paeds Flashcards
management for acute otitis media ? q
no abx, will resolve on its own. give ibruprof/paracet
if sx worsen/ do not improve after 3 days - amoxicciliin i first line
what is perthes and what age group and how present ?
avascarlar necrosis of femoral head
4-8 y/o
reduced ROM / pain over a couple of weeks
osteomyeltiis most commonly cause by what organism ?
staph aureus
what is ewings sarcoma ?
Ewing
sarcoma is a malignant bone tumour that most commonly affects long bones.
Presenting features depend on the size and location of the tumour, but bone pain is classically worst at night. There may be swelling or tenderness over the site
and tumours may be incidentally discovered following a pathological fracture
manage a severe/lifethreatening asthma attack steps
ADMIT TO HOSPITAL
- oxygen
- nebulised salbutomol
- nebulised ibratropium bromide
- nebulised mag sulphate
- prednisolone (can be IM if oral not poss)
- 2nd line treatments (if above fails): IV salbutamol/ IV aminophylline/ IV magnesium sulphate
- Discuss with senior clinician, PICU or paediatrician
manage a moderate asthma attack
ADMIT TO HOSPITAL
- oxygen
- salbutamol (metered dose inhaler + spacer)
- ipratropium bromide oral (given if poor response to above)
- prednisolone (oral)
features of life threatening asthma attack
peak expiratory flow rate (PEFR) less than 33% of expected,
oxygen saturation
less than 92%,
altered consciousness,
exhaustion,
cyanosis
silent chest
what happens after kid has had meningitis and its been treated ?
Patients should be reviewed by a
paediatrician 4–6 weeks after discharge and a formal audiological assessment
should be offered.
3 nephritic and 3 nephrotic
nephrotic
- minimal change disease
- focal segmental glomerulosclerosis
- membraneous glomerulonephritis
nephritic
1. post strep glomerulonephritis
2. IgA glomerulonephritis
3. rapidly progressing glomerulonephritis
how to manage paeds dka ?
- Initial fluid bolus at 10ml/kg of 0.9% NaCl over 30 minutes
- give 0.9% saline with 40 mmol/L potassium chloride
- once plasma glucose is < 14 mmol/L Change to 0.9% saline + 5% glucose
- Start IV insulin infusion 1-2 hours after beginning IV fluid therapy in children with DKA
*remeber continuous ecg to check for hypokalaemia
crohns vs UC
presentation
UC =
Diffuse abdominal
pain, rectal
bleeding, and
mucus
crohns=c
Right iliac fossa pain,
failure to thrive between
attacks, loose stools, and
rectal bleeding
crohns vs uc
exam findings
both =
Clubbing, anterior uveitis, erythema nodosum,
pyoderma gangrenosum, and signs of anaemia
just crohns=
Aphthous ulcers, fissures,
and fistulae
crohns vs uc
commonly affected areas and distribution and pattern
uc =
rectum, rectum and colon, continuous lesions
crohns=
terminal ileum, anywhere from mouth to anus, skip (disconinuous) lesions
crohns vs uc
depth of inflamm
uc =
submucosa and mucosa only
crohns =
transmural
crohns vs uc complications
uc =
Colonic
adenocarcinoma
and toxic
megacolon
crohns=
Abscesses, fistulae,
adhesions, strictures,
fissures, obstruction and
perforation
different child hearing tests and when theyre carried out
The newborn hearing test is carried out in the first 4–5 weeks of life using the
automated otoacoustic emission test. If this suggests a hearing problem, the newborn is offered an
automated auditory brainstem response test.
Visual reinforcement audiometry is
used in children aged 6 months to 2.5 years,
pure tone audiometry is used to screen a child’s hearing before starting school at 4–5 years of age
tympanometry is used to assess for otitis media with effusion (glue ear).
what heart stuff is turners associated with?
bicuspid aortic valve, aortic
stenosis, and coarctation of the aorta
how is acne managed
- benzoyl peroxidase, adapalene, azaleic acid
- oral abx for 3 month (doxycycline)
- alt abx
- isotretinoin (accutane)
what is the word when you get too much billirubin as a neonate and it messes up the brain ?
kernicterus
how is pulse scored on apgar
2 >100
1 < 100
0 nil
how is resp scored on apgar
2 = strong / crying
1 = weak, irregular
0 = nil
how is colour scored on apgar
2 = pink
1 = pink body / blue extremtieis
0 = blue all over
how is muscle tone scored on apgat
2 = active movement
1 = linmb flexion
0 = flaccid
hw is reflex scored on apgar
2 = cries on stimaulation / coughs / sneezes
1 = grimace
0 = nil
what is a normal apgar score ?
7 or above
is it bad to have blue extremities when you’re born ?
Apgar score is therefore 9. This is likely to be describing a
case of acrocyanosis — a benign condition that causes peripheral cyanosis
immediately after birth in healthy infants and resolves within 48 hours
threadworm caused by ?
Enterobius vermicularis
Children aged 3 months or
older with acute pyelonephritis/upper UTI - how managed ?
7–10 day course of
either oral cephalexin or oral co-amoxiclav.
Children aged 3 months or older
with cystitis/lower UTI management ?
should be given a 3-day course of oral trimethoprim or
oral nitrofurantoin
failure to pass
meconium within 48 hours, bilious vomiting, and abdominal distention - diagnosis
Hirschsprung disease
difference between lukaemia and lymphoma
leukaemia = abnormal cells accumulate in blood or bone marrow
lymphoma = form solid tumours in lypmh nodes, thmus, spleen
how to differentiate AML vs ALL in clincial presentation
ALL =
children more likely &
Lymphadenopathy +++
CNS involvement +++
Testicular enlargement
Thymic enlargement (mediastinum)
AML =
Lymphadenopathy less common
Quick subtype facts:
M3: Acute promyelocytic leukaemia 15;17– prone to DIC & bleeding
M4+5: Monoblasts/monocytes - Skin / gum infiltration + hypokalaemia
staging for hodgkins lymphoma
ann-arbor staging
Staging (Ann-Arbor)
Stage 1 – one LN region (LN region can include spleen)
Stage 2 – two or more LN regions on the same side of the diaphragm
Stage 3 – two or more LN regions on opposite sides of the diaphragm
Stage 4 – extra nodal sites (liver, BM)
A: No constitutional symptoms B: Constitutional symptoms
E.g. Stage 2a – patient with involvement in 3 LN regions above the diaphragm, pain after alcohol and SVC syndrome but no weight loss, night sweats etc.
management for viral induced wheeze
salbutomol - burst therapy
how to manage bronchiolitis ?
mainly supportive
humidifed oxygen
rsv stands for ?
respiratory syncytial virus (RSV)
neonate has conjuctivitis what are implications ?
Ophthalmia neonatorum simply means infection of the newborn eye.
Responsible organisms include
Chlamydia trachomatis
Neisseria gonorrhoeae
Suspected ophthalmia neonatorum should be referred for same-day ophthalmology/paediatric assessment.
how to manage whooping cough ?
Pharmacological Treatment - if admission is not needed, prescribe an antibiotic if the onset of the cough is within 21 days.
o < 1 month old = clarithromycin
o >1 months old and not pregnant = azithromycin
o If macrolides contraindicated, give co-trimoxazole
neonate is irritability and jitteriness, drowsiness and poor feeding
neonatal hypoglycaemia
how long for delivery for cat 1 and cat 2 c section?
cat 1 = 30 mins
cat 2 = 75 mins
perthes painful or painless limp ?
can be either
purpuric rash, athralgia, recent viral illness, proteinuria
IgA vascultitis (henoch-schonlein purpura)
surgery for biliary atresia ?
- Kasai hepatoportoenterostomy
ideally within first 60 days of life
what is Klinefelter’s syndrome
give features
is associated with karyotype 47, XXY.
Features
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia - increased incidence of breast cancer
elevated gonadotrophin levels but low testosterone
for cyanotic congenital heart defect what do you need to give baby
Prostaglandin E1 infusion (alprostadil)
this keeps ductus arteriosis open
baby stools contain undigested food ?
toddler’s diarrheoa
surgery for pyloric stenosis
Management is with Ramstedt pyloromyotomy
which heart abnormaility associated with downs syundrome ?
AVSD
name of criteria for septic arthiritis
The Kocher criteria for the diagnosis of septic arthritis:
fever >38.5 degrees C
non-weight bearing
raised ESR
raised WCC
which abx for septic arthiritis ?
- Prolonged course of antibiotics (initially IV for 2 weeks, followed by 4 weeks of oral antibiotics)
o Neonate to <3 months:
IV cefotaxime
o 3 months to </=5 years:
IV ceftriaxone
If penicillin allergic, give clindamycin
o >/=6 years
IV flucloxacillin
If penicillin allergic, give clindamycin
if suspected testicular torsion how do you manage ?
o IV fluids, NBM, antiemetics, analgesia
straight to surgery
difference between kawasaki and scarlet fever + management
kawasaki:
- high-grade fever which lasts for > 5 days. Fever is characteristically resistant to antipyretics
- conjunctival injection
- bright red, cracked lips
- strawberry tongue
- cervical lymphadenopathy
- red palms of the hands and the soles of the feet which later peel
mx = aspirin
scarlet fever:
- Scarlet fever has an incubation period of 2-4 days and typically presents with:
- fever: typically lasts 24 to 48 hours
- malaise, headache,
- nausea/vomiting
- sore throat
- ‘strawberry’ tongue
- rash (sandpaper rash)/fine punctate erythema
mx= oral penicillin V for 10 days (also called phenoxymethylpenicillin)
difference between kawasaki rash onset and scarlet fever rash onset …
kawasaki = 5-14 days after fever
scarlet fever = 12-48 hours after fever
for severe / life threatening asthma when do you give salbutomal and when do you give ipratropium??
you give them together
eye infection in neonate discuss ??
Ophthalmia neonatorum (conjunctivitis in the neonate)
Responsible organisms include
* Chlamydia trachomatis
* Neisseria gonorrhoeae
Management
* Mild bacterial conjunctivitis:
o Chloramphenicol eye drops
* Moderate-severe bacterial conjunctivitis:
o Chlamydial (most common):
Oral erythromycin
o Gonococcal:
Single dose of parenteral (IV or IM) cefotaxime/ ceftriaxone
o Pseudomonal:
Gentamicin eye drops plus systemic antibiotics
* Viral: no specific antiviral, may use topical antihistamine and artificial tears to relieve itching
* For chlamydia or gonococcal infections, the mother and her sexual partner also require treatment
neonatal group b strep infection how to prevent / manage?
