Paeds things you forget Flashcards
What is most common kidney stone in kids?
Phosphate stone - due to proteus UTI alkalinising urine.
What is fever in kids?
>
- This is red flag if <3m. >39 is fever if >3m.
Red flag infection signs in kids
o Fever >38C if <3m or >39C if 3-6m.
o Colour – pale, mottled, cyanosed.
o Level of consciousness reduced / neck stiffness / bulging fontanelle / status epilepticus / focal neurological signs/seizures
o Significant respiratory distress
o Bile-stained vomiting
o Severe dehydration or shock
Non-specific infection/meningitis abx given to neonates
<3m - cefotaxime. Add ampicillin if <1m to cover Listeria
>3m - ceftriaxone (contraindicated in <3m as displaces bilirubin from binding sites)
Aciclovir if encephalitis considered.
Most common cause of meningitis at different ages:
Neonate to 3m - BEL (Group B strep, E.coli, Listeria)
1m to 6yrs - NHS (N.meningitides, S.pneumoniae, Hib)
>6yrs - N.meningitides, S.pneumoniae
Meningitis prophylaxis
Ciprofloxacin, or Rifampicin
Name a group A and a group B strep
Group A - S.pyogenes
Group B - S.agalactiae
Way to remember, the letter’s dont match
Mumps Px, Ix, Cx
Px - Parotitis, fever, malaise.
Ix - Plasma amylase (may be raised due to pancreatic involvement)
Cx - Orchitis
5C’s of measles
Also 2 Tx’s
Cranky (malaise), cough, coryza, conjunctivitis, coplik spots
Also a rash spreading from behind the ears (maculopapular, effects whole body)
Generally supportive care, if severe:
Ribavirin, Vitamin A supplements
Facts about Kawasaki:
a) What size vessel?
b) What happens to platelets?
c) Ages effected?
d) Diagnostic criteria?
e) Tx (hospital admission? 2 drugs? What if aneurysm?)
a) Medium vessel vasculitis
b) thrombocytosis leading to thrombosis
c) 6m to 4yrs, peaks at age 1.
d) Fever >5 days + 4/5 of Conjunctivitis, Rash, cervical
lymphAdenopathy, Strawberry tongue, swollen/red/peeling Hands
e) Yes admit to ITU. IVIg 10 days, High dose Aspirin 6wks, Warfarin)
Treatment of Chicken Pox? Inc. school exclusion and pregnant mums.
Paracetamol + Diphenhydramine (skin emollient) or antihistamine (NSAIDs contraindicated)
If severe and >2, aciclovir.
Generally excluded for 5 days after onset of rash, or all lesions crusted over.
Pregnant women exposed are tested for immunity (look for varicella antibodies); Ig recommended within 10 days if non-immune, and aciclovir if infection occurs.
School exclusion for the following: Chicken pox, Diarrhoea/vomiting, Mumps, Measles and Rubella, whooping cough
Which xanthems require no school exclusion?
Chicken pox - until lesions have crusted (5 days)
Diarrhoea/vomiting - 2 things so can only come back to school 2 days symptoms free
Mumps has 5 letters, so 5 days after symptoms onset. Same for Rubella (measles 4 days though)
Whooping cough - whoop whoop 2 days since starting abx.
Scarlet fever - 1 day since starting abx.
No exclusion - Slapped cheek (B19), Roseola, EBV, head lice, threatworms and Hand foot and mouth (cox)
Antenatal infection. Features of CMV, VZV, Toxoplasmosis and Rubella infection in pregnancy
Congenital CMV - hearing loss, thrombocytopenia (petechial rash), microcephaly. No Tx, serology to diagnose.
VZV - hypertrophic scars (not petechial rash), limb defects (hypoplasia), ocular defects. Non-immune mum exposed then 10days Ig, aciclovir if infection occurs, similar for baby.
Rubella - triad of sensorineural deafness, ocular defects, CHD (PDA, pulmonary artery stenosis). No Tx.
Toxoplasmosis - cerebral calcification, chorioretinitis, hydrocephalus (mental handicap, convulsions, spasticity, visual impairment). Tx with Spiramycin. If vertical transmission Pyrimethamine + folinic acid.
Loss of internal or external rotation in SCFE?
Inability to internally rotate on flexion of the hip (so there is obligatory external rotation)
In in (inability to internally rotate)
What do you add after SABA and ICS in >/< 5’ for asthma
If >5 you add salmeterol a LABA ( the S of salmeterol looks like a 5 indicating it can be used >5.
If <5 you add montelukast.
Nevermind, it is LTRA for both.
Which kids with pneumonia / bronchiolitis do you admit to hospital?
SASI
* Severe resp distress (grunting, RR >70, marked recessions
* Apnoeas
* Saturations <90% (<92% if <6months)
* Inadequate fluid intake (50-75% of usual)
Levels of asthma attack severity
Moderate - can talk, PEFR >50%, O2 >92%
Severe - cannot talk, PEFR 30-50%, O2 <92%, use of accessory muscles
Life-threatening - silent chest, cyanosis, reduced LOC, exhaustion, normal PCO2
What is first, second line Tx for faecal impaction?
First line - macrogol (osmotic) laxative + electrolytes (Movicol paediatric plan would be polythene glycol and electrolytes)
Second line - Stimulant laxative can be added (e.g. Senna)
If movicol doesnt work, a different osmotic laxative can be used, e.g. lactulose.
NB diet on its own wont treat foetal impaction but is first line for chronic constipation. Bulk laxatives are of value.
What is sandifer syndrome
Unusual movements of head/back associated with reflux. Usually resolves by 2yrs of age.
Management of ITP in kids?
The majority resolve spontaneously over 6-8wks and require no Mx, however safety net. Avoid contact sports.
Only start prednisolone if platelet count is raised. Splenectomy if life threatening.
Tx of AOM? When are abx indicated?
Generally, watch and wait as AOM spontaneously reoslves in 80% of 4 days. Indications for immediate abx = <2, bilateral AOM, systemically unwell.
If abx indicated - first line = 5 day course of amoxicillin, Clarithromycin is 2nd line abx if allergic.
Refer to ENT if >6 episodes in 12m or effusion for >3m bilaterally or >6m unilaterally.
Describe 4 benign skin lesions that may be found on NIPE
Epstein pearls - small white pearls along the midline of the palate.
Milia - white pimples on nose and cheeks
Mongolian blue spots - blue/black macular discoloration looks like bruise. Fade over first few years.
Erythema toxicum - neonatal urticaria 2-3days . White pinpoint papules w/ eosinophils.
What is naveus flammeus?
Port wine stain - present from birth, usually grows with infant. Due to vascular malformation of capillaries. May be associated with Sturge-Weber syndrome.
What is carvernous haemangioma?
Strawberry naevus - not usually present at birth (differentiates from naveus flammeus), but appears in first month. More common in preterm. No Tx but topical propranolol may speed regression.
What are cafe au lait patches related to?
Neurofibromatosis if 5+
Describe irritant dermatitis (nappy rash) Px and Mx
Cx
Irritant effect of urine on skin, worse if mixed with faeces.
Erythematous, scalded appearance. Flexures are spared.
Mild - protective emollient. More severe - topical steroids.
Cx - candida infection may complicate nappy rashes - erythematous, involves flexures and satellite lesions. Tx with topical antifungal.
Describe infantile seborrheic dermatitis Px, Mx
First 3 months of life, starts on scalp as thick, yellow layer (cradle cap). May extend to flexures and napkin area. NOT itchy like eczema.
Mild - emollients. Severe - ointment w/ sulphur/salicylic acid. Mild topical steroid.
