not improved by day 7 or
o there is uncertainty about the diagnosis of gastroenteritis - Perform stool microbiology if
o you suspect septicaemia or
o there is blood and/or mucus in the stool or
o the child is immunocompromised - Do not routinely perform blood tests, however measure UE, creatinine, glucose and urea if
o IV fluids are going to be used.
o There are symptoms/signs of hypernatraemia (jittery, increased muscle tone, hyperreflexia, convulsions, drowsiness or coma) - Measure acid-base status and chloride concentration if shock is suspected
management of gastroenteritis
continue with usual feeds including breastfeeding, encourage oral intake, offer ORS as a supplement if at increased risk of dehydration, discourage foot juices and fizzy drinks (the sugar will draw water into the gut making it worse)
if dehydrated IV therapy (glucose-saline) if shock, evidence of dehydration despite ORS, if child is persitently vomiting whrn ORS is given OR can just give ORS orally plus maintenance fluids (consdier NG if refusing oral) amount of ORS = <5 give 50ml/kg over 4 hours with maintenance fluids, >5 then give 200ml ORS after loose stools in addition to child's normal intake
other
off liscence ondansetron
antibiotics if suspected or confirmed septicaemia <6m with salmonella
following rehydration - start milk straight away, re-introduce solids slowly, avoid fruit juices and carbondted drinks until diarrhoea resolves, wait to return to school until 48 hours after, avoid towel sharing, clean toilet
avoid any anti-diarrhoeals
4 typical symptoms of NEC
feeding intolerance
bilious vomiting
haematochezia/bloody stools
distension
others = decreased bowel sounds, palpable abdominal mass, respiratory distress, shock, bradycardia, visible intestinal loops, sepsis, lethargy
key points in a pregnancy history
Was the mother under hospital-led maternity care (and if so, why)?
Was this a high-risk pregnancy?
Did the mother or baby develop any problems during the pregnancy?
Pregnancy gestation?
Method of birth?
Any complications with the birth (both mother and infant)?
investigations for NEC
Bloods inc. culture, metabolic acidosis
US
AXR - pneumatosis intestinalis, dilated bowel loops, may see signs of perforation
management of NEC
NBM
NG
IV fluids resuscitation
IV Abx - broad spec for 10-14 days
ventilatory and circulatory support if required (vasopressors like dopamine)
Surgery in up to 50% - main indication is perforation
when does NEC present
usually first 2 weeks of life
3 random investigations for constipation
bowel transit studies
anal manometry
spinal imaging if neuro cause
what sort of laxative is movicol vs lactulose
movicol = osmotic lactulose = osmotic
management of constipation
movicol first line
nice say to add a stimulant laxative like senna if movicol doesn’t lead to disimpaction after 2 weeks
if Movicol is not tolerated, substitute a stimulant laxative like senna, either on its own or if stools are hard, then in combination with something to soften it like lactulose
can then offer a large volume polyethylene glycol (PEG) electrolyte solution bowel clean out (may require NG administration for rapid infusion)
enemas if no response to above
where is the typical transition zone in hirschprung’s
rectum or sigmoid = short segment disease
in 10% it extends past the sigmoid to the splenic flexure = long segment disease
rarely the whole colon is affected = total colonic aganlionosis
3 common symptoms of hirschprungs
bilious vomiting
distension
failure to pass meconium
diagnosis of hirschprungs
Bloods US AXR - distal obstruction Contrast enema - not if perforated - narrow distal end of colon Rectal biopsy - no ganglion cells
contrast enema can rule out differentials such as meconium plug syndrome, meconium ileus (thicker than normal), intestinal atresia, malrotation
management of hirschprungs
NBM IV fluids IV Abx - esp if enterocolitits NG Rectal washouts Surgery - with pullthrough procedure (traditionally a 3 stage procedure was perofmred) - will require multiple biopsies to determine site of transition zone
most have a normal life after surgery - may have some degree of incontinence until they’re a teenager - short bowel syndrome is another complication
main complication of hirschprungs
enterocolitis due to stasis of feces - treat with IV broad spec abx and fluid resuscitation
most common site for intussception
most commonly the ileum into the caecum through the ileo-caecal valve
can be following lymphoid hyperplasia of payer’s patch will creates a lead point for peristalsis to pull it through (or meckle’s) - although most is idiopathic
presentation of intussception - rare after 2 years
Spasms of colic w pallor/ screaming/ drawing-up legs
Lethargic/normal between episodes
Later- bile-stained vomit and red currant jelly stools
Dance’s sign
Sausage shaped mass
investigations for intussception
Bloods - metabolic acidosis