Prevention
* Offer intrapartum benzylpenicillin (or vancomycin if allergic to penicillin) to pregnant women who have had:
o a previous baby with an invasive group B streptococcal infection
o group B streptococcal colonisation, bacteriuria, or infection in the current pregnancy
o are in pre-term labour
Neonatal infection management
* Penicillin (IV Benzylpenicillin) and gentamicin
* First-line antibiotics recommended in NICE NG195 guidelines, but local antibiotic policies may vary
how to manage haemolytic disease of the newborn
o Resuscitation
A to E approach particularly if preterm, anaemic or hydropic(swelling/taking up fluid)
o Phototherapy
if significant jaundice (test with transcutaneous bilirubin)
o Exchange transfusion if:
Bilirubin rapidly rising (>8-10 μmol/l/hr) despite adequate phototherapy
Severe hyperbilirubinaemia insufficiently responsive to phototherapy and supportive care
Significant anaemia (Hb <100 g/l)
o IVIG
Only for immune haemolysis; if bilirubin continues to rise by > 8.5mmol/L/hour
how to manage neonate hep B virus ?
- Infants of mothers who are HBsAg positive should receive exposure immunization schedule:
o Monovalent Hepatitis B vaccine within 24 hours of birth (also at 4 weeks and 1 year of age)
o 6-in-1 vaccine (DT/aP/IPV/Hib/HepB) at usual times (8, 12 and 16 weeks) - HBIG should be given to the neonate if:
o Mother is HBsAg positive (even if she is HBeAg negative)
o Mother had acute hepatitis B during pregnancy
o Mother had an HBV DNA level equal or above 1x10^6IUs/ml in any antenatal sample during the current pregnancy - HBIG should be ideally given simultaneously as initial Hep B vaccine, but at a different site
- Acute Hep B infection: supportive care
neonate at risk of hypoxic brain injury what can you do ?
hypoxic ischaemic encephalopathy:
Babies born near or at term with HIE can benefit from therapeutic hypothermia
how to manage listeria neonatal infection?
Management
* Amoxicillin and gentamicin
o If blood cultures or CSF comes back as positive for Listeria
asymmetrical patchy opacities on chest x-ray in neonate + how would you manavge ?
meconium aspiration syndrome
more common in post term delivery / also could have meconium stained amniotic fluid
- If normal term infant with meconium-stained amniotic fluid but no history of GBS, observation is recommended
- If there are risk factors or laboratory findings that are suggestive of infection, consider antibiotics
o IV ampicillin AND gentamicin
premature neonate developing feeding intolerance, vomiting, lethargy and abdominal distension which progresses into bloody stools at around 9 days of age + how to manage ?
Necrotising Enterocolitis
Management
* Stop enteral feeding and medications
o TPN may be required if feeds stopped >24 hours
o For confirmed NEC cases feeds stopped for 7 days
* NG tube
o Used to drain fluid and gas from the gut
o Monitor hourly gastric aspirates
* Broad-spectrum IV antibiotics
o Must cover both aerobic and anaerobic organisms
o For example: cefotaxime and vancomycin
* IV Fluids
o For cardiovascular support, may require addition of inotropes
* Surgery
o Indicated if:
Perforation
Failure to respond to medical treatment
o Laparotomy with resection of necrosed bowel with either a primary anastomosis or a defunctioning stoma
Pneumatosis intestinalis. Seen as gas in the bowel wall on x-ray
necrotising enterocolititis
threshold for managing neonatal hypoglycaemia and what to do ?
If pre-feed glucose <2mmol/L or symptomatic (BNFC)
o Immediate glucose IV infusion
if above this, just encourage feeding.
how to manage increased unconjugated biliirubin - jaundice in neonate ?
serum bilirubin threshold graph
- subthreshold no treatment
- in between the 2 lines on graph - phototherapy
- above top line –> exchange transfusion
ground-glass shadowing and
air bronchograms.
Respiratory distress syndrome
how to manage RDS ?
Management
* ABC resuscitation
o Review history and examine baby to identify cause of respiratory distress
* Respiratory support
o Intubation and ventilation
Used when severe RDS
o Endotracheal surfactant
o Continuous positive airway pressure (CPAP)
Helps keep the lungs inflated
o Supplementary oxygen
Aim between 91-95% for preterm neonates
- Fluids
- IV antibiotics
o Broad spectrum combination
Such as benzylpenicillin and gentamicin (unless listeria in which case start amoxicillin and gentamicin) - CXR
o Do ASAP unless mild respiratory distress where this can be delayed
managment of toxoplasmosis in newborn
Management of symptomatic babies
* Refer to paediatric infectious diseases
* Pyrimethamine + Sulfadiazine + Folinic acid
o Continue all 3 for 1 year
* Monitor LFTs and FBCs every 4-6 weeks
* + Glucocorticoids (prednisolone)
o If CSF protein >1g or active chorioretinitis threatens vision
Transient tachypnoea of the newborn - what is it
Transient tachypnoea of the newborn (TTN) is the commonest cause of respiratory distress in the newborn period. It is caused by delayed resorption of fluid in the lungs
It is more common following caesarean sections, possibly due to the lung fluid not being ‘squeezed out’ during the passage through the birth canal
Chest x-ray may show hyperinflation of the lungs and fluid in the horizontal fissure.
mx –> largely observational
common organisms for neonatal sepsis ? + how to manage ?
are Group B Streptococcus, Escherichia coli, and Listeria monocytogenes.
The antibiotics used to treat early-onset sepsis may vary depending on the trust, but they typically include a penicillin (e.g. benzylpenicillin) and an aminoglycoside (e.g. gentamicin) to cover Gramnegatives
murmur for ASD
Classically causes a mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with fixed splitting of the second heart sound
how is coartation of aorta managed ?
- 98% occur distal to the left subclavian artery, usually at the origin of the ductus arteriosus
- Most common presentation is at 48 hours old when the ductus arteriosus closes
Management - Prostaglandin E1 infusion
o To maintain duct patency - Surgical repair
o End-to-end anastomosis or arch reconstruction with patch placement or bypass graft
o Older patients may require stent insertion or surgical resection
which pharmocological agent do you need to give in cyanotic heart disease ??
Maintain duct patency: key to early survival
o Start prostaglandin E1 infusion
how to manage PDA
if cyanotic disease you need to keep it open so give prostaglandin E1
if not then close it up… give them:
o IV Indomethacin – 1st line treatment
o Prostacyclin synthetase inhibitor
o Ibuprofen
Usually done in premature/VLBW infants
* If pharmacological methods are unsuccessful, surgical ligation or percutaneous catheter device closure may be used
what is rheumatic fever ?
Rheumatic fever develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection.
Type 2 hypersensitivity reaction….
diagnosis for rheumatic fever
Diagnosis is based on evidence of recent streptococcal infection accompanied by:
2 major criteria
1 major with 2 minor criteria
Evidence of recent streptococcal infection
raised or rising streptococci antibodies,
positive throat swab
positive rapid group A streptococcal antigen test
Major criteria
erythema marginatum
Sydenham’s chorea: this is often a late feature
polyarthritis
carditis and valvulitis (eg, pancarditis)
The latest iteration of the Jones criteria (published in 2015) state that rheumatic carditis cannot be based on pericarditis or myocarditis alone and that there must be evidence of endocarditis (the clinical correlate of which is valvulitis which manifests as a regurgitant murmur)
subcutaneous nodules
Minor criteria
raised ESR or CRP
pyrexia
arthralgia (not if arthritis a major criteria)
prolonged PR interval
how to manage rheumatic fever?
Prophylaxis
* Benzathine penicillin every 3-4 weeks
Management
1. Naproxen
- Anti-streptococcal antibiotics if persistent infection = e.g. penicillin V, benzathine benzylpenicillin, amoxicillin)
- Symptomatic heart failure
o Treated with diuretics and ACE inhibitors
o Prednisolone may be required
how to manage supraventricular tachycardia ?
- vagal manouveres
- adenosine
- DC cardiovert / amiodarone
if haemo unstable –> DC cardiovert
how to manage TofF TET spell/ hypercyanotic spell
o Place the patient in the knee-to-chest position
o Supplementary oxygen
o IV fluids
o Beta blockers (relax the right ventricle and improve flow to the pulmonary vessels)
o Morphine (decrease the respiratory drive)
o Sodium bicarbonate (counteracts any metabolic acidosis)
o Phenylephrine infusion (increase systemic vascular resistance)
how to manage TofF?
- If severe with worsening cyanosis:
o Prostaglandin E1 infusion
o Blalock-Taussig shunt
surgery performed from 4 months of age onwards
give an example of prostaglandin E1?
Prostaglandin E1 infusion (alprostadil)
surgery for tricupsuid atresia >
- Blalock-Taussig shunt insertion
murmur with VSD?
loud pansystolic murmur heard best at the lower left sternal edge in the third and fourth intercostal spaces; quiet pulmonary second heart sound
what murmur with TofF?
ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)
what do patients with a VSD need to be careful with ??
Whilst the VSD is present, bacterial endocarditis should be prevented by maintaining good dental hygiene
o Prophylactic amoxicillin to patients at high risk of developing endocarditis e.g. during surgical procedures
path of acute otitis media
whilst viral upper respiratory tract infections (URTIs) typically precede otitis media, most infections are secondary to bacteria, particularly Streptococcus pneumonaie, Haemophilus influenzae and Moraxella catarrhalis
viral URTIs are thought to disturb the normal nasopharyngeal microbiome, allowing bacteria to infect the middle ear via the Eustachian tube
how to manage acute otitis media ?
don’t really need abx - normally resolves in 3 days
if it doesnt the you can give abx
Amoxicillin - 5-7 days is first-line
Penicillin allergy: clarithromycin, erythromycin
what procedure for acute otitis media with effusion ?
Myringotomy is the most common surgical option for OME. It involves making
an incision in the tympanic membrane to drain the fluid, followed by insertion of
grommets which stay in place for 6–12 moths to prevent recurrence
what organism causes acute epiglottisis?
haemophilus influenza type B
rapid onset
high temperature, generally unwell
stridor
drooling of saliva
‘tripod’ position: the patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position
acute epiglottitis
how to manage acute epiglottitis ?
- Secure airway, do NOT examine the throat
o Direct rigid laryngoscopy and intubation is the most common approach - Take a blood culture
abx = ceftriaxone
managment for angioedema ?