Describe atopic eczema in kids Px, Mx
First year of life (uncommon in first 2m like infantile seborrheic dermatitis). Itchy rash predominantly face and trunk (older has flexor/friction surfaces).
Can get eczema herpeticum.
Mx - avoid irritants (soap) and mittens.
Emollients.
Topical corticosteroids need to be used with care. Avoid face.
>2 - immunomodulators cream.
Skin prick testing for cow’s milk protein allergy.
Describe stephen johnson and TEN
Steven johnson is <10% skin involved. If >30% then toxic epidermal necrolysis (TEN).
It is a severe type 4 skin reaction - skin can peel off.
Admit to burn unit/hospital. IVIg, abx, antihistamines.
Cx - dehydration, sepsis.
Some neonatal DS features
Hypotonia
Poor moro reflex
upslanted palpebral fissures
Single palmar crease
Bushfield spots in iris
Low set ears
Global developmental delay
Edward’s what is JEF18?
Trisomy 18
undersized Jaw (micrognathia)
Edward’s
Feet - rocker bottom feet (also can get this in patau’s)
Edward’s and patau’s are similar. What sets them apart?
Polydactyly in patau’s
Angelman’s inheritance?
Imprinting of paternal copy.
Kids are happy and excitable with severe disability.
Fragile X inheritance and Px
X-linked dominant transmission. Expansion of CGG triplet repeat on X-chromosome.
Big long head and big balls but floppy and autistic.
Features of turner’s
Short stature, wide nipples, webbed neck, bicuspid aortic valve/coarctation of aorta, primary amenorrhoea, hypothyroidism.
Describe Pierre-robin syndrome
Micrognathia, Posterior displacement of tongue, Cleft palate.
Small boy with a robin in his mouth
Describe inguinal hernia in kids
Usually indirect through inguinal canal. In premature babies with weak/friable, direct.
Px with lump in groin, can be strangulated = obstruction, pain, vomiting.
Tx - surgery.
Hydrocele / Varicocele
Differentiation from inguinal hernia and Mx
Can get above it.
Usually resolve spontaneously. Surgery considered if persists beyond 2yrs.
Undescended testes Mx, Cx
Present in 5%, more common in premature.
If bilateral undescended testes, karyotype must be established and should be reviewed by senior within 24hrs.
Imagining not helpful.
If 1 not descended, watch and wait for 3m.
Orchidopexy is usually performed at/before 1yr as spontaneous descent unlikely thereafter.
Torsion, reduced fertility, malignancy.
Describe foreskin retraction, rash ballooning
Not retractile before 3yr, then gradually becomes it.
Can become red as part of napkin rash - leave alone unless extensive/purulent discharge.
Ballooning rarely causes any trouble.
When do you worry about phimosis?
Puberty. It is normal up to 3yrs.
BXO (balanitis xerotica obliterans) causes progressive scarring and doesnt invert - worry about this.
<12 - reassurances and hygiene. Steroids if BXO. No surgery.
>12 - try topical corticosteroid. If doesnt work then surgery.
Paraphimosis - ring of narrower skin, requires emergency reduction surgery.
Hypospadias location, associations, Mx
80% on distal shaft of ventral penis. Hooded appearance. Hooded foreskin – ventral deficiency. It does join at the front.
Caudi – penis is bent forward instead of being straight.
Ventral meatus – wee comes out of the bottom side of the penis. It is usually distal.
Associated with cryptorchidism.
Surgery is not mandatory but if needed 2-3yrs of like (after 3months). It is important NOT circumcised.
Determinant of growth hormones
After birth
Childhood
Puberty
Thyroid hormone
GH producing IGF-1. Vit D also needed.
Testosterone/oestradiol
What is occipital plagiocephaly?
Babies on back sleeping can mould the head. It improves as more mobile. No Tx.
How can puberty be investigated?
Bone age measurement w/ x-ray of wrist.
Pelvic US looking at uterine size
Precocious puberty ages, types, Ix
8 in females, 9 in males.
Gonadotrophin dependent (true/central) from premature activation of hypothalamus. Puberty is consant.
Gonadotrophin independent (false, pseudo) from excess sex steroids outside of pituitary gland. Puberty is dissonant.
Differentiate w/ LHRH test. Give GnRH and see if LH/FSH rises. If not then pseudo.
Is PP more worrying in males or females?
In females PP usually just premature onset of normal puberty.
Gonadotrophin independent (CAH, adrenal tumours - virilisation, pubic hair before breast development).
Males PP usually pathological (gonadotrophin dependent due to tumour). MRI.
Late puberty: ages, types and causes in those types.
Cx. Which gender more worrying?
14 in females, 15 in males.
Constitutional delay - most common.
Hypogonadotrophic hypogonadism - Kallmann’s, tumours, systemic disease (CF, AN, CD, excessive exercise).
Hypergonadotrophic hypogonadism - Klinefelter, Turner, gonadal damage (chemo, radio, surgery, trauma).
Psychological, reproduction defects, reduced bone mass.
Late puberty is more worrying in girls, as boys just less sensitive to hormones (karyotype girls)
Describe gender effected, Ax, Px, Mx of:
- Klinefelter
- Turner’s
- Kallmann’s
Kallmann (hypo hypo) - M>F. Lack of GnRH hormones. Px at with late puberty and anosmia. Ix w/ LHRH test. Requires lifelong testosterone or oestrogen (+progesterone). Risk of osteoporosis
Klinefelter’s (hyper hypo) - Male w/ extra X chromosome. There is tall stature (SHOX -height gene on X chromosome). Small testes, infertility, lack of puberty. Can be gynaecomastia. Karyotype. Requires testosterone replacement.
Turner’s is girls with delayed puberty, short stature, webbed neck. Karyotyping. Give oestrogen and maybe GH.
Where is main site of haemopoiesis in foetus?
Liver
Describe O2 sats and Hb levels at in utero/at birth.
Also, WBC and plt counts
O2 is around 70% at birth hence Hb is high. These start to normalise over the weeks.
WBC is high but plts in normal adult ranges.
Preterm will have low stores of iron, folic acid and B12.
How can you distinguish red cell aplasia (congenital, TEC, B19) from other forms of anaemia?
Low reticulocytes (can be raised in IDA etc.)
Describe HS inheritance, Px and Mx
Autosomal dominant
Haemolysis - anaemia, hepatosplenomegaly, jaundice, dark wee, gallstones. Aplastic crisis if B19 infection (slapped cheek).
Diagnosed on blood film.
Oral folic acid. If severe then splenectomy (>7yrs old as sepsis risk).
Describe G6PD inheritance, Px and Mx
X-linked recessive
Haemolysis - anaemia, hepatosplenomegaly, jaundice, dark wee, gallstones triggered by fava beans and certain abx/drugs.
Bite cells on blood film, measure G6PD.
Avoid triggers, transfusions rarely.
Px and Mx of sickle cell anaemia
Anaemia w/ jaundice from haemolysis
Infection susceptibility (hyposplenism)
Vaso-occlusive crisis (cold, dehydration, exercise, hypoxia) - hand-foot syndrome (dactylitis), acute chest syndrome, AVN of femoral head.
Priapism
Requires immunisations, folic acid (anaemia). Hydroxycarbamide (increase HbF production) and BM transplant.
Acute crisis - analgesia, hydration, abx, O2.
Inheritance and Mx of haemophilia
X-linked recessive
Acute - tranexamic acid, recombinant factors (8 for a, 9 for b)
Chronic
- Avoid IM injections, aspirin and NSAIDs.
- Prophylactic f8 if severe
- Desmopressin (DDAVP) for mild A
Biliary atresia
- Aetiology/pathophysiology
- Px
- Ix
- Tx
Fibro-obliterative obstruction of extrahepatic and intrahepatic ducts. Aetiology unknown. Chronic liver failure and death within 2yrs if not treated.