US - target sign
AXR - small bowel obstruction and sausage shaped mass
Contrast enema - obstruction
management of intussception
IV fluids
NG
Radiological reduction - rectal insufflation of air - painful may need morphine
Surgery if this fails - can resect or try to decompress - try identify if patholgoical lead point is present if possible
most common type of volvulus in children vs adults
adults = sigmoid
babies and small children = midgut
otheres = caecum
diagnosis of volvulus in children (presents in baby or small child - more common in premature)
Bloods - metabolic acidosis
US - rule out intussusception and may see abdominal mass
AXR
Upper GI contrast study - bird beak sign
selected patients may need studies of lower bowel with barium enema
managemnet of volvulus in children
(Flatus tube and sigmoidoscopy (endoscopic detorsion) for sigmoid)
NBM
NG tube
IV fluids
Ladd’s procedure - and any dead bowel removed
management of biliary atresia
abx to prevent cholangitis UDCA to encourage bile flow fat soluble vitamines kasai procedure before 8 weeks of age liver transplant if fials
notes on sickle cell crisis
vaso-occlusive crises - commonly hands and feet
dactylitis
acute chest syndrome - precipitated by cold weater, dehydration, infection
stroke
infections - are functionally hyposplenic by 1 year so need pen V prophylaxis
aplstic crisis typically after parvovirus b19
priapism
avsaculr necrosis
retinopathy
delayed growth
treat with daily folic acid, vaccines, pen v prophylaxis, hydroxycarbamide, bone marrow transplant
management of asthma in children
UNDER 5 saba saba and ics saba and ics and leukotriene antagonist refer
5-12 saba saba and ics saba and ics and luekotriene antagonist saba and ics and laba switch to MART increase steroid dose refer
ICS is recommended when beta 2 agonist is being used more than 3 times per week, have asthma symptoms 3 times a week, symptoms disturb sleep at least once a week AND consider if a child >5 has had an exacerbation in previous two years that required systemic steroids
discharge wheeze plan
remeber to give this after an acute exacerbation
- Written information about inhaler technique, how long to continue with steroids, when to restart a preventer inhaler, and information about any other drugs
length of course of oral prednisolone in asthma exacerbation
3 days in children
5 days in adults
when to dicharge in asthma exacerbation
o SaO2 >94%, bronchodilators taken at intervals of 4-hourly or longer
o Review by GP 48 hours later
o Always give a discharge wheeze plan
(NB adults is - need to be stable on discharge medication for 12-24 hours)
cause and epidemiology of bronchiolitis
under 2 years
peaks at 3-6 months
caused by RSV
symptoms and investigations for bronchiolitis
avoid overfeeding in bronchiolitis because this can restrict feeding
NICE say <2 years w 1-3 day history of coryzal symptoms followed by all 3 of
persistent cough (non-productive)
tachypnoea or chest recession
wheeze or crackles
symptoms generally last 10 days (day 2-4 is worst)
pulse oximety
viral throat swab for RSV and other viruses via PCR - or can do naspharyngeal aspirate
can say you would do a capillary blood gas if not improving on treatment
(ABG if severely unwell)
blood and urine culture if pyrexic
CXR can be performed if deteriorating but should not routinely be performed or used to determine need for Abx becasue bronchiolitis can mimic pneumonia
management of bronchiolitis - not bronchodilators because children dont have sufficient receptors in airways to resond (start form 1 years)
decide if home or hospital - hosp if apnoea, looks unwell to healthcare professional, respiratory distress, >70/min, central cyanosis, <92% sats
primary care - anti-pyretics if distressed, saline nasal drops, feed little and often (obligate nasal breathers), lots of fluids
secondary
oxygen via nasal specs or a headbox
NG feeding as needed (if not tolerating then TPN)
hypertonic saline
upper airway suction if secretions / nasal suction
nebulised adrenaline has best evidence compared to other nebulised bronchodilators
CPAP in impeding resp failure if not improving on simple oxygen
if still not improving - do itubation via calling anaesthetists
antiviral therapy with ribavirin should be reserved for immunodeficient patients and those with underlying heart or lung disease, although its benefit is uncertain
antibiotic for tonsillitis and pharyngitis
phenoxymethylpenicillin
avoid amoxicillin because it may cause a rash in cases of EBV (tonsillitis is usually due to group A beta-haemolytic strep or EBV)
antibiotic for otitis media
amoxicillin
management of pneumonia
admit if <92%, RR >70, CRT >2…
oxygen if <92%
antipyretics if needed
antibiotics - amoxicillin first line for 7-14 days - for severe then co-amoxiclav (and if associated with influenza)
IV abx if cannot absorb oral or in those with severe symptoms
IV fluids if needed