- Patients with rapidly developing angio-oedema without anaphylaxis:
o Chlorphenamine and hydrocortisone - Patients with symptoms requiring treatment:
o Cetirizine (or other non-sedating antihistamine such as fexofenadine, or loratadine)
o Oral corticosteroid (for example prednisolone 40 mg daily for up to 7 days)
manage asthma in kids both age groups
< 5 y/o
1. SABA
2. paed mod dose ICS
3. LTRA (montelukast)
4. stop LTRA –> refer to paeds
5-16 y/o
1. SABA
2. paed low does ICS
3. montelukast
4. stop montelukast, start LABA
5. stop ICS , stop LABA. start MART with paed low dose ICS
6. Increase ICS to moderate dose
7. refer to paeds
gold standard for diagnosing bronchiectasis
High resolution CT is the gold standard investigation to diagnose bronchiectasis
o Radiological features indicative of bronchiectasis include:
o Bronchial wall thickening
o Diameter of bronchus larger than that of the bronchial artery (‘signet ring’ sign)
o Visible peripheral bronchi
CF bronchiectasis common organism is ?
o Pseudomonas spp. Is characteristic of CF bronchiectasis
features of RSV bronchiolotiis
- coryzal symptoms (including mild fever) precede:
- dry cough
- increasing breathlessness
- wheezing, fine inspiratory crackles (not always present)
- feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission
managemnt of bronchiolitis
- humidified o2
- CPAP
- upper airway suciton
4.fluids
features of cow milk protein allergy
regurgitation and vomiting
diarrhoea
urticaria, atopic eczema
‘colic’ symptoms: irritability, crying
wheeze, chronic cough
rarely angioedema and anaphylaxis may occur
how to manage cows milk protein allergy
breastfeeding mum:
exclude cow’s milk from her diet
bottlefed:
* Trial of extensively hydrolysed formula
epideiomology of croup
- peak incidence at 6 months - 3 years
- more common in autumn
features of croup
- cough
- barking, seal-like
- worse at night
- stridor
- remember, the throat should be not examined due to the risk of precipitating airway obstruction
- fever
- coryzal symptoms
- increased work of breathing e.g. retraction
how to manage croup ?
every gets oral dexamethasone
moderate croup can give oxyen
severe croup can also give nebulsied adrenaline (1 in 1000)
Cystic firbosis diagnosis ?
Sweat test
patient’s with CF have abnormally high sweat chloride
normal value < 40 mEq/l, CF indicated by > 60 mEq/l
common mutation in CF
F508 delta
how do you holistically manage a CF patient ?
o Pulmonary – physiotherapy, mucolytics
o Infection – prophylactic antibiotics, monitoring
o Nutrition – enzyme tablets, high-calorie diet, monitor growth
o Psychosocial – provide support for child and carers
gold standard for diagnosis of food allergy ?
Food challenge
o After 6-12 months of being symptoms-free consider a food challenge
This involves administration of increasing quantities of the food allergen under medical supervision, starting with direct mucosal exposure (allergen contact with the lips), and then titrated oral ingestion as tolerated. If no symptoms are provoked, the test is negative and clinical allergy can be excluded
foreign body inhalation pathway ?
- ecnourage cooughing
- back blows
- abdo thrusts
in hosputal
1. flexi bronchoscopy / or rigid bronchoscopy
2. surgery / trachotomy
what is laryngomalacia and what are features
Laryngomalacia is the most common congenital laryngeal abnormality characterised by flaccidity of the supraglottic structures. The larynx is soft and floppy as a result and collapses during breathing.
Features
Inspiratory stridor: high-pitched and crowing. This is usually intermittent, occurring in the supine position e.g. when the child lies on its back, when feeding or when agitated
Symptoms increase in severity during the first 8 months but tend to resolve by 18-24 months
Respiratory distress, failure to thrive and cyanosis are rare
which pathogen causes scarlet fever and how do you manage it ?
Group A haemolytic streptococci (usually Streptococcus pyogenes
Pencillin V (phenoxymethylpenicllin)
how does scarlet fever present ?
- fever: typically lasts 24 to 48 hours
- malaise, headache, nausea/vomiting
- sore throat
- ‘strawberry’ tongue
- rash
fine punctate erythema (‘pinhead’) which generally appears first on the torso and spares the palms and soles
children often have a flushed appearance with circumoral pallor. The rash is often more obvious in the flexures
it is often described as having a rough ‘sandpaper’ texture
desquamination occurs later in the course of the illness, particularly around the fingers and toes
sore throat scoring system in paeds sore throat
FeverPAIN score (4 or 5) or Centor score (3 or 4)
management for sore throat (tonsilitis / parhyngitis )
sore throat is tonsilittis / pharingitis
normally from GAS inection
therefore treat with Penicilin V
score used to assess severity of urticaria ? hwo do you manage it
- Urticaria Activity Score (UAS7)
cetirizine (anti histamine)
how does viral induced wheeze present + how to manage ?
wheeze
salbutamol
Burst Therapy is often used for viral-induced wheeze
features of whooping cough
catarrhal phase
* symptoms are similar to a viral upper respiratory tract infection
* lasts around 1-2 weeks
paroxysmal phase
* the cough increases in severity
* coughing bouts are usually worse at night and after feeding, may be ended by vomiting & associated central cyanosis
* inspiratory whoop: not always present (caused by forced inspiration against a closed glottis)
* infants may have spells of apnoea
* persistent coughing may cause subconjunctival haemorrhages or even anoxia leading to syncope & seizures
* lasts between 2-8 weeks
* convalescent phase
* the cough subsides over weeks to months
how to manage whooping cough ? which pathogen + give type ?
bordetella pertussis (gram neg coccobacillli)
- Pharmacological Treatment - if admission is not needed, prescribe an antibiotic if the onset of the cough is within 21 days.
o < 1 month old = clarithromycin
o >1 months old and not pregnant = azithromycin
o If macrolides contraindicated, give co-trimoxazole
Do not use in infants <6 weeks of age
appendicitis in kids - things to think about
Appendicitis is one of the most common acute surgical problems facing children. Diagnosis is often made difficult by a presentation which is far from the classically history of:
central abdominal pain which later radiates to the right iliac fossa
low-grade pyrexia
minimal vomiting
Children who are younger or have a retrocaecal/pelvic appendix are more likely to present in an atypical way
Appendicitis is uncommon in children under 4 years old but in this group often presents with perforation
how does coeliac present in kids ?
Features may coincide with the introduction of cereals (i.e. gluten)
failure to thrive
diarrhoea
abdominal distension
older children may present with anaemia
many cases are not diagnosed to adulthood
what are the differrent types of laxatives ?
o Bulk-forming: fybogel, methylcellulose
o Osmotic: lactulose, Movicol
o Stimulant: Bisacodyl, senna, sodium picosulphate
o Stool-softener: arachis oil, docusate sodium
important questions to ask in constipation hx to rule out sinister cause…
Red Flag for Constipation
- Ribbon stool
- >24 hrs meconium at birth
- Distension
- any blood
Amber Flag for Constipation
- Faltering growth
Ribbon stool pattern — may indicate anal stenosis (more likely to present in a child younger than 1 year of age)
when shoudl neonates pass meconium
Meconium should be passed ideally within the first 24 hours and less frequently within the first 48 hours
how to manage simple constipation in kids
if impaction:
1. movicol (osmotic lax), can increase dose over 2 weeks, also diet advice. (movicol are satchet packets)
2. if unresponsive can give senna (stimulative laxative)
3. if stools are hard can also use lactulose/docusate
if no impaction:
1. movicol
2. if movicol not tolerated can give senna (stimulative laxative)
3. if stools are hard can also use lactulose/docusate
crohns in kids management
The shift in guidance to start anti-TNF agents such as infliximab as a first-line treatment (‘top-down therapy’) as opposed to the previous ‘step-up’ model was informed by studies such as the TISKIDS and REACH trials where this approach was associated with much better outcomes for children
failure to thrive differentials
- Inadequate nutritional intake. e,g, neglect, poverty, iron def anaemia, maternal malnurtiion if breastfeeding
- Difficulty feeding - poor breastfeeding/suck, cleft lip, cleft palate, pyloric stenosis,
- Malabsorption - crohns, coeliac, CF, perniciois anaemia
- Increased energy requirements - CF, hyperthyroid, malignancy. HIV
- Inability to process nutrition - type 1 diabetes, inborn errors of metabolism
how to manage GORD ?
- Breastfeeding: offer assessment → alginate therapy
- Formula: review feeding history → smaller, more frequent feeds → thickeners → alginate therapy
what is hirschprung disease ?
Hirschsprung’s disease is caused by an aganglionic segment of bowel due to a developmental failure of the parasympathetic Auerbach and Meissner plexuses.
parasympathetic neuroblasts fail to migrate from the neural crest to the distal colon → developmental failure of the parasympathetic Auerbach and Meissner plexuses → uncoordinated peristalsis → functional obstruction
how does hirschprung’s disease present ?
Possible presentations
neonatal period e.g. failure or delay to pass meconium
older children: constipation, abdominal distensionh
gold standard diagnosis for hirschsprungs disease ?
rectal biopsy
how to manage hirschsprungs disease ?
bowel irrigation
surgery = anorectal pull through
how does intussuseption present ?
- intermittent, severe, crampy, progressive abdominal pain
- inconsolable crying
- during paroxysm the infant will characteristically draw their knees up and turn pale
- vomiting
- bloodstained stool - ‘red-currant jelly’ - is a late sign
- sausage-shaped mass in the right upper quadrant
Ix for intussuseptin and give findings
abdo ultrasound
target like mass
how to manage intussuseption
- A-E
- NG aspitation
- IV fluids
- Clindamycin + gentamicin
- rectal air insufflation
surgery = if peritonitis / big problem
anatomy reason for intussuseption??
- If recurrent intussusception - consider investigating for a pathological lead point (e.g. Meckel’s diverticulum)
most common cause of painless massive GI bleeding in kids age 1-2?
meckel’s diverticulum
Presentation (usually asymptomatic)
* abdominal pain mimicking appendicitis
* rectal bleeding
* Meckel’s diverticulum is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years
* intestinal obstruction
* secondary to an omphalomesenteric band (most commonly), volvulus and intussusception
ix for meckels diverticulum ?
Investigation
* if the child is haemodynamically stable with less severe or intermittent bleeding then a ‘Meckel’s scan’ should be considered
* uses 99m technetium pertechnetate, which has an affinity for gastric mucosa
* mesenteric arteriography may also be used in more severe cases e.g. transfusion is required
surgery for intestinal malrotation / volvulus
Ladd procedure - detorting the bowel and surgically dividing the Ladd bands
how does volvulus / malrotation present ?
constipation
abdominal bloating
abdominal pain
nausea/vomiting
what is mesenteric adenitis and how is it managed ?
Mesenteric adenitis is inflamed lymph nodes within the mesentery. It can cause similar symptoms to appendicitis and can be difficult to distinguish between the two.
It often follows a recent viral infection and needs no treatment
pain can take 2-4 weeks to resolve
how does peptic ulcer present ?
epigastric pain
nausea
duodenal ulcers
more common than gastric ulcers
epigastric pain when hungry, relieved by eating
gastric ulcers
epigastric pain worsened by eating
how does pyloric stenosis present ?