Obstructive jaundice picture. Faltering growth. Hepatosplenomegaly (portal HTN).
Raised CB, abnormal LFTs. US. Diagnosis confirmed by cholangiogram. Diagnosis before 6-8wks preferable.
Kasai hepato-porto enterostomy. Nutrition/fat soluble vitamin supplements. Ursodeoxycholic acid.
Wilm’s tumour aetiology, Px, Ix, Mx
tumour of pluripotent embryonic renal precursor cells. Usually age 2-5.
Unilateral, large, painless, abdominal/flank mass. Haematuria in 10-25%. Anaemia in 25% (haemorrhagic, IDA). Can have varicocele.
Abdo US first line, Surgical resection diagnostic.
Nephrectomy, chemo/radio.
Neuroblastoma aetiology, Px, Ix, Mx
Neural crest tissue in adrenal medulla/SNS.
Most have abdo mass but can be anywhere along sympathetic chain. Usually <5yrs. Symptoms of mets.
Urinary catecholamine levels 1st line. Confirmation w/ biopsy.
Surgery.
Rhabdomyosarcoma aetiology, Px, Ix, Mx
Sarcoma - malignant connective tissue, Rhabdomyo - striated muscle. <18. Primitive mesenchymal tissue.
Head and neck most common sites (proptosis, nasal obstruction), can involve bladder.
Biopsy.
Tx depends on age/site - surgery, chemo/radio.
Most common brain tumour, Px, Ix, Tx
Astrocytoma (40%) Medulloblastoma (20%)
Recurrent vomiting, ataxia, behaviour change, siezures, eye problems (double vision), developmental delay, macrocephaly.
MRI scan, LP may be CI.
Surgery relieving hydrocephalus.
Which type of lymphoma more common in kids?
NHL in childhood.
HL is more in adolescence.
Describe bone tumours (osteosarcoma >Ewing sarcoma) Px, Ix, mx
Uncommon before puberty. Male predominance. Limbs most common site.
Persistent localised bone pain on waking. Otherwise well.
Plain X-ray -> MRI.
Chemo/surgery.
When should primitive reflexes disappear?
Abnormal if retained past first year of life.
What is the order we broadly develop the 4 fields of development?
Gross motor - during first year of life.
Vision/fine motor - from 1yr onwards.
Hearing, speech, language - from 18m of age
Social, emotional, behavioural - from 2.5yrs
Describe hearing tests and when they are done
OAE - newborn screening. Simple, quick but misses auditory neuropathy. High false positive rate in first 24hrs.
ABR - if OAE abnormal. Lower rate of false positives, but baby needs to be asleep.
Distraction testing 7-9m, done if missed newborn screening. You turn towards sounds.
Visual reinforcement 10-18m (up to 3yrs). Turn towards toys.
Pure tone audiometry - from 4yrs. Done at entry to most schools in UK.
Define impairment, disability, disadvantage
- Impairment – loss or abnormality of physiological function or anatomical structure
- Disability – any restriction or lack of ability due to the impairment
- Disadvantage –results from disability, and limits or prevents fulfilment of a normal role. It is situationally specific, e.g. a child with a learning disability may be a good skier.
Describe aetiology of CP
80% antenatal - CVH, ischaemia, maldevelopment, chorioamnionitis, TORCH infections, teratogens
10% perinatal - HIE, asphyxia
10% postanal - meningitis, head trauma, hyperbilirubinaemia
Describe general and subtypes Px of CP
Motor dysfunction - abnormal posture/tone (clasp knife) with delayed motor milestones. feeding difficulty, gait abnormality, asymmetric hand function <12m. Primitive reflexes persist.
Spastic (90%) - UMN lesion. Can be
- Hemiplegia - unilateral, often vascular cause.
- Quadriplegia - bilateral, severe, trunk involved, opisthotonos, seizures.
- Diplegia - 4 limbs effected but legs much worse. Associated w/ preterm and periventricular leukomalacia.
Dyskinetic (6%) - BG/SN damage. Uncontrolled involuntary movements (chorea, athetosis) and DROOLING. HIE most common cause, then hyperbilirubinaemia (kernicterus)
Ataxic (4%) - cerebellum damage. Symmetrical, genetic cause.
CP Ix & Mx
MRI on everyone.
For hypertonia - Botox injection, baclofen, deep brain stimulation.
General - PT, OT, SALT, sleep support etc.
Define ADHD diagnostic criteria
Functional impairment in >/2 domains (e.g. school and home).
3 core behaviours are:
- Hyperactivity - fidgety, talkative, noisy, cant remain seated.
- Inattention - easily distracted, not listening, forgetful, organisational problems
- Impulsivity - blurts out answers, interrupts, cant wait turns.
Need 6/9 inattentive symptoms and 6/9 hyperactivity/impulsivity.
Describe Mx of ADHD
1st line school stuff, rules etc.
If >5, hyperactivity responds symptomatically to medication.
- Stimulants - methylphenidate or dexamphetamine
- Non-stimulants - atomoxetine (3rd line).
All 3 are cardiotoxic so ECG before starting Tx.
Must monitor growth on methylphenidate.
Amphetamines work by boosting noradrenaline and dopamine in prefontal cortex by inhibiting presynaptic dopamine transporters.
Describe refractive errors (which is more common) and Mx
Hypermetropia (long sight) - most common refractive error in young children. Convex lens
Myopia (short sight) - most common refractive error if born preterm. Concave lens.
Describe squint/strabismus
- Manifest
- Latent
Ix, Mx, Cx
Misalignment of visual axes of eyes. Main RF are FHx, prematurity.
Manifest always appears not aligned. When you cover normal eye, abnormal one corrects itself. All muscles/nerves working just born not lined up. Suffix -TROPIA (esotropia inward)
- Causes - usually refractive error (hypermetropia associated w/ esotropia).
- can be seen on cover/uncover test and corneal reflections.
Latent - eyes appear aligned, only deviates when covered. Suffix -PHORIA (esophoria). Many of the population have this a little bit.
- can ONLY be detect on the alternate test.
Define the terms concomitant (non-paralytic) and incomitant (paralytic)
Both types of manifest squint
Concomitant - where size of deviation does not vary with direction of gaze. Most esotropias are like this. This means the eyes are moving the same.
Incomitant - it does change. Can be due to nerve palsies (CN6). These paralytic squints need EMERGENCY investigations.
Mx of squints and amblyopia
Conservative - glasses, prisms for diplopia, orthoptic exercise.
Tx underlying cause - srgery.
NB most amblyopia is asymptomatic. Requires patching of the good eye for periods of day. If >7 improvement unlikely.
If due to strabismus, optic correction then patching/atropine penalisation.
Mx of DKA
- Fluids - resuscitation w/ bolus of 0.9% saline with 40mmol/L KCl (10ml/kg).
Then give replacement. Add 5% glucose when <14mmol/L.
NB usually a bolus is 20ml/kg but for DKA and HF it is 10ml/Kg due to fluid overload Cx. Do not subtract initial bolus from maintenance (however do if they are not shocked)
- Insulin infusion after fluids running for 1hr. Do not give bolus.
- May give potassium if low from insulin.
Signs of hypo and who should you check glucose levels in?
Sweating, pallor, CNS signs, irritability, headache, seizures, coma.
Check glucose in anyone who:
- Becomes septicaemic
- Has a prolonged seizure
- develops an altered state of consciousness.
Signs of hypo and who should you check glucose levels in?
Sweating, pallor, CNS signs, irritability, headache, seizures, coma.