viral induced wheeze vs bronchiolitis (NB acute ashtma exacerbation unlikeyl firs tpresention - usually have history of wheeze or somethig)
broncholitis has fine inspiratory crackles
both have wheeze
bronchiolitis is mainly <1 year but can be up to 2
management of viral induced wheeze
as for acute asthma - salbutamol, motelukast, oxygen (can use ipratropium if not working)
rarely need ventilation/intubation
aim for O2 >92%
but do not response to inhaled steroids
prescribe antibiotics if suggest bacterial infection like amoxicillin
usually will grow out of this by age 6 - usually due to RSV, rhinovirus or influenza
(will be well in between asthma unlike asthma where they may have difficulty breathing at night and in sports)
how is CF picked up on newborn spot check
IRT is measured (immunoreactive trypsinogen)
what can CF present with
meconium ileus
haemorrhagic disease of newborn - lack of vit K
prolonged jaudice - due to thickened biliary secretions which causes plugging
recurrent infections
failure to thrive
nasal polyps
pancreatitis
chronic pulmonary disease
infertility
rectal prolapse due to frequent coughing and hard to pass stools
investigatinos for cf
NICE say can diagnose when
- No symptoms but infant screen positive, and sweat and gene tests for confirmation
- Symptoms with sweat or gene test to confirm
- Symptoms but normal sweat or gene results - this is rare
sweat test - chlroide >60mmol/L with sodium>chlroide - 2 occasions
genetic testing
spirometry >5 years
sputum microbiology on regular basis
check for vitamin levels
baseline bloods and glucose for diabetes
pancreatic insufficiency via stool elastase - low in indufficiency (and present of fat globules in stool)
semen analysis
cxr or ct of thorax in lung disease
baseline bloods, glucose tolerance test and bone profile at annual assessmsnets
heel prick tests for immuno-reactive trypsinogen
managmenet of cf
LUNG
chest physio
regular sputum cultures
exercise
prophylactic abx - e..g. fluclox up to age 3, consider up to 6
chronic abx if colonised with p aeruginosa
if they get an infection do high dose and at least 2w - may need IV
oral azithromycin for people with repeated exacerbations or deteriorating lung function
annual flu vaccine
bronchodilators
neb dornase alfa (recombinant enzyme) to aid sputum removal - neb mannitol in those than cant use dornase alfa
nebulised hypertonic saline also thins mucus
treat polyps (nasal steroids at first then polypectomy)
transplant - a major operation that is not without risks and requires life-long immunosuppression - medications which have many serious side-effects. It also does not address extra-pulmonary manifestations of CF
infection control - avoid cross-infection - need own clinic room which is cleaned before, and side room in hospital
PANCREAS/GI creon with all meals high protein, fat and calorie diet fat soluble vitamin supplements liver transplant in liver failure (before this can try UDCA)
INFERTILTY
ICSI with surgical retrieval of sperm - but risk of passing it on
OSTEOPROSIS
vitamin d and calcium and regular dxa
juvenille idiopathic arthritis key points
morning stiffness, pain, swelling, knees, ankles and wrists first
clinical diagnosis - esr, crp often raised, ana can be positive, rf and hlab27 can be positive
manage with physio, ot, hydrotherapy, exericse, nsaids, steroid injections, methotrexate in polyarthritis, biological agents for refractor like anti-tnf
presentation, investigations and management of testicular torsion
acute pain (may come on with exericse), may have episodes of brief similar pain when torsion corrects itsel, n and v, easing pain may = torision correcting itself, red, swollwn, lifting over symphysis increases pain, bell clapper position, absent cremasteric reflex, higher than other one
investigate with us and doppler, urinalysis for uti, but if high suspicion then surgery asap
management - reduce torsion manualls then bilateral orchidopexy within 6 hours after symptom onset
can put in prosthesis at time or later date if orchiectomy has to be performed
when to refer with cryptochoridism
bilateral testes - refer within 24hours
unilateral at birth - re-exaiine at 4-5 months
at 4-5 months - arrange referall to paedatric surgery to be seen by 6 months
short term relief for enuresis
sublingual desmopressin
others = eneuresis alarms, waking child in night, start charts
tetrad of henoch schonlein purpura
palpable purpuric non-blanching rash
joint pain / arthritis - especially in knees and ankles (permanent deformity doesnt occur)
gi symptoms +/- blood diarrhoea- may precede rash
renal involvement - IgA nephritis with microscopic haematuria and proteinuria (nephrotic syndrome may also occur)
it is often triggered by preceding URTI or gi infection
often have a low-grade fever
differentials for a non-blanching rash
meninogococcal septicaemia leukaemia ITP - idiopathic thrombotyopenic purpura haemolytic uraemic syndrome HSP