Pyloric stenosis typically presents in the second to fourth weeks of life with vomiting, although rarely may present later at up to four months. It is caused by hypertrophy of the circular muscles of the pylorus.
NON BILOUS VOMITING
- ‘projectile’ vomiting, typically 30 minutes after a feed
- constipation and dehydration may also be present
- a palpable mass may be present in the upper abdomen
- hypochloraemic, hypokalaemic alkalosis due to persistent vomiting
target sign on ultrasound ?
pyloric stenosis or intussusecption
definitive management of pyloric stenosis ?
- Definitive treatment is by performing a Ramstedt pyloromyotomy
how to manage paeds UC?
- Proctitis
o 1st line - Topical aminosalicylate for 4 weeks, - Mild UC:
o 5-ASA - Moderate UC:
o Oral prednisolone for 2-4wks and taper - Severe UC:
o Medical emergency
o High dose IV Methylprednisolone
o Surgical Treatment
how to manage primary sclerosing cholangitis
ursodeoxycholic acid
how does biliary atresia present ?
Patients typically present in the first few weeks of life with:
- Jaundice extending beyond the physiological two weeks
- Dark urine and pale stools
- Appetite and growth disturbance, however, may be normal in some cases
Signs:
Jaundice
Hepatomegaly with splenomegaly
Abnormal growth
Cardiac murmurs if associated cardiac abnormalities present
The perinatal form presents in the first two weeks of life, and the postnatal form presents within the first 2-8 weeks of life
Biliary atresia occurs in 1 in every 10,000-15,000 live births
ix for biliary atresia
Ultrasound of the biliary tree and liver: May show distension and tract abnormalities
Percutaneous liver biopsy with intraoperative cholangioscopy
important to avoid which painkiller in hep A
paracetamol
scoring system for wilson’s disease severityu
- Nazar score or Kings Wilson score used to assess severity
how does wilson’s present ? + outline it + ix + manage
Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues. Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion. Wilson’s disease is caused by a defect in the ATP7B gene located on chromosome 13.
The onset of symptoms is usually between 10 - 25 years. Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease
Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea:
- liver: hepatitis, cirrhosis
neurological:
- basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
- also: asterixis, chorea, dementia, parkinsonism
- Kayser-Fleischer rings
green-brown rings in the periphery of the iris due to copper accumulation in
Descemet membrane present in around 50% of patients with isolated hepatic Wilson’s disease and 90% who have neurological involvement
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
Investigations
slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
free (non-ceruloplasmin-bound) serum copper is increased
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene
mx = penicillamine (chelates copper) has been the traditional first-line treatment
contraindications to lumbar puncture in meningitis
Contraindication to lumbar puncture (any signs of raised ICP)
focal neurological signs
papilloedema
significant bulging of the fontanelle
disseminated intravascular coagulation
signs of cerebral herniation
how to manage bacterial meningitis in kids ?
< 3 months = amoxicillin/ampicillin + cefotaxime
> 3 months = ceftriaxone
dexamethsone (don’t give if < 3months)
- Presenting in primary care: single dose of IM/IV benzylpenicillin
all children should be followed up 4/6 weeks for hearing assessment
meningitis presentation in babies and toddlers
- fever
- drowsy, floppy, unresponsive
- refusing food
- vomiting
- tense bulging fontanelle
- unusual cry
- rapid breathing
- seizures
how does chicken pox present ?
- fever initially
- itchy, rash starting on head/trunk before spreading.
- Initially macular then papular then vesicular
systemic upset is usually mild
counsel for chicken pox
mainly supportive treatment
- fluids, smooth cotton frabirc, nails short
- paracetamol, topical calamine lotion for itch
- infective until lesions have crusted over so until this point no school, no pregnant ladies, no immunocompromised
- admit to hospital if serious complications
how does dengue present ?
Dengue fever
fever
headache (often retro-orbital)
myalgia, bone pain and arthralgia (‘break-bone fever’)
pleuritic pain
facial flushing (dengue)
maculopapular rash
haemorrhagic manifestations e.g. positive tourniquet test, petechiae, purpura/ecchymosis, epistaxis
‘warning signs’ include:
abdominal pain
hepatomegaly
persistent vomiting
clinical fluid accumulation (ascites, pleural effusion)
Severe dengue (dengue haemorrhagic fever)
this is a form of disseminated intravascular coagulation (DIC) resulting in:
thrombocytopenia
spontaneous bleeding
around 20-30% of these patients go on to develop dengue shock syndrome (DSS)
how does EBV/ infective mononucleosis present ?
The classic triad of sore throat, pyrexia and lymphadenopathy
management and counsel for EBV / infective mononucleosis
- Explain the expected course of the illness
o Symptoms usually last for 2–4 weeks.
o Tiredness is common
o Exclusion from work or school is not necessary but tailor activities to what they find comfortable
o Limit spread by avoiding kissing and sharing of eating utensils
o Avoid heavy lifting and contact or collision sports for the first month of the illness - due to risk of splenic rupture
supportive management (rest, paracemolm . iburpofen)
features and management of roseola infantum
Features
* high fever: lasting a few days, followed later by a
* maculopapular rash
* Nagayama spots: papular enanthem on the uvula and soft palate
* febrile convulsions occur in around 10-15%
* diarrhoea and cough are also commonly seen
supportive mx (paraceotmol & ibrufpofen)
risk of febrile seizures
how does erythema infectiosum present ?
The illness may consist of a mild feverish illness which is hardly noticeable.
- noticeable rash which appears after a few days.
- The rose-red rash makes the cheeks appear bright red, hence the name ‘slapped cheek syndrome’.
- The rash may spread to the rest of the body but unlike many other rashes, it only rarely involves the palms and soles.
The child begins to feel better as the rash appears and the rash usually peaks after a week and then fades.
Most children recover and need no specific treatment. School exclusion is unnecessary as the child is not infectious once the rash emerges. In adults, the virus may cause acute arthritis.
outline impetigo - features and what its caused by ? + give mx
caused by either Staphylcoccus aureus or Streptococcus pyogenes.
It can be a primary infection or a complication of an existing skin condition such as eczema (in this case), scabies or insect bites.
Features
‘golden’, crusted skin lesions typically found around the mouth
very contagious
tx = topical fusidic acid
slapped cheek caused by which pathogen ?
human parvovirus b19
features of kawasaki disease and mx
Features
* high-grade fever which lasts for > 5 days. Fever is characteristically resistant to antipyretics
* conjunctival injection
* bright red, cracked lips
* strawberry tongue
* cervical lymphadenopathy
* red palms of the hands and the soles of the feet which later peel
mx = high dose aspirin / IVIG
school exclusion for measles ?
- Stay away from school for at least 4 days after the development of the rash
features of measles and how it presents + mx
prodromal phase
irritable
conjunctivitis
fever
Koplik spots
typically develop before the rash
white spots (‘grain of salt’) on the buccal mucosa
rash
starts behind ears then to the whole body
discrete maculopapular rash becoming blotchy & confluent
desquamation that typically spares the palms and soles may occur after a week
diarrhoea occurs in around 10% of patients
mx = supportive , stay away from sschool at least 4 days after developement of rash
school exclusion with mumps
- Stay away from school for 5 days after the development of parotitis
how does mumps present ?
Clinical features
fever
malaise, muscular pain
parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%
how does rubella present ?
Features
prodrome, e.g. low-grade fever
rash: maculopapular, initially on the face before spreading to the whole body, usually fades by the 3-5 day
lymphadenopathy: suboccipital and postauricular
mx for tyhphoid
- Supportive care: IV fluids and antipyretics
- Suspected: Ceftriaxone and azithromycin
- Known:
o Ciprofloxacin 7d treatment
o If no response after 4/5d of treatment add azithromycin
o If encephalopathic, add high-dose dexamethasone
rubella school exclusion
- Stay away from school for at least 5 days after initial development of rash
what is eczema herpaticum ?
Eczema herpeticum describes a severe primary infection of the skin by herpes simplex virus 1 or 2.
It is more commonly seen in children with atopic eczema and often presents as a rapidly progressing painful rash.
admit and tx = acyclovir
general overview of eczema management
- emolient
- topical corticosteroids - hydrocortisone
- Topical Calcineurin Inhibitors
wet wraps / bandages
non-sedating anti-histamine (cetirizine)
tacrolimus
infected eczema = flucoxacillin
what is guttate psoriasis
Guttate psoriasis is more common in children and adolescents. It may be precipitated by a streptococcal infection 2-4 weeks prior to the lesions appearing.
Features
tear drop papules on the trunk and limbs
gutta is Latin for drop
pink, scaly patches or plques of psoriasis
tends to be acute onset over days
mx = phototherapy
collection of small blood vessels forming a lump under the skin / strawberry mark
what is it ? and how do you treat
Haemangioma
Most haemangiomas will have disappeared completely by the age of five to seven years.