Check glucose in anyone who:
- Becomes septicaemic
- Has a prolonged seizure
- develops an altered state of consciousness.
What to TSH levels do after birth?
Low in utero.
TSH surge after birth causing very high T4 and T3.
These decline to normal adult range within a week.
Most common causes of congenital hypothyroidism worldwide, in UK, in consanguineous relationships
Iodine deficiency - worldwide
Maldescent/athyrosis - uk. Thyroid doesnt descend from sublingual position
Dyshormonogensis - consanguineous. Just dont make it.
CAH inheritance, Px, Ix, Mx
Autosomal dominant
At birth - virilised genitalia (enlarged clitoris, fused labia or enlarged penis, hyperpigmentation of scrotum)
At puberty - pseudo precocious. Premature adrenarche.
Salt losing crisis - age 1-3 due to lack of aldosterone. Weight loss, FTT, hypotension, vomiting, low Na/high K+, acidosis.
17a - hydroxyprogesterone.
Surgery to genitalia. Crisis w/ NaCl, glucose and hydrocortisone.
Lifelong glucocorticoids (e.g. hydrocortisone) to suppress ACTH. Mineralocorticoids.
Which obese children should you be suspicious of Cushing’s syndrome?
Obese children who are short/with growth failure. Can be pituitary adenoma.
Give dexamethasone at night to suppress levels, measure cortisol in the morning.
MRI
Resect tumours.
AIS aetiology, pathophysiology, Px, Ix, Mx, Cx
X-linked recessive inheritance.
XY chromosomes but no testosterone due to defect on X. No testosterone receptors means wolffian ducts dont develop. Teste development doesnt require androgens so normal.
Px - male with atypical genitalia. May feel inguinal mass being testes in abdomen. Normal thelarche (breast development) but no pubic hair growth and inability to have vaginal intercourse.
Confirmed with androgen receptor gene sequencing.
Symptom Mx - HRT, genital surgery. Most raised as females.
Fluids calculations
- Estimating weight
- Amount given as maintenance
- Amount given as replacement
- Amount given as bolus
Weight=2 × (age +4).
100ml/kg/day first 10kg of weight
50ml/kg/day next 10kg of weight
20ml/kg/day for any more.
Fluid deficit (mL) = % dehydration x weight (kg) x 10
Then add this to maintenance.
- 5% dehydrated if some signs of dehydration
- 10% dehydrated if signs of shock
Resuscitation - 10ml/Kg over <10minutes. NICE says dont subtract from maintenance
Kawasaki vessel effected, what happens to plts, how long Tx
Medium
Thrombocytosis - clots
10 days IVIg, may continue
6 weeks high dose aspirin.
Cause, Tx and school exclusion of impetigo.
Usually with S.aureus but also group A strep.
Treatment:
* If no signs of infection – Benzoyl peroxide (Hydrogen peroxide)
* If signs of infection but systemically well – topical fusidic acid
* Systemically unwell – oral flucloxacillin
Need to be excluded from school until either all lesions have healed or 48hrs after starting abx.
Agent, Px, Tx of Rosella infantum
HHV6 or 7.
Fever which lasts 3-5days. As it resolves, a pink maculopapular rash (painless, non-pruritic, blanching) on chest and spreads to limbs. Lasts 2 days.
Can cause febrile seizures.
No Tx required.
Agent, Px, Tx of Molluscum contagiosum
Poxvirus
Flesh coloured lesions with central dimpling (not fluid filled, skin filled).
Self-limiting. No school exclusion required. Avoid sharing clothes etc.
Age affected by coxsackie, rash type and Tx
<10 most commonly but can effect any age.
Painful erythematous macules/papules with a greyish vesicle.
Symptom Tx only - hydration, paracetamol.
Erythema infectiosum / slapped cheek / 5th disease describe:
- Rash, Px
- What does fbc show?
- Tx (inc school exclusion)
- Cx
Starts with mild prodromal illness - headache, rhinitis, sore throat etc.
7-10days later classic slapped cheek rash which spares the nose. Can get arthropathy.
Will be anaemia and reticulocytes ARE NOT raised.
Generally self limiting, just supportive treatment.
If severe IVIg / red cell transfusion. School exclusion not required.
People with high RBC turnover/destruction (HS, SCD, IDA, thalassaemia) can get transient aplastic crisis.
Mumps cause, Px, Ix, Tx, Cx
Paramyxovirus
Fever, malaise, parotitis, usually unilateral -> bilateral. Can be pain on eating.
Plasma amylase raised.
Generally mild and self-lmiting.
hearing loss can fail. Orchitis is most feared Cx.
What is tinea capitis?
Scalp ringworm. Treated the same as normal ringworm.
Scabies Px, Ix, Tx
Severe itching, worse in warm conditions and at night.
O/E - burrows, papules, vesciles between fingers and toes. In infants more in palms, soles and trunk.
Diagnosis on clinical grounds (burrows and itching on other family members).
Tx w/ permethrin cream, avoid eyes. Benzyl benzoate below neck. Malathion lotion.
Which Ix for UTI in kids show what?
- US scan initially. Shows size and drainage of kidneys and bladder.
- MCUG – shows VUR, bladder shape/size and a posterior urethra. It is invasive though.
- DMSA scan – shows relative renal function and renal scarring.
Tx of UTI in kids:
- <3m or seriously ill
- >3m and acute pyelo
- Children with cystitis
- <3m with suspicion of UTI or seriously ill – referred to hospital immediately. They require IV abx (e.g. co-amoxiclav) for at least 5-7days at which point oral prophylaxis can be commenced.
- > 3m and acute pyelonephritis are usually treated with oral trimethoprim for 7 days, or IV co-amoxiclav.
- Children with cystitis – can be treated with oral trimethoprim/nitrofurantoin for 3 days.
Cx of nephrotic syndrome (minimal change) and their management
Hypovolaemia - intravascular compartment becomes volume depleted. Pt has abdo pain / feels faint. Usually sodium retention. Tx with IV fluid.
Oedema - if severe 20% albumin (can cause pulmonary oedema from overload) and furosemide (can worse hypovolaemia).
Thrombosis
Infection - pneumococcus in particular, get vaccinations.
Hypercholesterolaemia.
What is urine like in glomerulonephritis?
Brown / coca cola like.
Lower urinary tract haematuria is usually red and UTI / stone / trauma.
General pathophys and so Px of acute nephritis. Also Mx.
Inflammation leads to increased cellularity and so glomerular blood flow, therefore decreased GFR. Leads to:
- decreased urine output and volume overload
- HTN which can cause seizures.
- Oedema
- Haematuria and proteinuria.
Monitor water/electrolytes and used diuretics when necessary.
Post strep nephritis Px, Ix, Mx
3-4 weeks after strep throat or skin inection. Haematuria, swelling, decreased urine output.
FBC shows anaemia, U&Es show signs of AKI.
Immunology - raised ASOT/anti-DNAse B titre, low C3/4.
Culture from swabs
Urinalysis - micro/macroscopic haematuria, proteinuria (dipstick) and microscopy (RBC cast).
Can be managed at home if kidney function okay. Consider fluid/electrolyte balance, dialysis?. Penicillin for strep infection.
HSP aetiology, Px, Ix, Mx
Unknown, probably due to raised IgA.
Often preceded by URTI. Characteristic urticarial -> purpuric palpable rash on extensor surfaces with trunkal sparing.
Also fever, arthralgia, oedeoma, colicky abdo pain (intussusception) w/ glomerulonephritis.
Clinical diagnosis w/ urine dip. Needs to be repeated after 6-10m to detect persisting haematuria/proteinuria.
Oral steroids (IV or cyclophosphamide if severe). Adjuncts - acei/ARBs.