investigations and management of HSP
investigations - clinical. urinarlysis for haematuria and proteinuria, raised esr, crp, UE for renal involvement, serum albumin for nephrotic, serum creatinine for renal involvement, protein: creatinine ratio to quantify proteinuria, serum IgA raised, abdominal US for obstruction (4% associated with intussception), renal biopsy if persistent nephrotic syndorme
autoantibody screen for other ct disorders like ANA for sle
is self limiting; rest, rehydration, nsdais, monitoring of urine and bp once monthly for 6-12m (provide urine, then bp)
steroids can be considered for severe gi pain or renal invovelemnt
admission in some cases if abdominal or renal complications
most common causes of tonsillitis
group a beta-haemolytic strep/strep pyogenes
EBV
rarely diptheria
virtually any other virus can also cause it e.g. adenovirus
differentials for tonsillitis
common cold
pharyngitis
glandular fever- petechiae on palate, atypical lymphocytosis
tonsillar malignancy
epiglottitis
quinsy or peritonsillar abscess
hand foot and mouth disease (supportive treatment only)
feverpain score
no cough or coryza attends within 3 days fever in last 24 hours purlulent tonsils severely inflammed tonsils
2 or 3 consider delayed prescription
4 or 5 consider antibioitcs
tonsillitis managmenet
low feverpain/centor - reassurance, watchful waiting, antipyretics
centor pain 3 or 4/fever pain 4 or 5
studies have shown abx decreases symptom duration by less than 1 day
can do delayed antibiotic statedgy
phenoxymethylpenicillin - avoid amoxicillin due to possibility of glandular fever
analgeisa inc topical ones for swallowing
immediate abx if very unwell or complications like peritonsillar abscess
steroids for those with glandular fever that might need hosp admission with severe dysphagia
tonsillectomy if >7 eps in 1 yr, >5 eps in 2 years, >3 eps in 3 years
viral croup cause and alternative name and peak incidence
laryngotracheobronchitis
parainfluenza
affects 6m- 3 years - peak incidence of 2 years
previous intubation is a risk factor
presentation of croup
normally starts with nonspecific symptoms of viral URTI - runny nose, cough, fever
after couple days - barking cough and hoarseness which is worse at night and when child is running around playing
can have low grade fever
stridor
normal chest sounds
tends to last 3-7 days but can persist for up to 2w
investigations for croup
- Normally clinical diagnosis
- SaO2 <95% indicates significant respiratory impairment
- It is important to weigh the benefits of investigations such as CXRs and blood tests against the risks of distressing the child and making the symptoms worse
o On a CXR can see a steeple sign (subglottic narrowing looks like a church steeple) - Can do bloods - CBG if necessary
- Never perform a throat examination on a patient with croup due to risk of airway obstruction / laryngospasm
management for croup (barking cough, hoarse voice, stridor = harsh sound on inspitaiton) peak incidence at 2
most can be managed at home
hospitalize if moderate or severe resp failure, any suspicion of peritonsillar abscess, epiglottitis, foreign body inhalation
keep child calm because cyring increases oxygen demand
paracetamol or ibuprofen for discomfort or fever
adequate fluids
advise to seek medical care if symptoms worsen e.g. intermittent stridor at result or high fever or HR as could indicate bacterial tracheitis
single dose of dex
in hospital
oxygen
nebulizewd adrenaline
single dose of dex - can be repeated if more severe or use IV
thigns suggesting they need amission = stridor at rest, resp distress, lethargy (not acting normal) or very freuqnt barking cough
cause of epiglottitis and age of presentation, diagnosis and management
haemophlius influenza type b - others = strep, psueomonas
2-5 years
diagnose via flexible laryngoscopy
- Usually is conservative with IV or oral Abx with oxygen
- Intubation may be needed
- Surgical tracheostomy may be required in patients with severe obstruction where intubation isn’t possible (or nasotracheal tube is a step before this)
management of foreign body inhalation
- If the obstruction is a soft bolus, then the use of smooth muscle relaxant (hyoscine butylbromide) and swallowing a fizzy drink may be successful
- Direct visualisation
o Anaesthetise the throat using a xylocaine spray
o Use a good light to examine the patient and use forceps to grasp and remove the object - If there is airway compromise or the object is known to be sharp or nothing is seen on direct visualisation, there needs to be urgent referral for endoscopic removal under general anaesthetic
- In rare cases where endoscopy/bronchoscopy cannot remove the object, then thoracotomy (open surgery) may be required
peritonsillar abscess vs retropharyngeal abscess
- A peritonsillar abscess can cause trismus (difficulty opening the mouth)