- If there is functional impairment (near eyes, nose, mouth) or cosmetic disfigurement:
o Beta-blocker: PO (propranolol) or topical (timolol)
o Corticosteroid: PO or topical
o Until theoretical involution or 12m
o If cosmetically-sensitive or high-risk/ulceration, can additionally consider:
Pulsed laser dye
Surgical excision
how does hand foot and mouth disease present ? and mx
Clinical features
* mild systemic upset: sore throat, fever
* oral ulcers
* followed later by vesicles on the palms and soles of the feet
Hand, foot and mouth disease is a self-limiting condition affecting children. It is caused by the intestinal viruses of the Picornaviridae family (most commonly coxsackie A16 and enterovirus 71). It is very contagious and typically occurs in outbreaks at nursery
self limiting / symptomatic tx
features of infantile seborrhoeic dermatitis
- ‘Cradle-cap’
- Erythematous scaly eruption in first 2 months of life
- Progresses to thick yellow adherent layer
- Starts on scalp, spreads to the face, flexures and napkin area
- Not itchy
- Management –
o Infants: baby shampoo/oil, barrier emollients, topical antifungal creams (clotrimazole, miconazole)
o Children/adolescents: ketoconazole shampoo/creams, selenium sulphide shampoo, coal tar, salicylic acid ointment
features of atopic eczema
- Itchy rash typically in face, trunk and flexor surfaces (age-dependent)
- Common in first year of life
- Associated with asthma and hay fever
- Scratching causes excoriation, crusting, infection and eventually lichenification
- Management – avoid precipitants, emollients, topical corticosteroids, occlusive bandages, antihistamine, antibiotics, immunomodulators
how to manage nappy rash
o Disposable nappies are better than towel nappies
o Expose nappy area to air where possible
o Apply barrier cream (e.g. Sudocrem)
o Mild steroid cream (e.g. 1% hydrocortisone) in severe cases
o Manage suspected candida nappy rash with topical imidazole (cease the use of barrier cream until candida has settled)
features of candida infection paeds
- Both causes and complicates napkin rashes
- Spares flexures
- Satellite pustules
- Management – ensure good hygiene, topical antifungals
features of molluscum contagiosum
- Caused by a poxvirus
- Pearly papules with central umbilication through which the infectious central core is shed
- Usually disappear spontaneously
- Management (if needed) – cryotherapy, topical antibacterials to prevent/treat secondary bacterial infection
features of scabies
- Caused by Sarcoptes scabiei
- Severe itching worse at night and in warmth
- Ask about family’s living situation
- Between fingers and toes, axillae, palms, soles and trunk in younger children
Treatment – treat child and whole family, 5% permethrin cream or 0.5% malathion lotion to whole body below neck, washed off after 12 hours
features of ring worm
- Annular lesions with a crusted edge caused by dermatophyte fungi
- Kerion – severe inflammatory pustular ringworm
- Treatment – topical antifungals, systemic antifungal for severe infection, treat source (often animals)
features of erythema multiforme
- Target lesions, can also be vesicular or bullous
- Caused by herpes simplex, Mycoplasma pneumonia and other infections and drugs
- Usually resolves spontaneously within a few weeks
features of psoriasis
- Most commonly guttate psoriasis following strep/viral URTI
- Small erythematous patches with silvery scale on trunk and upper limbs
- Rare before 2 years, rarely chronic
- Management – emollients, coal tar, dithranol (for resistant cases), calcipotriol (over 6 years of age)
- Can be associated with arthritis
features of acne vulgaris
- Can occur 1 – 2 years before onset of puberty
- Due to obstruction of sebum flow in sebaceous follicle
- Open/closed comedones, papules, pustules, nodules, cysts on face, neck, back, shoulders
- Can produce scarring
- Treatment – topical – benzoyl peroxide, antibiotics, retinoids. Systemic – oral antibiotics (tetracyclines only licensed if over 12 years old), isotretinoin
features of erythema nodosum
- Tender discrete red nodules on the shins
- Caused by Strep, primary TB, IBD, drugs
- Treatment – treat underlying cause, compression, anti-inflammatories
features of meningococcal septicaemia rash
- Caused by Neisseria meningitides septicaemia
- Characteristic non-blanching purpuric lesions irregular in size and outline with a necrotic centre
- Called ‘purpura fulminans’ if widespread
- Often non-specific initial presentation – fever, vomiting, poor feeding, irritability, lethargy, seizures, reduced consciousness, shock; later bulging fontanelle, neck stiffness and opisthotonus
- Typically headache, neck stiffness and photophobia
- Diagnosis – LP (turbid fluid, polmorphs, high protein, low glucose)
- Management – rapid initiation of antibiotics – 3rd generation cephalosporin e.g. ceftriaxone)
features of Erythema infectiosum / fifth disease / slapped cheek syndrome
- Common infection caused by parvovirus B19
- Often asymptomatic
- Rash – initially ‘slapped cheek’, progresses to maculopapular lace-like rash on trunk and limbs
- Rash associated with fever, malaise, headache and myalgia
- Infects erythroblastoid red cell precursors in BM, so causes aplastic crisis in sickle cell (↑ RBC turnover), also in immunocompromised
- Maternal transmission can cause hydrops and foetal death due to severe anaemia
- Paracetamol or ibuprofen and encourage adequate fluid intake
- Secondary arthritis may be treated with ibuprofen
head lice mx
- wet combing
- dimeticone lotion (insecticide)
3.
tx periorbital cellultiis
cefotaxime or clindamycin)
ringworm mx
Tinea Corporis (body), Tinea Cruris (jock)
o Mild infections - terbinafine cream, clotrimazole
o If marked inflammation- hydrocortisone 1% cream
o severe infections:
1st line: oral terbinafine
2nd line: oral itraconazole
o Topical aluminium acetate (in some)
- Tinea Capitis (head)
o Systemic antifungal therapy (e.g. griseofulvin or terbinafine)
o 2nd line: itraconazole or fluconazole
o Adding topical antifungal shampoo is recommended in some patients (e.g. selenium sulfide or ketoconazole topical) - NOTE: any animal source of the infection will also need treatment
- Advice
o Wear loose-fitting cotton clothing
o Wash affected areas of skin daily
o Dry thoroughly after washing
o Avoid scratching
o Do not share towels
o Wash clothes and bed linen frequently
o No need for school exclusion
scabies mx
permethrin 5% cream
apply to whole body
normal age for children being dry ?
- Most children are dry by day and night by the age of 5 years
o Children are dry by day only by the age of 4 years
mx for enuresis
o BED
Behavioral - Advise onreduced fluid intake before bed, diet and toileting behaviour & Reward systems (e.g. star charts)
Enuresis alarm
Desmopressin: may be used 1st line if > 7 years or if short-term control is needed (e.g. holiday)
outline henoch schonlein purpura
IgA vascultitis
HSP is an immune-mediated small vessel vasculitis. IgA and complement components (C3) are deposited in vessel walls leading to inflammation.
The mechanism underlying this is not entirely clear, but HSP can follow an upper respiratory tract infection, so it is thought to be triggered by an abnormal immune system response.
Features
palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure
how does UTI present in children ?
Presentation in childhood depends on age:
* infants: poor feeding, vomiting, irritability
* younger children: abdominal pain, fever, dysuria
* older children: dysuria, frequency, haematuria
* features which may suggest an upper UTI include: temperature > 38ºC, loin pain/tenderness
how to collect urine in child ?
Urine collection method
clean catch is preferable
if not possible then urine collection pads should be used
cotton wool balls, gauze and sanitary towels are not suitable
invasive methods such as suprapubic aspiration should only be used if non-invasive methods are not possible
causes of epididimoorchitis
o Sexually transmitted infection
* Age <35 yrs
* 1+ sexual partner in last 12 months
* Urethral discharge
o Gonorrhoeal
* Previous gonorrhoeal infection
* Purulent urethral discharge
* Men who have sex with men
* Black ethnicity
o Enteric organisms associated with UTIs
* Age >35 yrs
* Low risk sexual history
* History of penetrative anal sex
* Recent catheterisation
o Consider testing for HIV, hepatitis, syphilis, trichomoniasis and mumps
how to manage a hydrocele ?
- < 2 years (congenital hydrocoele) = most resolve spontaneously before the age of 2 so observation is appropriate unless there is bowel palpable in the groin and provided there is no evidence of underlying pathology
- 2-11 years - hydrocele persists beyond 2 years
o Open repair
o Laparoscopic exploration
o Bilateral repair
o Abdominoscrotal hydrocoeles - require surgery through an abdominal incision - 11-18 years - commonly non-communicating hydrocoele
o Idiopathic hydrocoele - observation is appropriate, however, surgery may be considered if it is large or uncomfortable
o Hydrocoele after varicocelectomy - conservative management is the initial approach, surgery is considered in cases that do not resolve
o Filarial-related hydrocoele (parasitic infection) - complete excision of the tunica vaginalis
young boy with ball pain - what should you think about … outline the features + how to manage
pain is usually severe and of sudden onset
the pain may be referred to the lower abdomen
nausea and vomiting may be present
on examination, there is usually a swollen, tender testis retracted upwards. The skin may be reddened
cremasteric reflex is lost
elevation of the testis does not ease the pain (Prehn’s sign)
management:
- Presenting within 4-6 hours of symptom-onset has a greater likelihood of testicular viability
Management
* If suspected admit immediately to urology or paediatric surgery
o IV fluids, NBM, antiemetics, analgesia
mx Wilm’s Tumour (Nephroblastoma)
*
Surgery (nephrectomy) and chemotherapy (may be post-operative or pre-operative)
mx beta thalassaemia major
regular blood transfusions
non-accidental injury – red flags:
o Bruises are on a child who is not yet independently mobile (crawling, cruising, or walking).
o Bruises have indicative features - unusually large, multiple sites or in clusters, similar shape and size, patterned in the shape of a hand print, ligature, stick, tooth, grip, or implement (such as a belt).
o Bruises are found in indicative places - any non-bony part of the body or face (including the eyes, ears, cheeks, back, abdomen, buttocks, arms, and genitalia).
o Explanation for the bruising is implausible, inadequate, or inconsistent
o Delay in presentation.
o If suspicions of NAI, screen for other injuries and perform skeletal survey to investigate. Inform safeguarding team.
prophylaxis in sickle cell for kids
- Immunisation against encapsulated organisms (e.g. S. pneumoniae and H. influenzae type B)
- Daily oral penicillin
- Daily oral folic acid
- Vaso-occlusive crises should be minimised by avoiding exposure to cold, dehydration, excessive exercise, undue stress or hypoxia
different type of bleeding for platelet disrder vs coagulation disorder
platelet=
Site Skin, mucus membranes (epistaxis, gum, vaginal, GI)
coagulation =
Soft tissues, joints, muscles
Role of von Willebrand factor and therefore consequences of VWD
- large glycoprotein which forms massive multimers up to 1,000,000 Da in size
- promotes platelet adhesion to damaged endothelium
- carrier molecule for factor VIII
Types
type 1: partial reduction in vWF (80% of patients)
type 2*: abnormal form of vWF
type 3**: total lack of vWF (autosomal recessive)
Investigation
prolonged bleeding time
APTT may be prolonged (it stablises factor 8)
factor VIII levels may be moderately reduced
defective platelet aggregation with ristocetin
acute and chronic management of acute sickle cell crisis
Management of Acute Crises
* Oral and IV analgesia (avoid morphine < 12 years)
* Good hydration (oral or IV)
* Infection should be treated with antibiotics
* Oxygen (if reduced saturation)
* Exchange transfusion is indicated for acute chest syndrome, priapism and stroke
Management of Chronic Problems
* Children who have recurrent hospital admission (>3 in 12 months) for acute chest syndrome or vaso-occlusive crises could benefit from hydroxycarbamide (stimulated HbF production)
o Monitor for white blood cell suppression (side-effect of hydroxycarbamide)
* Splenectomy with immunisation against encapsulated organisms
* Bone marrow transplant may be considered in severe cases
types of von willebrand disease
Types
type 1: partial reduction in vWF (80% of patients)
type 2*: abnormal form of vWF
type 3**: total lack of vWF (autosomal recessive)
ballooning under the foreskin during urination
paraphimosis
mx for retinoblastoma
- Average age of diagnosis: 18 months
- In propriety, goals of treatment: Save life, save eye, save vision
- Frequent eye examinations under anaesthesia to assess the response to treatment
Management
* Gross vitreous seeding present (tumor cells floating within the vitreous cavity)
o 1st LINE: Enucleation (surgical removal of the eye without resection of the lids or extraocular muscles
o Infiltration of the iris, ciliary body or sclera: Adjuvant chemotherapy: carboplatin, etoposide, and vincristine
* Minimal or no vitreous seeding present
o 1st LINE: systemic chemotherapy (carboplatin, vincristine, etoposide)
o PLUS: focal therapy (cryotherapy or laser therapy)
* Family history of retinoblastoma/detected at birth
o Usually treated by laser alone
o Followed up with an examination under anaesthesia every month for at least 1 year
* Vitreous seeding after chemotherapy and/or focal therapy
o 1st LINE: external beam radiotherapy
- Most patients are cured (90%)
- However, many will be visually impaired
- Significant risk of second malignancy (especially sarcoma) among survivors of hereditary retinoblastoma
bruising in kids what should you think striaght away ?