What is IgAN compared to HSP?
Same thing, but just the kidney injury, no rash etc.
Causes of uni and bilateral renal masses?
Uni - multicystic kidney, obstructed hydronephrosis, wilm’s tumour
Bi - AR/ADPKD, tuberous sclerosis.
Define weight faltering
Drop by 2 centile spaces.
Mx of weight faltering/FTT
Observed meal times / food diaries.
If <6m with severe weight faltering, hospital admission may be necessary for MDT and active refeeding.
Weight starts to rise usually starts 4-8weeks past intervention.
Px of CMPA vs CMPI and Mx
(then lactose intolerance)
Both present when top up feeds (formula milk) started.
CMPA - 10-15mins after feeds with vomiting/regurg, abdo pain, malabsorption/diarrhoea, urticaria, angioedema, atopic eczema.
CMPI is local gut injury only - diarrhoea, blood in stool, abdo colic.
CMPA has skin prick for cow’s milk and specific IgE. Gold std is double blind placebo controlled challenge.
Mx w/ hydrolysed replacement. If this doesnt work then amino acid based formula.
Lactose intolerance is explosive watery stools and flatulence.
Describe foetal circulation
Blood flows through 1 umbilical vein, ductus venosum and into RA, RV, out pulmonary trunk through PDA (or through foramen ovale. This is due to high pressure in pulmonary circulation.
Then flows around body and out of 2 umbilical arteries which take the deoxygenated blood back to placenta.
Describe the S’s of an innocent heart murmur
aSymptomatic
Soft blowing
Systolic only
left Sternal edge
no added Sounds
normal heart Sounds
Describe venous hums and stills murmur
Venous hum - due to turbulent blood flow in the great veins returning to the heart. Head as a continuous blowing noise below both clavicles. Disappears when supine. Older kids than PDA
Still’s murmur - lower left sternal edge, vibratory sound, low pitched. Occurs in 2-7yr olds.
General Mx for L-R shunts
Stabilise the patient, Increase calorie intake/NG tube, Diuretics and ACEi to prevent HF symptoms, Surgical repair.
Describe murmur’s in:
- ASD
- VSD
- PDA
- Coarctation
- Tetralogy
- TGA
- Tricuspid
ASD - a split double (fixed split S2 heart sound), ejection systolic murmur heard loudest at upper left sternal border.
VSD - very systolic (pan/holosystolic) heard loudest at lower left sternal edge.
PDA - continuous (diastolic) machinery murmur heard at left upper sternal border, associated w/ prematurity and rubella
Coarctation - ejection systolic, radiates to back, apical click, radiofemoral delay
ToF - ejection systolic heard loudest at upper left sternal angle (due to right outflow obstruction/PS)
TGA - NO MURMUR, but loud S2 and prominent RV impulse
Tricuspid - ejection systolic and prominent apical impulse.
VSD Mx
Majority - just observe.
If signs of HF or pulmonary HTN then treat - diuretics (furosemide) often combined with captopril. Once HF is adequately treated, open surgery / percutaneous closure to close VSD.
What is hyperoxia (nitrogen washout) test?
Cyanosed infant, determines if CHD is the cause.
Place in 100% O2 for 10mins, if PaO2 remains low then it is CHD.
5T’s of cyanotic heart disease and Mx of cyanosed infant
TGA, TOF, tricuspid atresia, tricuspid regurg, truncus arteriosus
Stabilise airway, breathing, circulation with artificial ventilation.
Start PG infusion (duct dependent)
Monitor SE of PG - apnoea, jitteriness, seizures, flushing, vasodilation, hypotension.
TOF - Aetiology, Mx of hyper-cyanotic spells and X-ray appearance
DiGeorge syndrome (22q deletion), DS. Spells due to RV outflow spasm so no blood goes to lungs.
Sedation (to reduce metabolic O2 demand) and pain relief (morphine)
IV propranolol which works as vasoconstrictor and relieves sub-pulmonary muscular obstruction.
IV volume administration
Bicarb if acidotic.
CXR shows boot shaped heart.
What is tricuspid atresia?
Only the LV is effective, the RV is small. There is cyanosis. LV has to hypertrophy to compensate.
Tx w/ Blalock-Tsaussig insertion.
Aetiology, Px, Ix Mx of AS in kids
Turner’s syndrome causes bicuspid aortic valve. NB the left side of the heart can be very small (differentiates from tricuspid atresia)
Asymptomatic murmur, reduced exercise tolerance, chest pain on exertion, syncope. If severe, may be HF. Same Signs as adults - slow rising pulses, carotid palpable thrill, ejection systolic murmur.
CXR Prominent LV (ECG shows LVH too).
Tx if severe w/ balloon valvotomy. May require aortic valve replacement.
Px Ix, Mx of coarctation of aorta
Acute circulatory collapse at 2days when the duct closes. There will be asymmetry w/ right arm and left arm/leg depending on where the constriction is relative to left Ccarotid/subclavian arteries. May be radiofemoral delay.
CXR - cardiomegaly from HF. Rib notching and 3 sign. ECG normal/LVH.
ABC. PG’s. Surgical repair soon after diagnosis.
Which maternal condition can cause congenital complete heart block?
SLE - anti-Ro/La antibodies cause atrophy of the AVN.
Often death in utero/HF in neonatal period.
Rheumatic fever Ax, Px, Ix, Mx, Cx
Multisystem autoimmune disorder proceeding group A strep (s.pyogenes) infection - causes scarlet fever (hence we give 10days abx for this). Molecular mimicry is RF.
Px - latent interval of 2-6wks following pharyngeal skin infection. There is carditis (chest pain, palpitations, SOB), arthritis, chorea (restlessness/jerky), erythema marginatum (red rings on trunk), SC nodules.
Clinical diagnosis w/ Jone’s criteria
In acute phase - Aspirin. Symptomatic HF Tx (direutics/ACEi).
Long term penicillin V prophylaxis may help.
Rheumatic heart disease (mitral stenosis).
Describe Jone’s criteria for rheumatic fever
2 major or 1maj + 2min
Major - carditis (endo/myo), migratory arthritis (red/hot/swollen), chorea, erythema marginatum, SC nodules.
Minor - fever, polyarthralgia, prolonged PR on ECG, raised ESR/CRP.
Describe Ebstein’s anomaly
Atrialisation of RV and large RA. Low insertion of tricuspid valve.
Caused by lithium exposure in utero.
Cyanosis, a wave in JVP, hepatomegaly, tricuspid regurg. RBBB.
In which children is GOR more common in?
GOR Px
What defines GORD?
Ix for GOR
Tx for GOR
Preterm, CP, following surgery.
Presents with recurrent regurgitation/vomiting but otherwise well. It is a benign self-limiting condition.
Faltering growth, oesophagitis +/- structure, apnoea, aspiration (wheezing/hoarseness/recurrent pneumonia), IDA, seizure-like events, torticolis (sandifer)
GOR diagnosed clinically. If Cx can do 24hr pH monitoring, endoscopy/contrast studies.
Uncomplicated - reassurance, adding inert thickening agents, position 30degree head-up, sleep on back.
GORD Mx with acid suppression (antacids, H2RA, PPIs). Ranitidine not used as carcinogenic.
PS - age effected, ABG results, diagnosis
2-12wks.
Hypochloraemic, hypokalaemic metabolic alkalosis.
US
Infant colic
Age effected
Px
Mx
Differentials
Typically starts in first weeks and resolves from 3-12months.
Crying, drawing up of knees and passage of flatus.
Support and reassurance (gripe water)
CMPA, GOR
Meckel diverticulum
Ax/pathophys
Px
Ix
Mx
Ileal remnant of vitello-intestinal duct. Contains ectopic gastric mucosa.