- A retropharyngeal abscess can cause torticollis (stiff neck)
- Both can cause fever, drooling, dysphagia, odynophagia (painful swallowing), muffled voice, dyspnoea, STRIDOR
causes of stridor
- Apyrexial illness such as foreign bodies, anaphylaxis, injuries, and tumours
- Pyrexial illness such as epiglottitis, croup, retropharyngeal abscess and diphtheria
neuroblastoma urine
usually raised urinary catecholamins - vma and hma found in urine
symptoms of juvenille hypothyroidism
as for adults, but can also include delayed puberty and SUFE - slipped upper femoral epiphysis
diagnosis of CAH
raised 17-OHP due to deficiency in 21-hydroxylase
low glucose
low sodium and high potassium
corticotropin stimulation test (similar presence to short synatchen test)
pelvic US in person with ambigious genitalis to see if presence of uterus
karotype and genetic analysis
types of cerebral palsy
spastic - increased tone and reflexes, scissor gait, can be hemiplegic, paraplegic or quadriplegic - problem in cortex
athetoid/dyskinetic - hyperkinesia (increased activity) described as stormy movement (choreea = irregular and sudden, athetosis = slow, writhing movements, dystonia = twisting movements) - problem in basal ganglia
ataxic - loss of coordination - problem in cerebellum
mixed
nb cp is a static disorder and non-progressive
causes and presentation of cp and diagnosis
causes = birth asphyxia, birth trauma, intraventricular haemorrhage, meningitis, head trauma, genetic mutation
present with low APGAR score, early motor features like fidgety movements, abnormal tone, late rolling/crawling, early hand preference before 1 year, not walking by 18 months, persistent primitve reflexes
is associated with learning difficulties, epilepsy, squints, hearing impairement
diagnosis is clincial - can do eeg to detect damage from hypoxia or mri if cause unknown
management of cp
physios, OTs, speech therapists
spasticity can be eased with diazepam, baclofen
botulinum toxin a can be considered if focal spasticity
mobility aids with wheelchair
mental health care
surgery for scoliosis, tendon lengthening, osteotomy
diagnosis of adhd
6 or more symptoms from either 2 category
Inattention
o Forgetful in daily activities
o Easily distracted
o Loses things necessary for tasks e.g. school materials
o Trouble organising tasks
o Does not follow instructions and fails to finish schoolwork or chores
o Does not seem to listen when spoken to directly
o Often doesn’t listen when spoken to directly
o Fails to give close attention to details or makes careless mistakes in schoolwork or other activities
Hyperactivity and impulsivity
o Often fidgets with or taps hands or feet or squirms in seat
o Leaves seat in situations where remaining seated is expected
o Runs or climbs in situations where it isn’t appropriate
o Unable to play or take part in leisure activities quietly
o Is often ‘on the go’ acting as if ‘driven by a motor’
o Often talks excessively
o Often blurts out an answer before a question has been completed
o Often has trouble waiting his/her turn
o Often interrupts or intrudes on others (e.g. butts into conversations or games)
in addition - several symptoms present before 12 years and in 2 or more settings, with clear evidence it inteferes with school or social functioning
management of adhd
10 week watch and wait period to see if symptoms change or resolve first
offer referal to child psychaitrist or CAMHS and group-based ADHD focused support and CBT and social skills training
liase with school
teachers should have approprate training for behavioural strategies in the classroom
stress importance of balanced diet and exericse
medication only used if environmental modification and support groups have failed
methylphenidate/ritalin first line - only if >5
do baseline physical assessment before - are potentially cardiotoxic
SE include stunted growth, HTN, palpitations, disturbed sleep, problems with anxiety/depression/agresion, decreased appeteite - so monitor growth, BP and pulse
what is spinal muscular atrophy
autosomal recessive disorder that leads to degeneration of anterior horn of spinal cord
causes muscle weakness, wasting, absent reflexes
seizure differentials
epilepsy
non-epileptic paroxysmal episodes aka dissociative seizures aka pseudoseizures
benign neonatal speep myoclonus
breath holding attacks
masturbation
reflex anoxic seizures where heart stops due to excessive activity of vagus nerve
benign paroxysmal torticollis
syncope
daydreaming can look similar to absence seizure
fabricated seizure
marcus gunn phenomenon - rapid movements of eyelids each time jaw moves
infantile spasms/wests syndrome
hallucinations in psychiatric disorders
differentials for eeg changes with seizure
epilepsy metabolic - hypoglycaemia, sodium, low calsium, low mg head trauma meningitis or encephaltisis poisons febrile seizures
neonatal seizure management