NAI
blood results in DIC
- ↓ platelets, ↓ fibrinogen, ↑ PT & APTT, ↑ fibrinogen degradation products
signs of acute haemolysis in g6pd
- Parents should be advised on the signs of acute haemolysis (jaundice, pallor, dark urine)
ITP Mx
- In 80% of children, the disease is acute, benign and self-limiting
- It will resolve spontaneously within 6-8 weeks
- Most children can be managed at home
- Treatment is indicated if there is evidence of major bleeding (e.g. intracranial or gastrointestinal) or persistent minor bleeding that affects daily life (e.g. excessive epistaxis)
Management - Life- or Organ-threatening bleeding
o IVIG + corticosteroid + platelet transfusion
o Antifibrinolytics (Aminocaproic and tranexamic acid) may be used - Newly Diagnosed Child
o Asymptomatic or Minor Bleeding
Observation (most will achieve a normal platelet count eventually)
Most manifestations are limited to the skin
o Major Bleeding
Corticosteroids
IVIG OR anti-D immunoglobulin - Child with Chronic Disease
o Mycophenolate mofetil
o Rituximab
o Eltrombopag (thrombopoietin receptor agonist)
o 2nd line: splenectomy (if persistent)
mx for haemophilia A and B
- Recombinant factor VIII concentrate for haemophilia A
o 10-15% of patients will develop antibodies to factor VIII treatment - Recombinant factor IX concentrate for haemophilia B
Management
* Acute bleeds are treated with factor concentrates and anti-fibrinolytics (e.g. aminocaproic acid, tranexamic acid)
* NOTE: these should be given by prompt IV infusion whenever there is any bleeding
* Analgesia and physiotherapy may be required for deep bleeds into muscles and joints
* Orthopaedic and pain team review may also be necessary
* In patients with haemophilia, the following should be AVOIDED:
o IM injections
o Aspirin
o NSAIDs
outline sickle cell management acute and chronic
Prophylaxis
* Immunisation against encapsulated organisms (e.g. S. pneumoniae and H. influenzae type B)
* Daily oral penicillin
* Daily oral folic acid
* Vaso-occlusive crises should be minimised by avoiding exposure to cold, dehydration, excessive exercise, undue stress or hypoxia
Management of Acute Crises
* Oral and IV analgesia (avoid morphine < 12 years)
* Good hydration (oral or IV)
* Infection should be treated with antibiotics
* Oxygen (if reduced saturation)
* Exchange transfusion is indicated for acute chest syndrome, priapism and stroke
Management of Chronic Problems
* Children who have recurrent hospital admission (>3 in 12 months) for acute chest syndrome or vaso-occlusive crises could benefit from hydroxycarbamide (stimulated HbF production)
o Monitor for white blood cell suppression (side-effect of hydroxycarbamide)
* Splenectomy with immunisation against encapsulated organisms
* Bone marrow transplant may be considered in severe cases
Prognosis
* Can cause premature death due to complications
* 50% of patients with the most severe form of sickle cell disease will die < 40 years
DDH risk factors
Risk factors
* female sex: 6 times greater risk
* breech presentation
* positive family history
* firstborn children
* oligohydramnios
* birth weight > 5 kg
* congenital calcaneovalgus foot deformity
clinical exam findings in DDH + ix
Clinical examination
* Barlow test: attempts to dislocate an articulated femoral head
* Ortolani test: attempts to relocate a dislocated femoral head
* other important factors include:
* symmetry of leg length
* level of knees when hips and knees are bilaterally flexed
* restricted abduction of the hip in flexion
Imaging
ultrasound is generally used to confirm the diagnosis if clinically suspected
however, if the infant is > 4.5 months then x-ray is the first line investigation
how is DDH screened ?
Screening for DDH
the following infants require a routine ultrasound examination
* first-degree family history of hip problems in early life
* breech presentation at or after 36 weeks gestation, irrespective of presentation at birth or mode of delivery (they need an ultrasound of the pelvis at 6 weeks)
* multiple pregnancy
* all infants are screened at both the newborn check and also the six-week baby check using the Barlow and Ortolani tests
mx for DDH
- Summary
o Most unstable hips will resolve spontaneously by 3-6 weeks
o Pavlik harness in children younger than 4-5 months
o Older children may require surgery
o Female sex at greater risk
how does juvenile idiopathic arthritis present ?
Features of systemic onset JIA include
* pyrexia
* salmon-pink rash
* lymphadenopathy
* arthritis
* uveitis
* anorexia and weight loss
REMEMBER YOU CAN GET A FEVER!!
Investigations
ANA may be positive, especially in oligoarticular JIA
rheumatoid factor is usually negative
Juvenile idiopathic arthritis (JIA) refers to persistent joint swelling lasting longer
than 6 weeks in patients under the age of 16 years.
mx forf juvenile idiopathic arthritis ?
Management
* Pharmacological management:
o Simple analgesia e.g. Paracetamol
o NSAIDs are useful for controlling pain and stiffness
o Consider weak opioids e.g. codeine
* Intra-articular, oral or IV corticosteroids are useful adjunctive agents (whilst waiting for second-line agents to have an effect) – avoided if possible due to risk of growth suppression and osteoporosis
* DMARDs - used when the disease fails to respond to conventional treatments
o 1st line: oral or SC methotrexate
o 2nd line: sulfasalazine
* Other treatments: Inflammatory cytokine blockade e.g. TNF-alpha inhibitors, interleukin receptor antagonists, anti-emetics
outline osgood schlatter disease
Osgood-Schlatter disease (tibial apophysitis) is a type of osteochondrosis characterised by inflammation at the tibial tuberosity. It is a traction apophysitis thought to be caused by repeated avulsion of the apophysis into which the patellar tendon is inserted
Management is supportive
- Seen in sporty teenagers (‘osGOOD at sports)
Management - Advise about pain relief
o Analgesia - paracetamol or NSAIDs
o Intermittent application of ice packs over the tibial tuberosity (10-15 mins up to 3 times per day, including after exercise)
o Protective knee pads (may relieve pain when kneeling) - Reassure the patient and parents that this will resolve over time but may persist until the end of a growth spurt
- Reassure that usually stopping all sporting activity is not necessary
o Reduce sporting activity (intensity, frequency or duration)
o Change the type of exercise to limit the amount of running and jumping requiring powerful quadriceps contraction if they cannot tolerate normal activity
o As symptoms decrease, they can gradually increase their exercise levels
o Introduce low-impact quadriceps exercises (e.g. isometric quadriceps contractions, straight leg raises, cycling or swimming) - Reassure that usually stopping all sporting activity is not necessary
- If symptoms do not improve or worsen OR symptoms persist into adulthood despite the above management, refer for specialist assessment by orthopaedic surgeon.
o ADVICE
Victorian Paediatric Orthopaedic Network fact sheet on Osgood-Schlatter disease has an explanation of the condition as well as instruction on some useful stretches
Proper stretching before and after exercise may reduce symptoms
what is this ?
Knee pain and swelling, typically after exercise
Knee catching, locking and/or giving way
Feeling a painful ‘clunk’ when flexing or extending the knee
Osteochondritis Dissecans
Osteochondritis dissecans (OCD) is a pathological process affecting the subchondral bone (most often in the knee joint) with secondary effects on the joint cartilage, including pain, oedema, free bodies and mechanical dysfunctions. It generally affects children and young adults. OCD may progress to degenerative changes if untreated.
Patients typically present with a subacute onset of:
Knee pain and swelling, typically after exercise
Knee catching, locking and/or giving way: more constant and severe symptoms are associated with the presence of loose bodies
Feeling a painful ‘clunk’ when flexing or extending the knee - indicating the involvement of the lateral femoral condyle
Signs:
Joint effusion
Tenderness on palpation of the articular cartilage of the medial femoral condyle, when the knee is flexed
Wilson’s sign for detecting medial condyle lesion - with the knee at 90° flexion and tibia internally rotated, the gradual extension of the joint leads to pain at about 30°, external rotation of the tibia at this point relieves the pain
Investigations:
X-ray (anteroposterior, lateral and tunnel views) - may show the subchondral crescent sign or loose bodies
MRI - used to evaluate cartilage, visualise loose bodies, stage and assess the stability of the lesion
Management
Early diagnosis is important
Clinical signs may be subtle in the early stages hence there should be a low threshold for imaging and/or orthopaedic opinion.
- Pain relief (paracetamol or ibuprofen)
- Rest and quadriceps exercises
- Sometimes surgical intervention is needed (to remove intra-articular loose bodies)
anterior knee pain exacerbated by running, climbing stairs, and getting up from a chair.
Passive movements are usually painless, but repeated extension may produce
pain and a grating feeling, and crepitus or a small effusion may be palpable.
what is it ?
Chondromalacia patellae
Chondromalacia patellae is defined as anterior knee pain caused by degeneration
of the articular cartilage on the posterior surface of the patella. It is particularly
common in young adults as a result of overuse in physical activities. The pain
may be exacerbated by running, climbing stairs, and getting up from a chair.
Passive movements are usually painless, but repeated extension may produce
pain and a grating feeling, and crepitus or a small effusion may be palpable.
Patients should receive physiotherapy to strengthen the quadriceps.
- hip pain: develops progressively over a few weeks
- limp
- stiffness and reduced range of hip movement
perthes
what age group for perthes ?