Most asymptomatic, or severe lower rectal bleeding in <2yrs. Can present w/ intussusception, volvulus, diverticulitis
Technetium scan demonstrates gastric mucosa
Wedge excision (surgical resection) if symptomatic.
Any child with dark green vomiting needs which Ix?
Urgent upper GI constrast to assess intestinal rotation, unless signs of vascular compromise where laparotomy required.
GE - most common viral and bacterial cause?
Types of dehydration Px
Ix
Mx
Cx
Rotavirus causes 60% in <2yrs. C.jejuni.
Isonatraemic/hyponatraemic (drinking lots). Water shifts intracellular causing increased brain volume/seizures. ECF depletion = greater shock per unit water loss.
Hypernatraemic (high insensible losses). Water shifts ECF so less signs of shock. Cerebral shrinkage -> jitteriness, hypertonia/reflexia, seizures.
Usually no Ix, just assess dehydration. If septic/bloody stools then stool culture.
Oral rehydration solution mainstay. If hypernatraemic then maybe just water. If persistent vomiting or deteriorating then IV fluids. NO abx or anti-diarrhoeals.
How does coeliac present in kids?
Malabsorptive syndrome at 8-24months (after weaning onto solids).
There is faltering growth, abdo distension, buttock wasting, abnormal stools. Anaemia.
Is a risk of osteopenia.
CD compared to UC in kids,
Mx
CD is more common than UC unlike in adults.
CD induce remission w/ whole protein modular feeds (polymeric diet) for 6-8wks. 2nd line is systemic steroids. Maintenance w/ azathioprine, mercaptopurine, methotrexate.
UC - aminosalicylates for induction and maintenance. May require topical steroids.
Mx of constipation in kids
Some organic causes of it
Diet. If impaction/encopresis then osmotic laxatives (macrogol). May add stimulant but be careful if risk of perforation.
Hirschsprung, spinal cord, anorectal abnormalities, hypothyroidism, coeliac, hypercalcaemia. Dehydration.
Describe Hirschsprung associations, Px, Ix and Mx
Associated with DS, MEN2a. Complex inheritance pattern.
Presents with bilious vomiting, abdo distension, delayed meconium in first 48hrs. Explosive passage.
Plain AXR. Contrast enema. Definitive diagnosis is w/ colonic biopsy.
Bowel irrigation then surgical Mx (swenson procedure).
can lead to ischaemic enterocolitis.
RF for DDH
Fat (macrosomia), female, first born, foot first (breech), FHx, fair (caucasian), fluid (oligohydramnios).
Scoliosis onset and Mx as per cobb angle
Most commonly adolescent idiopathic scoliosis which is usually late onset effecting girls 10-14 during pubertal growth spurt. Can be congenital or 2o to neuromusc disorders.
Coronal Cobb angle <10 degrees then regular exercises with observation.
21-45 Cobb angle then bracing and regular exercise.
Cobb angle >45 then surgical spinal arthrodesis and regular exercises.
What are the rules of growing pains / nocturnal idiopathic pain?
Pain often wakes the child from sleep but pain settles with massage or comforting. The rules of growing pains are:
* Age 3-12
* Pains symmetrical in lower limbs and not limited to joints
* Pains never present at the start of the day after waking
* Physical activities not limited, no limp.
* Physical examination normal (including pGALS), with the exception of joint hypermobility in some, and otherwise well.
Osgood schlatter’s Px
Tenderness to palpation of tibial tubercle - warmth. BIlateral in 25-50%. Activity limitation.
Clinical diagnosis, sometimes plain X-rays.
Mx - self limiting so conservative (ICE, NSAIDs, PT, immobilisation). Very rarely, surgical excision.
Signs of TS, Ix and Mx
Mild/moderate hip pain/limp. URTI within recent weeks. Limited movement. Hip is abducted and externally rotated. Positive log role.
If suspicion then aspirate and cultures mandatory.
TS has no pain at rest, normal XR (USS may show effusion though). Can give NSAIDs, rest.
Describe Kocher criteria?
- Non-weight bearing
- Fever >38.5ºC
- WCC >12 * 109/L
- ESR >40mm/hr
More likely to be SA if 2 or more.
SCFE Ax, Px, Ix, Mx
10-15yr old boys, obese. Also weakness to the metaphysis (obesity, endocrine disorders - hypothyroid, renal osteodystrophy).
Several week Hx of vague groin/hip/thigh pain with a limp, bilateral in 40%. Obligatory external rotation.
Bilateral AP x-rays. Klein’s lines do not intersect the femoral head.
Surgical pinning and prophylactic fixation.
Can lead to osteonecrosis of femoral head.
Perthe’s describe and Mx
Avascular necrosis of femoral epiphysis due to interruption of blood supply. Revascularisation over 18-36m. It is usually self-limiting.
Short stature, delayed bone age and hyperactivity (lots of sports) is the phenotype. There is limp, hip pain and limited ROM.
<6 - mobilisation + monitoring PT to optimise movement. Non-surgical containment.
>6 - surgical containment (if there is severe deformity).
Cx - OA, stiffness, reduced ROM, limb length inequality.
Definition of JIA and describe the 5 types:
persistent joint swelling (>6wks duration) presenting before 16yrs in the absence of infection or any other cause.
- Oligoarticular (most common) – 1, 2, 3, 4 joints involved, often asymmetrical. Normally ANA+ and associated with high risk of uveitis. Best prognosis.
- Polyarticular (25%) - >4 joints involved, often symmetrical and more destructive.
- Systemic onset JIA (10%) – with fever and SALMON PINK rash.
- Psoriatic – think of PA in adults (dactylitis, nail pitting, psoriasis, etc.).
- Enthesitis related – inflammation of enthesitis (ligament/tendon attaches to bone). Think like AS – back pain.
JIA Px, Ix and Mx
Gelling (stiffness after rest), morning joint stiffness, intermittent limp. There will be swelling/effusion/warmth O/E.
Extra-articular - psoriasis, dactylitis, nail pitting, fever, uveitis, salmon-pink rash.
Lab tests/imaging (although diagnosis made clinically). Yearly ophthalmology for anterior uveitis (asymptomatic). ‘
For Sx - NSAIDs, steroid injections.
DMARDS if polyarticular - methotrexate (monitor LFTs, BM suppression). Consider sulfasalazine/leflunomide.
Avoid systemic corticosteroids/biologics but may be required.
4 Cx of JIA
Chronic anterior uveitiis (can lead to cataract/glaucoma).
Flexion contracture of joints - PT
Growth failure - systemic disease/corticosteroids.
MAS - high fever, hepatosplenomegaly, purpuric rash and pancytopenia. Give steroids.
Also, anaemia, osteoporosis.
Osteogenesis imperfecta inheritance, Px, Tx
AD (disorder of collagen metabolism).
Fractures in childhood, blue sclera (also hearing loss)
Bisphosphonates to reduce fracture rates.
4 causes of HIE/asphyxia and Mx
- Failure of gas exchange across placenta – excessive or prolonged uterine contractions, placental abruption, ruptured uterus
- interruption of umbilical blood flow – cord compression including shoulder dystocia, cord prolapse
- inadequate maternal placental perfusion, maternal hypotension or HTN in compromised fetus – IUGR, anaemia
- Failure of cardiorespiratory adaptation at birth – failure to breathe.
If >36wks can reduce brain damage by wrapping in cooling blanket if <6hrs of birth. Resp support, anticonvulsants, fluid restrict.
3 reasons why neonates get physiological jaundice
High Hb conc at birth
RBC lifespan is only 70 days
Hepatic bilirubin metabolism is less good.