> 3 minute then phenobarbital loading dose
can give further dose if still persisting
then step up to levetiracetam or phenytoin then midazalam
3 main causes of meningitis
strep pneumoniae
neiseria meningitides
haemophlius type b
in neonate - 3m - group B strep is another important cause - usually acquired from the mother at birth - as well as e coli and listeria monocytogenes
encephalitis vs encephalopathy
encephalitis = encephalopathy secondary to infective process
encephalopathy is degeneration of brain function / impaired cognition +/- focal neurological signs - is typicallty matched with a typical eeg trace with abundance of slow waves
and reduced consciousness via GCS
triad of viral encephalitis and presentation in neonates
fever
headache
altered mental staus
a disseminated infection causes constitutional signs like shock, jaundice, GI bleeding, rash
neonatal HSE usually presents between 4 and 11 days after birth, with lethargy, irritability, poor feeding, tremors, seizures and a bulging fontanelle (is associated with temporal lobe epilepsy)
investigations for encephalitis
neuro exam
gcs
bloods inclulding glucose
when stable LP - PCR tests, wcc, glucose, lactate, protein
neuroimaging with mri - provides sensitive detection of demyelination and can show oedematous changes seen in early phases
EEG - frequently abnormal and can somtimes help determine localisation in early stages
sections of child protection act
44 = emergency protection order - social worker applies to court - lasts 7 days and social workers can gain parental responsibility if necessary
46 = the child may be kept at the police station or removed to accommodation such as relative’s home, foster care or via children’s services - up to 72 hours - parental responsibility is still required for medical examinations
47 = to decide whether and what type of action is required to safeguard a child who is suspected of suffering harm (the child’s parents/carers will be interviewed, as well as the child (unless the child is too young). The assessment will also include information from the child’s school, doctor and other professionals a conference must be held within 15 days of when enquiries were initiated)
Children may be defined as ‘children in need’ (section 17) following investigation, these are children who need input from local authority service to maintain a reasonable standard of health or to prevent harm- the parents still have PR, but there is input and assistance to the child’s care
differential for a non accidental injury
bleeding disorder
non-pathological bruising e.g. petechial haemorrhage of the upper body following a tantrum or vomiting, bruising following scratching
precocious vs delayed puberty ages
precocious = before age 8 in females and age 9 in males
delayed = 14 in females, 16 in males
causes of precocious puberty
central/true - gonadotrophin dependent
idiopathic
tumours e.g. of hypothalamus
other cns lesions like arachnoid cyst, hydrocephalus
peripheral ovarian or testicular tumours mccune albright syndrome CAH or adrenal tumour hcg secreting tumour iatrogenic due to exogenous sex steroid administration
treatment of central precocious puberty
suppression of axis with long acting gnrh analogue
constant stimulation of gnrh receptor results in down regulartion of the receptor
administered via sc or im injection
genetic mechanisms of ds
meiotic non-disjunction - pair of 21 chromosomes dont separate in meiosis
robertsonian translocation - usually with 14 and 21 - parnets with a balanced translocation can either have a child with a balanced translocation, a child with ds with the unbalaned form or a child with normal chromosomes
mosaicism
features of ds
short neck, flat back of head, lighter spots in iris (brushfield spots), epicanthic folds (fold in upper eyelid), single palmar crease
hypotonia congeital heat defects - commonly avsd duodenal atresia hirschprungs umbilical hernia, imperforate anus
in later life increased risk of - otitis media, cataracts, hypothyroidism, ALL, coeliac, AD, epilepsy
investigations for sepsis
- Diagnosis of sepsis is clinical
- Observation after giving antipyretics can help distinguish sepsis from a less severe infection
- FBC and other baseline bloods
- CRP and ESR
- Blood culture
- Viral PCR for N meningitides
- Blood gas - metabolic acidosis with raised lactate
- Urine culture
- Stool culture if diarrhoea present
- <3 months and those with high WCC - LP should be performed
- CXR can be considered if chest signs present
- Other cultures - wound culture, all ports of any indwelling catheters, sputum swab
- Refer to nice traffic light system for identification of a serious illness
managemenet for sepsis
a-e and sepsis 6
monitor urine output with catheterisation if necessary
oxygen high flow
IV/IO fluids in 20ml/kg boluses (if repeated boluses are required, consider intubation and ventilation as pulmonary oedema is more likely)