4-8 y/o
arthritis, uveitis, and urethritis
Reactive Arthritis
can’t see, can’t pee, can’t climb a tree
how does septic arthritis present , give ix + mx
Symptoms
joint pain
limp
fever
systemically unwell: lethargy
Signs
swollen, red joint
typically, only minimal movement of the affected joint is possible
Investigations
joint aspiration: for culture. Will show a raised WBC
raised inflammatory markers
blood cultures
The Kocher criteria for the diagnosis of septic arthritis:
fever >38.5 degrees C
non-weight bearing
raised ESR
raised WCC
- Prolonged course of antibiotics (initially IV for 2 weeks, followed by 4 weeks of oral antibiotics)
o Neonate to <3 months:
IV cefotaxime
o 3 months to </=5 years:
IV ceftriaxone
If penicillin allergic, give clindamycin
o >/=6 years
IV flucloxacillin
If penicillin allergic, give clindamycin
o Oral stepdown:
Co-amoxiclav
Flucloxacillin - Joint aspiration - affected joints should be aspirated to dryness as often as required (through closed needle aspiration or arthroscopically)
- Washing out of the joint or surgical drainage may be required
Slipped Capital Femoral Epiphysis (SUFE)
Slipped upper femoral epiphysis
Typically seen in obese male adolescents. Pain is often referred to the knee. Limitation to internal rotation is usually seen. Knee pain is usually present 2 months prior to hip slipping. Bilateral in 20%.
X-rays will show the femoral head displaced and falling inferolaterally (like a melting ice cream cone) The Southwick angle gives indication of disease severity
- Ensure patient remains non-weight-bearing, analgesia, immediate orthopaedic referral
- Surgical repair
- In situ screw fixation across the growth plate
Viva Tips
What are the X-ray findings?
o Trethowan’s sign: line of Klein does not intersect superior femoral epiphyses/asymmetry between line of Klein’s on either side
features of rickets and mx
Rickets is a term that describes inadequately mineralised bone in developing and growing bones. This results in soft and easily deformed bones. It is usually due to vitamin D deficiency. In adults, the equivalent condition is termed osteomalacia
Predisposing factors
dietary deficiency of calcium, for example in developing countries
prolonged breastfeeding
unsupplemented cow’s milk formula
lack of sunlight
Features
aching bones and joints
lower limb abnormalities:
in toddlers genu varum (bow legs)
in older children - genu valgum (knock knees)
‘rickety rosary’ - swelling at the costochondral junction
kyphoscoliosis
craniotabes - soft skull bones in early life
Harrison’s sulcus
Investigations
low vitamin D levels
reduced serum calcium - symptoms may results from hypocalcaemia
raised alkaline phosphatase
mx=
* If calcium deficient rickets with vitamin D deficiency
o Daily calcium AND
o Ergocalciferol (vit D2) / colecalciferol (vit D3)
* If pseudo-vitamin D deficiency (defect in 1-alpha hydroxylase)
o Calcitriol / alfacalcidol
* Phosphate salts are used in hypophosphataemic rickets
* Dietary: oily fish, egg yolk
how does transient synovitis present ?
Transient synovitis is sometimes referred to as irritable hip. It generally presents as acute hip pain following a recent viral infection. It is the commonest cause of hip pain in children. The typical age group is 3-8 years.
Features
* limp/refusal to weight bear
* groin or hip pain
* a low-grade fever is present in a minority of patients
* high fever should raise the suspicion of other causes such as septic arthritis
diagnosis of ADHD ?
diagnosis of attention deficit hyperactivity disorder (ADHD) which requires the presence of symptoms for at least 6 months in at least two different environments. If not hitting criteria then watchful waiting is important
classification of cerebral palsy
Classification
spastic (70%)
subtypes include hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons
dyskinetic
caused by damage to the basal ganglia and the substantia nigra
athetoid movements and oro-motor problems
ataxic
caused by damage to the cerebellum with typical cerebellar signs
mixed
risk factors for cerebral palsy
- Risk Factors
o Antenatal: Chorioamnionitis, maternal respiratory or GU infection
o Perinatal: Preterm birth, LBW, neonatal encephalopathy, neonatal sepsis, maternal infection (e.g. respiratory or genito-urinary)
o Postnatal: Meningitis, head trauma prior to 3 years
o Delayed motor milestones for cerebral palsy
(correct for gestational age)
Not sitting by 8 months
Not walking by 18 months
Hand preference before 1 year
o Refer all children with persistent toe walking
mx for cerebral palsy
- Summary
o Physiotherapy – encourage movement, improve strength and stop muscles from losing range of motion
o Speech therapy – improve language abilities
o Occupation therapy – identify everyday tasks that may be difficult and help make these tasks more accessible
o Medication
Stiffness – baclofen, diazepam
Sleeping – melatonin
Constipation – laxatives
Drooling – anticholinergic
gross motor development milestones
3 months Little or no head lag on being pulled to sit
Lying on abdomen, good head control
Held sitting, lumbar curve
6 months Lying on abdomen, arms extended
Lying on back, lifts and grasps feet
Pulls self to sitting
Held sitting, back straight
Rolls front to back
7-8 months Sits without support (Refer at 12 months)
9 months Pulls to standing
Crawls
12 months Cruises
Walks with one hand held
13-15 months Walks unsupported (Refer at 18 months)
18 months Squats to pick up a toy
2 years Runs
Walks upstairs and downstairs holding on to rail
3 years Rides a tricycle using pedals
Walks up stairs without holding on to rail
4 years Hops on one leg
speech and hearing development milestones
Age Milestone
3 months Quietens to parents voice
Turns towards sound
Squeals
6 months Double syllables ‘adah’, ‘erleh’
9 months Says ‘mama’ and ‘dada’
Understands ‘no’
12 months Knows and responds to own name
12-15 months Knows about 2-6 words (Refer at 18 months)
Understands simple commands - ‘give it to mummy’
2 years Combine two words
Points to parts of the body
2½ years Vocabulary of 200 words
3 years Talks in short sentences (e.g. 3-5 words)
Asks ‘what’ and ‘who’ questions
Identifies colours
Counts to 10 (little appreciation of numbers though)
4 years Asks ‘why’, ‘when’ and ‘how’ questions
fine motor development milestones
The tables below summarises the major fine motor and vision developmental milestones
Age Milestone
3 months Reaches for object
Holds rattle briefly if given to hand
Visually alert, particularly human faces
Fixes and follows to 180 degrees
6 months Holds in palmar grasp
Pass objects from one hand to another
Visually insatiable, looking around in every direction
9 months Points with finger
Early pincer
12 months Good pincer grip
Bangs toys together
Bricks
Age Milestone
15 months Tower of 2
18 months Tower of 3
2 years Tower of 6
3 years Tower of 9
Drawing
Age Milestone
18 months Circular scribble
2 years Copies vertical line
3 years Copies circle
4 years Copies cross
5 years Copies square and triangle
Book
Age Milestone
15 months Looks at book, pats page
18 months Turns pages, several at time
2 years Turns pages, one at time
social and play development mielstones
Developmental milestones: social behaviour and play
The table below summarises the major social behaviour and play milestones
Age Milestone
6 weeks Smiles (Refer at 10 weeks)
3 months Laughs
Enjoys friendly handling
6 months Not shy
9 months Shy
Takes everything to mouth
Feeding
Milestone Age
May put hand on bottle when being fed 6 months
Drinks from cup + uses spoon, develops over 3 month period 12 -15 months
Competent with spoon, doesn’t spill with cup 2 years
Uses spoon and fork 3 years
Uses knife and fork 5 years
Dressing
Milestone Age
Helps getting dressed/undressed 12-15 months
Takes off shoes, hat but unable to replace 18 months
Puts on hat and shoes 2 years
Can dress and undress independently except for laces and buttons 4 years
Play
Milestone Age
Plays ‘peek-a-boo’ 9 months
Waves ‘bye-bye’
Plays ‘pat-a-cake’ 12 months
Plays contentedly alone 18 months
Plays near others, not with them 2 years
Plays with other children 4 years
rescue therapy for seizure lasting longer than 5 mins ?
buccal midazolam
drug for tonic clonic seizures
sodium valproate
drug for absense seizures
ethosuximide
drug for focal seizures
levetiracetam, lamotrigine
age for febrile convulsions
6 months - 5 years old
causes of febrile seizure
Any febrile illness can cause febrile seizures, but around 80% are viral. Common causes include:
* Respiratory tract infections
* Otitis media (this will be the kid who is touching his ear a lot – could ask about this in Hx)
* Urinary tract infections
* Influenza.
what is recovery like after febrile convulsion?
The majority of children (75%) present with a simple febrile convulsion. This is typically a generalised tonic-clonic seizure, presenting with muscle stiffness and jerking or shaking of the limbs, without focal features. Additional features may include:
* Breathing difficulties
* Pallor
* Cyanosis
* Loss of consciousness
This is often followed by post-ictal drowsiness and confusion, which may last anywhere from several minutes to hours. Seizures rarely last longer than 10 minutes, occur once within 24 hours or within the same febrile illness, and resolve spontaneously, the vast majority with full recovery within 1 hour
febrile status epilepticus ?
febrile seizure lasting longer than 30 misn
red flag sx of headahce in kids
red flag symptoms:
o Waking at night or present on waking in the morning
o Features of meningism
o Vomiting or ataxia
o Aggravated by coughing, sneezing, or bending down
o Progressively worsens
o Change in conscious level or pervasive lethargy
o Within 5 days of head injury
o Squint or failure of upward gaze
o New onset cognitive dysfunction
important to ask about specificvs of teh seiure ?
An eyewitness history is key to establish the duration and nature of the seizure. Important features to ask about:
Presence of fever
* Onset
* Peak temperature
* Duration
Details of seizure
* Characteristics
* Duration
It is also important to clarify whether this is the first presentation of a seizure.
Additional factors to note include developmental history and immunisation history, including any recent immunisations.
mx for hydrocephalus
ventriculoperitoneal shunt
mx migraine
- paracetoml / ibruprofen
- nasal sumatriptan
- combination of above ^
portwine
stain in the distribution of the ophthalmic division of the trigeminal nerve with
associated intracranial lesions.
Sturge–Weber syndrome
café au lait spots, neurofibromas, optic gliomas, Lisch nodules, and sphenoid dysplasia.
neurofibromatosis type 1
schwannomas of the vestibulocochlear nerve (causing hearing loss), meningiomas, and spinal cord ependymomas.
neurofibromatosis type 2
mx for status epilepticus
- Step 1: (0 min)
o Secure airway
o Check ABC, high flow Oxygen2 if available
o Check blood glucose
o Confirm clinically that it is an epileptic seizure - Step 2: (5 min)
o If IV access, IV lorazepam
o If NO immediate IV access:
Buccal midazolam
Rectal diazepam - Step 3: (15 min)
o if no response, give a second dose of IV lorazepam
o Call for senior help
o Start to prepare phenytoin for step 4
o Re-confirm it is an epileptic seizure - Step 4: (25 min)
o Seek senior anaesthetist / inform ICU
o Phenytoin 20 mg/kg by intravenous infusion over 20 mins
or (if on regular phenytoin): Phenobarbital 20 mg/kg intravenously over 5 mins
o Consider rectal paraldehyde 0.8 ml/kg - Step 4: (45 min)
o Rapid sequence induction of anaesthesia using thiopental sodium - Consider dexamethasone if vasculitis/cerebral oedema is possible
- NOTE: treat reversible causes if identified (e.g. thiamine if malnourished or glucose if hypoglycaemic)
mx for CAH
- Affected females sometimes need corrective surgery for external genitalia (they have a uterus and ovaries so they are reared as girls)
- Definitive surgical correction is usually delayed until puberty
- Acute (salt losing crisis)
o IV saline (0.9% sodium chloride), IV hydrocortisone 200mg, IV dextrose - Long Term
o Life-long glucocorticoids (hydrocortisone) to suppress ACTH levels (and hence testosterone)
o Mineralocorticoids (fludrocortisone) if there is salt loss
o Monitoring growth, skeletal maturity, plasma androgens and 17α-hydroxyprogesterone levels
o Additional hormone replacement at times of illness or surgery
names of teh specific enzymes in CAH ?