UCB can cross BBB and cause kernicterus.
Causes of jaundice:
<24hrs
24-2wks
>2wks
<24hrs - congenital infection (GBS), haemolytic disorders (ABO, rh incompatibility, G6PD, HS, PKD).
24hrs-2weeks - physiological / breast milk jaundice, infection (UTI/torch), haemolysis (above), bruising at birth, polycythaemia, Crigler-Najjar
> 2wks - Above, hypothyroidism. Conjugated - biliary atresia, neonatal hepatitis.
Difference between ABO and Rh incompatibility
ABO - mum must be blood group O. Rh mum must be Rh negative.
ABO is more common but less severe than Rh.
ABO does NOT require sensitisation so can happen on first pregnancies (unlike Rh incompatibility). Means cannot be prevented (give RhOD Ig at 28wks, 34wks and before delivery)
ABO less severe because maternal IgG less specific and A, B antigen on RBCs weakly attached - mild anaemia, not usually jaundiced.
Conversley Rh can have hydrops foetalis, anaemia, jaundice (coca cola urine), hepatosplenomegaly and kernicterus.
Coomb’s test weakly positive in ABO and strongly positive in Rh.
How does TORCH and hypothyroidism cause prolonged jaundice?
Both via cholestasis -> decreased clearance of bilirubin.
Ix and Mx of newborn jaundice
Transcutaneous bilirubin (not accurate if <24hrs)
Blood sample (best).
Phototherapy (UBC -> Lumirubin excreted in urine).
IVIG and fluids
Exchange transfusion is last line.
What is kernicterus
Deposition of UCB in basal ganglia and brainstem nuclei.
Causes dyskinetic cerebral palsy (6% chorea / drooling one)
Other manifestations - lethargy, poor feeding, opisthotonos.
Resp distress in the newborn: Describe the following:
- Transient tachypnoea of newborn
- Meconium aspiration
- Persistent pulmonary HTN of the newborn
- Congenital diaphragmatic hernia
NB other causes are pneumonia, pneumothorax, milk aspiration.
RDS, BPD more preterm kids.
TTN is most common cause of resp distress. Caused by delayed resorption of lung fluid, usually post CS. CXR shows fluid in horizontal fissue and hyperinflation. Manage w/ observation (maybe O2), usually settles in days.
Meconium aspiration - usually term infant asphyxiated around delivery. Predisposes infection, pneumothorax (overinflated). Confirmed by CXR. Mechanical ventilation often required. Causes persistent pulmonary HTN of newborn.
Persistent pulmonary HTNon - life-threatening, usually 2o to birth asphyxia, meconium aspiration, RDS or sepsis. High PVR causes R-L shunting at atrium/ducts leading to cyanosis. CXR, echo to exclude CHD. Inhaled NO or sildenafil (vasodilators), if severe extracorporeal membrane oxygenation.
Congenital diaphragmatic hernia - left sided herniation of bowel through diaphragm. Resp distress with bowel sounds, can get pneumothorax. CXR/AXR diagnosis. NG tube and suction then repair. Main Cx is pulmonary hypoplasia / HTN. Mortality high.
Neonatal hypoglycaemia
- Causes
- Px
- Mx
IUGR/preterm (poor glycogen stores), GDM (hyperplasia of islet/insulin cells), hypothermia, neonatal sepsis, IEM.
Asymptomatic, autonomic (hypoglycaemia effects SNS) - jitteriness, irritability, tachypnoea, pallor, neuro (drowsy, seizures)
Mx
- Asymptomatic - normal feeding and monitor
- Symptomatic or very low glucose (<1.6) - admit to neonatal unit, IV infusion of 10% dextrose via central catheter.
Also manage if asymptomatic with 2 low glucose levels (<2.6).
Causes, Ix and Mx of cleft lip and palate
Most inherited polygenically or syndrome (trisomy 13, 15, 18)
Events in pregnancy - maternal AEDs, BDZs, smoking, rubella.
Can be detected on antenatal US screening
Surgical repair of lip 3m of age, of palate 6-12m of age.
Make sure feeding okay.
Describe difference between gastroschisis and exomphalos
Gastroschisis has no covering sack. Not associated with other congenital abnormalities so usually better clinically.
Greater risk of dehydration and protein loss. Doesnt necessarily require surgical Mx (put in a big back that shrinks.
Exomphalos (omphalocele) there is a membrane. Again conservative Mx. Check BM as this may occur as part of EMG syndrome (exomphalos, macroglossia, gigantism) - hypo.
What is the giveaway of duodenal atresia?
Down syndrome with double bubble sign on CXR (also get this with oesophageal atresia).
Difference between caput succedaneum and cephalhaematoma
CS - crosses sutures. Resolves in a few days.
Cephalhaematoma - bleeding below periosteum. Resolves over severe weeks.
Nerve roots effected in Erb’s (waiter’s tip) and Klumpke’s (claw hand) palsy
Erbs - C5, C6
Klumpke’s - C8-T1
Describe RDS (newborn respiratory distress syndrome)
AKA hyaline membrane disease. There is a deficiency of surfactant (type 2 pneumocytes) which lowers surface tension/alveolar collapse and impaired infusion.
More common in preterm, boys with GDM mums.
0-4hrs after birth - tachypnoea, laboured breathing/chest wall recession, cyanosis if severe.
Ix - CXR has diffuse, granular/ground glass appearance of lungs.
Prevent w/ glucocorticoids given antenatally (<34wks gestation).
Ambient oxygen and perhaps surfactant therapy onto the lungs.
Cx - pulmonary interstitial emphysema, pneumothorax
How is apnoea of prematurity treated?
20-30s intervals where stops breathing and bradycardia. Usually due to immaturity of central respiratory control.
Tx w/ caffeine. CPAP or mechanical ventilation may be required.
Describe BPD (chronic lung disease), Ix, Mx
Infants who still have an O2 requirement at postmenstrual age of 36 wks are described as having BPD (AKA chronic lung disease). Alveoli not had time to develop as grow slower post birth. Can be due to volume trauma from artificial ventilation.
CXR - widespread areas of opacification sometimes with cystic changes.
Some need prolonged artificial ventilation, most weaned onto CPAP or high flow nasal cannula over months. Steroids may help.
NEC - RF, Px, Ix, Tx
Increasing prematurity, no breast milk.
Typically seen in first wks of life. Feed intolerance, lethargy, vomit (bile stained), distended abdomen w/ visible peristalsis, stool w/ fresh blood, shocked, pain.
Diagnosed on AXR - distended bowel loops, thickened wall (pneumatosis, bowel wall oedema). May be perforation. ABG may show metabolic acidosis.
Stop oral feeds (parenteral nutrition always), broad spec abx, mechanical ventilation/circulatory support, surgery if perforation.
Describe preterm brain injury
brain haemorrhages occur in 20% of very low birthweight infants, seen on US scans. Most occur within 72hrs of life.
Usually small or large Intraventricular haemorrhages causing hydrocephalus.
Antenatal glucocortioids can reduce incidence.
Can lead to hydrocephalus requiring VP shunt.
Paed epilepsy Mx for:
- Childhood rolandic epilepsy
- Childhood absence epilepsy
- Infantile spasms / West syndrome
- Juvenile myoclonic epilepsy
- Febrile siezure (not epilepsy)
- Reflex anoxic seizure (not epilepsy)
- Rolandic epilepsy - usually benign. Usually no Tx, may require AEDs
- Absence - usually benign and no Tx, maybe ethosuximide.
- West - Vigabatrin (AED) and/or steroids.
- Juvenile myoclonic - sodium valproate works well but strict birth control
Febrile no Mx. If prolonged (>5mins) ask parents to call ambulance + buccal midazolam.