IV/IO antibiotics
in general, start with a third-generation cephalosporin (high dose cefotaxime or ceftriaxone) and use the following antibiotics for specific groups of patients (e.g. neonatal sepsis - IV benzylpenicillin with gentamicin, intra-abdominal cause – consider gut anaerobes – metronidazole, gentamicin)
blood sugar <3mmol/L - correct with 2ml/kg bolus of 10% dextrose
treat underlying condition
further management includes inotropes or intubation and ventilation
investigations and management for perthes
trendelenburg’s test - stand on one leg for 30 seconds - positive is when pelvic drops towards unsupported side rather than staying level
x ray can confirm - can do mri if negative and still suspicious
management with physiotherapy, analgesia, and restriction of movement/weight baring until ossification is complete <6
surgery if >6 - femoral or pelvic osteotomy (operation to cut a bone followed by realignment of the bone ends to allow healing)
sufe diagnosis and management
trendelenburg positive (stand on one leg for 30 seconds - positive is when pelvis drops towards unsupported side rather than staying level)
X ray if unconclusive if not MRI
classified as an emergency due to risk of avascular necrosis of femoral head - therefore mandates immediate referral to paediatric othopedics
management - restriction (should not weight bear), analgesia, surgical stabilistaion with internal fixation across the growth plate
examination findings with sufe
decreased rom - decreased internal rotation
confirmation and screening of ddh
the following require US at 6w after birth - first degres family history, breech presentaiton, multiple pregnancy
all other infants are also screened at 6w using barlow and ortalini - if positive then have us to confirm if under 6 months, or x ray if older
management - most unstable hips will spontaneously stabilise by 3-6w of age, any hip that remains unstable requires pavlik harness, or older children may require surgery
osgood schlatter disease
unilateral knee pain that is worse with movement and during exericse
investigations and management for pyloric stenosis
- A test feed should be performed with NG tube in situ and stomach aspirated - while the child is feeding, examiner can palpate for a pyloric mass and observe for visible peristalsis (can palpate an olive shaped mass)
- US will reveal hypertrophy
- cap blood gas - hypokalaemia, hypochloraemic metabolic alkalosis
- 20ml/kg boluses as required for resuscitation
- NG tube - aspirated at 4 hourly intervals
- Then rehydration should be commenced at 150ml/kg/day
- Blood gases and UE should be checked regularly
- Is managed surgically with Ramstedt’s pyloromyotomy - once stablised
- Baby can resume feeding over 6 hours, although there may be some residual vomiting
management of nephrotic syndrome
high dose steroids
the majority of children with minimal change disease will respond to steroids - but most will have a relapse
low salt diet to avoid worsening the odema
prophylactic antibioitsc - they will be leaking immunoglobulins through the kdinesy and therefore are at high risk of infection
features of ALL
peak at 2-5 years anaemia - lethargy, pallor thrombocytopenia - easy bruising, non-blanching rash leukopenia - frequent infections may complain of bone pain due to hyperplastic marrow weight loss malaise lymphadenopathy hepatosplenomegaly testicular enlargement fever is present in 50%
FBC will either show pancytonpeia or anaemia and thrombocytopenia with significant lymphcytosis
blood film - presence of blast cells
should have LP to check for cns involvement, bone marrow aspirate to confirm, cxr to exclude mediastinal mass
ddx = burising due to ITP trauma or NAI, recurrent infections due to immune deficiecny, reactive lymphadenopathy to infection, pancytopenia due to aplastic anaemia (lack of blasts on blood film) or other malignancies like neuroblastoma
manage with chemo, blood procuts, prophylactic antifungal treatment, resucitation as needed, abx if concurrent infection
how long do you need abx for uti for
children, adults = 3 days
males and pregnant women = 7 days
dka management in children
SHOCK
initial bolus of 20ml/kg of 0.9% saline over 15 minute i- up to 40 total before inotropes should be considered
NO SHOCK
10ml/kg over 1 hour
then ongoing fluids
0.05-0.1 units/kg per hour insulin like actrapid
check blood glucose hourly and ketones every 1-2 hours
consider potassium replcamaent
management of febrile seizures
having one febrile seizure is a risk factor for having another - but chances lessen with age
during an episode, parents should not restrain the child, support the child’s head, then turn it to the side to prevent injury and choking
after the convulsion, place the child into the recovery position
antipyretics if irritable with fever - but wil not reduce risk of febrile esizures
if >5 minutes call ambulance