21-hydroxylase deficiency (90%)
impairs the conversion of 17-hydroxyprogesterone to 11-deoxycortisol, leading to cortisol deficiency and excess androgen production
11-beta hydroxylase deficiency (5%)
results in hypertension due to excess deoxycorticosterone
17-hydroxylase deficiency (very rare)
leads to mineralocorticoid excess with low androgen and estrogen levels
short repeated spasms in kids
Infantile spasms
Infantile spasms, or West syndrome, is a type of childhood epilepsy which typically presents in the first 4 to 8 months of life and is more common in male infants. They are often associated with a serious underlying condition and carry a poor prognosis
Features
characteristic ‘salaam’ attacks: flexion of the head, trunk and arms followed by extension of the arms
this lasts only 1-2 seconds but may be repeated up to 50 times
progressive mental handicap
Investigation
the EEG shows hypsarrhythmia in two-thirds of infants
CT demonstrates diffuse or localised brain disease in 70% (e.g. tuberous sclerosis)
Management
poor prognosis
vigabatrin is now considered first-line therapy / high dose pregnisolone
ACTH is also used
how to manage cerebral oedema as a consequence of DKA ?
The osmotic pressure range between intravascular and brain cells during DKA treatment has also been proposed as a cause of cerebral edema. Diabetic ketoacidosis causes an increase in plasma osmolality, whereas osmolytes accumulate in brain cells, resulting in no osmotic pressure gap
mannitol or hypertonic sodium chloride
what can cause a first epsiode of DKA in t1dm kido?
- Discuss factors that led to this episode
- Advice on how to manage intercurrent illness (e.g. viral infections leading to increased insulin demand)
what are the different types of insulin therpay for t1dm in kids ?
o Three Types of Insulin Therapy
Multiple Daily Injection Basal-Bolus: injections of short-acting insulin or rapid-acting insulin analogue before meals, with 1 or more separate daily injections of intermediate acting insulin or long-acting insulin analogue
Continuous Subcutaneous Insulin Infusion (insulin pump therapy): programmable pump and insulin storage device that gives regular or continuous amounts of insulin (usually rapid-acting insulin or short-acting insulin) by a subcutaneous cannula
One, Two or Three Insulin Injections Per Day: injections of short-acting insulin or rapid-acting insulin analogue mixed with intermediate-acting insulin
o Offer multiple daily injection basal-bolus insulin regimens from diagnosis
o If this is inappropriate, consider continuous subcutaneous insulin infusion (CSII or pump therapy)
mx for hyperthyroidism
- 1st line: Medical - Carbimazole or propylthiouracil
- 2nd line: Radioiodine treatment, Surgery (partial thyroidectomy)
side effects of hyperthroid medication ?
- 1st line: Medical - Carbimazole or propylthiouracil
- Important: both thionamides are associated with a risk of neutropaenia
o Families should be safe-netted about seeking urgent medical attention and a blood count if a sore throat or fever occur whilst on treatment
hypocalcaemia mx
- Management of Acute Symptomatic Hypocalcaemia
o IV calcium gluconate - Management of Chronic Hypocalcaemia
o Oral calcium
o High dose vitamin D analogues
o Important: avoid hypercalciuria because it can lead to nephrocalcinosis so urinary excretion should be monitored
features of hypocalcaemia ?
CATS go numb
Convulsions
arrythmias
tetany
spasms and stridor
numb = parathesia
precocious puberty
cafe-au-lait spots
polyostotic fibrous dysplasia
short stature
McCune-Albright syndrome
define precocious puberty and what are the causes ?
Precocious puberty
Definition
‘development of secondary sexual characteristics before 8 years in females and 9 years in males’
more common in females
Some other terms
thelarche (the first stage of breast development)
adrenarche (the first stage of pubic hair development)
May be classified into:
- Gonadotrophin dependent (‘central’, ‘true’)
due to premature activation of the hypothalamic-pituitary-gonadal axis
FSH & LH raised - Gonadotrophin independent (‘pseudo’, ‘false’)
due to excess sex hormones
FSH & LH low
Males - uncommon and usually has an organic cause
Testes
bilateral enlargement = gonadotrophin release from intracranial lesion
unilateral enlargement = gonadal tumour
small testes = adrenal cause (tumour or adrenal hyperplasia)
Females - usually idiopathic or familial and follows normal sequence of puberty
Organic causes
are rare, associated with rapid onset, neurological symptoms and signs and dissonance
e.g. McCune Albright syndrome
mx hypoglycaemia
- Mild-to-Moderate Hypoglycaemia
o Give fast-acting glucose by mouth (usually liquid carbohydrate (e.g. Lucozade))
o May need to be given in small amounts if vomiting
o Recheck blood glucose within 15 mins and repeat fast-acting glucose if hypoglycaemia persists
o As symptoms improve, give oral complex long-acting carbohydrate to maintain blood glucose levels - SEVERE Hypoglycaemia
o Treat in hospital
Give IV 10% glucose (maximum dose of 500 mg/kg of bodyweight (5 ml/kg))
o If NOT in hospital: unresponsive or PO route cannot be used
IM glucagon or concentrated oral glucose solution (e.g. glucogel)
* IM glucagon: 500 µg for < 8 years; 1 mg for > 8 years
Seek medical help if blood glucose remains low after 10 mins
Once symptoms improve, give oral complex long-acting carbohydrate
* NOTE: alcohol is a risk factor for hypoglycaemia (they should eat carbohydrates before and after drinking)
in A-E outline A
Secretions, foreign body
Stridor
See-sawing
Open airway – jaw thrust and position:
* Infant – neutral position
* Children – ‘sniffing’ position
* NB. C-spine control
Remove obstruction if safe
in A-E outline B
Respiratory rate
Symmetry
Wheeze
Work of breathing
Auscultate and monitor
Oxygen
Support breathing
in A to E outline C
Pulse rate and volume
Blood pressure
Capillary refill time
Fluid/blood
Chest compressions
Defibrillation
Look at the colour and temperature of peripheries
Measure capillary refill time
Auscultate the heart
Insert 1 or 2 large bore cannulas
Reassess every 5 mins
Consider fluid bolus if hypotensive
in A to E outline D
Disability
Consciousness
Pupils
Posture
AVPU/GCS
Collateral history re. seizures, trauma, poison, sepsis, diabetes
what to give in anaphylaxis
- Give IM adrenaline 1: 1000 (as per age-related guidelines)
- Give high flow oxygen
- Give IV fluids
- Give IV chlorphenamine 10 mg + IV hydrocortisone 200 mg
neonatal resuss
- At birth, delayed cord clamping if possible
- Dry the baby, remove any wet towels and covers and start the clock or note the time
- Within 30 seconds: assess tone, breathing and heart rate
- Within 60 seconds: if gasping or not breathing – open the airway and give 5 inflation breaths
o Consider SpO2 and ECG monitoring - Re-assess: if no increase in heart rate, look for chest movement
- If chest NOT moving:
o Check mask, head and jaw position
o Consider 2-person airway control
o Consider suction, laryngeal mask/tracheal tube
o Repeat inflation breaths and look for a response
o Consider increasing inflation pressure - If NO increase in heart rate: look for chest movement
- When chest is moving: if heart rate is not detectable or slow (< 60/min) ventilate for 30 seconds
- Reassess heart rate: if still < 60 bpm
o Start chest compressions with ventilation breaths (3:1)
o Increase oxygen to 100%
o Consider intubation if not already done or laryngeal mask if not possible - Reassess heart rate every 30 seconds: if heart rate is not detectable or slow (< 60/min):
o Vascular access and drugs (e.g. atropine)
o Consider other factors, e.g. pneumothorax, hypovolaemia, congenital abnormality
in paeds life support if no signs of life / not breathing normally ?
5 rescue breaths
outline gillick competence
Gillick Competence
* At 16 years or older, a young person can be treated as an adult and be presumed to have capacity to decide
* Under the age of 16 years, children may have capacity to decide, depending on their ability to understand what is involved
* Where a competent child refuses treatment, a person with parental responsibility or the court may authorise investigation or treatment which is in the child’s best interests
* Family Law Reform Act (1969)
o Those over 16 can consent to treatment but CANNOT REFUSE TREATMENT under 18 years old, unless there is one consenting parent, even if the other disagrees
non accidental injury who to involve and what to do ?
- Variety of Presentations
o Bruising
o Broken bones
o Drowsiness (subdural haematoma)
o Neglect (e.g. unkempt)
o Failure to thrive - Is the child in DANGER?
o Could the siblings or parents be in danger?
o MAKE SURE THE CHILD IS IN A SAFE PLACE - Who to get involved?
o Senior colleagues
o Named doctor for child protection
o Contact social services and make a formal referral
o Consider contacting the police (Child Abuse Investigation Team (CAIT))
o Consider contacting Multi-Agency Safeguarding Hub (MASH)
This includes a variety of people that help manage different aspects of a child’s life - Investigations
o Skeletal survey
o CT +/- MRI head scan
o Bloods and bone profile
Rule out leukaemia, ITP etc.
o Ophthalmology referral (fundoscopy for retinal haemorrhages) - GENERAL RULE: if you are suspecting NAI, it is always safe to admit the child
school exclusion for scarlet fever ?
24 hours after abx
whooping cough school eclusion ?
48 hours after abx
measles school exclusion
4 days from onset of rash
rubella school exclusion
5 days from onset of rash
chickenpox school exlcusion
once all lesions crusted over
impetigo school exclusion
once all lesions have crusted over
mumps school exclsuion
5 days from onset of swollen glands
normal vitals for < 1
30 – 40 110 – 160 70 – 90
diarhoea and vomiting school exclusion
until sx settled for 48 hours
normal vitals 2 -5
20 – 30 95 – 140 80 – 100
noraml vitals 5-12
15 – 20 80 – 120 90 – 110
normal vitals > 12
12 – 16 60 - 100 100 - 120