Reflex anoxic - most grow out of it and no Tx required.
Tx algorithm for status epilepticus
ABCDE
5mins - BDZ (lorazepam, midazolam, diazepam)
10mins - 2nd BDZ
Levetiracetam
Prepare phenytoin
10mins later - IV phenytoin
Rapid sequence induction
Infantile spasms describe
- West syndrome triad
- Px
- Ix
- Aetiology
- Mx
Infantile spasms, hypsarrhythmia on EEG, developmental problems.
3-12m. Flexor spasms of head w/ extension of arms lasting 1-2s in bursts lasting 30s. Often on waking. Looks like colic. Learning disability.
EEG shows hypsarrhythmia.
Most common cause is tuberous sclerosis.
Mx - vigabatrin and/or steroids.
Benign rolandic epilepsy describe
- Px
- Tx
4-10yrs, most common epilepsy in childhood.
Rolandic area is centro-temporal area of hte brain which supplies face. Px w/ focal seizures w/ abnormal feelings in the tongue and face - twitching, numbness, drooling. May also be infrequent tonic clonic seizures.
Usually no AEDs required.
Describe juvenile myoclonic epilepsy
- Px
- Mx
Myoclonic seizures, generalised tonic clonic and absence seizures may also occur. These are most commonly shortly after waking. Learning unimpaired.
Tx w/ sodium valproate but strict birth control.
SMA pathophys and aetiology
Degeneration of anterior horn cells.
Autosomal recessive.
DMD inheritance, Px, Mx
X-linked recessive (1/3 de novo).
Waddling gait, language delay. 5 at diagnosis. Positive Gower’s (normal until age 3 - hands on legs to get up). Pseudohypertrophy of the calves.
PT/Splints for contractures. Overnight CPAP may improve QOL through nocturnal hypoxia.
Friedreich ataxia inheritance, Px
Autosomal recessive
Triplet repeat causing alck of frataxin protein.
There is worsening ataxia, dysarthria, distal wasting, absent reflexes.
Shaken baby syndrome triad
retinal haemorrhages, subdural haematoma, and encephalopathy (e.g. seizures/reduced level of consciousness).
Neurofibromatosis type 2 and tuberous sclerosis inheritance
Both AD
NF-2 - lots of brain tumours (schwannomas, meningiomas) - bilateral acoustic neuromata. Can be assied w/ MEN. 6+ cafe au lait spots.
TS - depigmented skin, butterfly rash, infantile spasms, learning difficulty
Scarlet fever bacteria, Px, Ix, Tx, Cx
Group A strep (pyogenes)
Fever, headache, N/V, tonsilitis
Sandpaper-like maculopapular rash starting in axillae/groin before spreading over the trunk.
Strawberry tongue. Forchheimer spots on the palate.
Take throat swab but dont delay starting 10days oral penicillin/erythromycin). Return to school 24hrs after starting abx. NOTIFIABLE DISEASE.
Scarlet fever is a mild illness but can be Cx by otitis media (most common), rheumatic fever (20 days after infection) acute glomerulonephritis.
Scarlet fever bacteria, Px, Ix, Tx, Cx
Group A strep (pyogenes)
Fever, headache, N/V, tonsilitis
Sandpaper-like maculopapular rash starting in axillae/groin before spreading over the trunk.
Strawberry tongue. Forchheimer spots on the palate.
Take throat swab but dont delay starting 10days oral penicillin/erythromycin). Return to school 24hrs after starting abx. NOTIFIABLE DISEASE.
Scarlet fever is a mild illness but can be Cx by otitis media (most common), rheumatic fever (20 days after infection) acute glomerulonephritis.
3 indications for tonsillectomy
Recurrent severe tonsilitis (not recurrent URTIs).
Peritonsillar abscess (quinsy)
OSA (adenoids also removed).
Laryngomalacia
- Ax
- Px (ages)
- Ix
- Tx
Congenital abnormality of larynx cartilage, that makes supraglottis collapse during inspiration -> intermittent stridor.
Usually stridor at birth, max Sx at 6-8m to gradual improvement/resolution at 12-24ms.
Frequently associated w/ GORD/feeding difficulties
Diagnosis clinical or flexible laryngeal endoscopy.
Tx - observation alone (Tx GORD). Endoscopic supraglottoplasty if v severe.
Croup name, virus, Px (ages, time of year), Ix, Mx,
Laryngotracheobronchitis
Parainfluenza virus type 1 or 3. Other viruses can cause it.
6m to 6 years (like febrile seizures). Cases tend to peak later autumn. Coryza/fever followed by seal-like barky cough, stridor, hoarseness (vocal cord inflammation), Inc WOB.
Usually abrupt onset, Sx at night.
Usually diagnosed on Hx/Exam. May do X-ray neck rarely.
Stat does oral corticosteroids works within 2hrs. Alternatively nebulised steroids. 2nd line combine w/ adrenaline / oxygen.
Which patients with croup would you admit?
Generally kmore likely if <12m due to narrow airway calibre.
Always <6m.
Stridor at rest is a red flag.
Systemically unwell
Signs of hypercapnia (decreased consciousness)
Triad for epiglottitis, abx and household prophylaxis
drooling, tripod, high fever (looks septic/toxic)
Cefotaxime, ceftriaxone, or ampicillin (started AFTER the airway is secured).
Rifampicin is offered to close household contacts as prophylaxis.
Bacterial tracheitis (pseudomembranous croup) bacteria, Px, Mx
Usually cuased by S.aureus.
Rare condition, similar to epiglottitis but copius thick airway secretions.
Mx - IV abx and intubation/ventilation if required.
Bronchiolitis prophylaxis given to who?
Palivizumab - monoclonal abx to RSV.
Preterm babies (<29wks) with chronic lung disease of prematurity (>21% O2 for 28 days after birth), haemodynamically significant CHD, and time of year (winter).
Mx of transient early wheeze and viral episodic wheeze
Transient early wheeze - just reassure. Salbutamol sometimes but often not helpful.
Viral episodic wheeze - aberrant immune response to viral infection when airways are small and narrow. PRN salbutamol helps (no regular inhaled steroids but sometimes oral in exacerbations).
Asthma management algorithm
- 1st – Inhaled b2 agonists (SABA – salbutamol). Onset of action fast (max 10-15mins), effective 2-4hrs w/ no SE. Used PRN and in high dose for acute attacks. Also used for viral induced wheeze.
+ICS (every child with asthma should be on ICS) Decrease airway inflammation reducing Sx, exacerbations and bronchial hypersensitivity. May slightly reduce height velocity but otherwise no SE. - 2nd - ¬+LRTA (oral montelukast). NICE recommends use this any age.
- 3rd - +LABA (salmeterol) some say >LTRA if >5. Or increase ICS, it is up to specialist.
Describe whooping cough, age effected, Px, Ix, Tx, Cx
URTI by Bordetella pertussis. Effects <6m most of the time but can effect any age.
Initial coryzal symptoms (stage 1) followed by 1-6wks of paroxysmal whooping cough. Inspiratory whoop, red/blue in the face, worse at night. Can be vomiting and epistaxis/conjunctivial haemorrhage. Lasts 3m.
PCR/serology confirms diagnosis. Lymphocytosis (intracellular)
If <1m azithromycin/clarithromycin (macrolides as intracellular). Second line is erythromycin (>1m as can cause PS) or trimethoprim.
Notify PHE.
Can cause pneumothorax.
Describe Kartagener’s syndrome
A rare, autosomal recessive genetic ciliary disorder comprising the triad of situs inversus, chronic sinusitis, and bronchiectasis.