if regular recurrence, GP may offer parents diazepam to shorten episodes (PR)
active cooling is not advised
only 1% of children with febrile seizures go on to develop epilepsy
management of PDA
Treat medically with diuretics or NSAIDs like indomethacin or ibuprofen
o This inhibits prostaglandin synthesis and closes the connection in the majority of cases
o If associated with another congenital heart defect amendable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair
Or closure via a coil or occlusion device at around 12 months, this is inserted via cardiac catheter
Rarely – surgical with ligation
6 month milsetones
GROSS MOTOR
sit supported w round back (straight at 8)
weight bear on feet
may be able to roll onto front
FINE MOTOR
palmar grasp
transfer objects
HEARING, SPEECH AND LANGUAGE
laughing, screaming, babbling
SOCIAL, EMOTIONAL + BEHAVIOURAL
chew and put food in mouth
express likes and dislikes
should know their name at 5-7m
ITP
cause is unknwonw -may be an autoimmune disorder that follows a viral illness
Most children with ITP will have bruising and petechiae (pinprick blood spots under the skin). Bruising usually
happens following minor knocks, but may occur without
any history of trauma
are otherwise well
may also have bleeding of gums or nose - girls may have heavy period
FBC for low platelets
isnt contagious
most will improve in 6w with or without treatment
most do not need treatment unless sevree bleeding - tranexamic acid, IV immunoglobulin, steoroids, platelet transfusions (but majority = none)
can return to school immediately if >20 palteltes, if not then after a week - avoid contact spots, no diving into shallow end, avoid ibuprofen (lowers plateltes)
bring to hospital immediately if prolonged bleeding anywhere, blood in urine or stools, heavy blow to head w LOC, heavy period)
presentation of HSP
non-blanching skin purpura - usually starts on legs then spread to buttocks - can also affect trunk and arms
typically raised
arthrtisis - mainly in knees and ankles - may be swollen and tender but permanent deformity doesn’t occur
abdominal pain +/- blood diarrhoea - in severe cases can lead to gi haemorrhage, intussusception and bowel infarction
renal involvement - IgA nephritis - microscopic haematuria and proteinuria
N+V
questions i forget in hist
any social workers involved in care
causes for admission
3 wet nappies a day is ok
RR 70 (maybe consider if 60)
resp distress
<92% sats
<50% feeding or dehydration
18 months developmental milestones
GROSS MOTOR
walk upstairs w one hand held
FINE MOTOR
build tower of 3-4 bricks
turn book pages
HEARING, SPEECH, LANGUAGE
points and identifies eyes, mouth, ears
should know 25-50 words but understands many more
SOCIAL, EMOTIONAL AND BEHAVIOURAL DEVELOPMENT
plays alone
can indicate if needs toilet
take off shoes
explaining CF
a genetic condition where the body isn’t able to make its secretion watery enough
this means that any body part that makes these secretions such as the lungs, pancreas and intestine can run into trouble with thick, sticky mucus
this is why people get a lot of chest infections and tummy problems
around 1 in 2500 are affected - you recieve a copy of DNA from your mum, and a copy from your dad, both of these copies have to be defective for CF to occur. This means your parents are both ‘carriers’ – they have one defective gene, but they don’t have symptoms because the other copy is working fine. Approximately 1 in every 25 people is one of these ‘carriers’ of the defective gen
there’s a 25% chance you will have a child with these gene
Currently there is no cure for the condition, so the main focus is on dealing with the problems that may arise. This includes using antibiotics to prevent chest infections, medicines to help open up the airways and shift the sticky mucus, and providing dietary advice and nutritional supplements to help their growth and development
The problem with the sticky mucus and the repeated infections is that it takes its toll on the lungs, and they become progressively more damaged over time, making CF a progressive condition. Currently the only treatment for this that we have is a lung transplant. Currently the life expectancy for people with CF is that over half will live beyond 40, however we anticipate that those children born with it now will live longer than this
what can i do? Ensuring your child eats well and does regular exercise is the best thing you can do, as they will need more calories and the exercise will help shift the mucus. Making sure nobody in the home is smoking, and generally reducing exposure to pollution and smoke will help reduce infections, as will making sure people at home are washing their hands regularly
3 year milestones
GROSS MOTOR
stand on one leg
tricycle
FINE MOTOR
9 cube tower
draw a face
HEARING SPEECH LANGUAGE
know their name and age
SOCIAL
goes to toilet on their own
knife and fork
