Paediatrics Flashcards
Which is preserved in FTT - head circumference, height or weight
Head circumference preserved relative to height
Height preserved relative to weight –> Normal height, tailing weight = FTT
Causes of short statue
Chronic disease
hypopituitarism
GH deficiency
Causes of increases height
Thyrotoxicosis
Precocious puberty
Marfan’s
homocystinuria
Causes of increased weight
Too much food/Not enough exercise Hypothyroidism Cushing's Prader-Willi Bardet-Bield Cohen syndrome PCOS
Causes of Hypothyroidism
Congenital: thyroid dysgenesis, dyshormonogenesis, athyreosis; also maternal anti-thyroid drugs
Acquired: prematurity, Hashimoto’s thyroiditis, hypopituitarism, x-rays, Down’s syndrome
Hypothyroidism Symptoms
Early: may be none at birth; prolonged neonatal jaundice; widely opened posterior fontanelle; poor feeding; hypotonia; dry skin; inactivity; sleepiness; slow feeding; little crying; constipation; coarse dry hair; flat nasal bridge; protruding tongue; hypotonia; umbilical hernia, slowly relaxing reflexes, bradycardia, poor growth and mental development
Late: low IQ, delayed puberty, short stature, delayed dentition
Nb: X-ray of left wrist/hand - bone age
Paediatric DM diagnostic criteria & Mx
Diagnostic criteria:
Signs of hyperglycaemia
Venous blood glucose: >7mmol/L (fasting) or >11.1mmol/L (random
Mx:
Involve patient, family and school
May be “partial remission phase” with start of insulin
Insulin: 1/3 dose should be rapid acting and 2/3 should be long acting; 2/3 should be given pre-breakfast and 1/3 pre-dinner
May need SC insulin infusion
Diet plan
DKA Dx
hyperglycaemia (>11.1mmol/L), acidosis (pH
DKA Mx
Do GCS
Resuscitate: oropharyngeal airway; 100% O2, ?intubation; 0.9% saline boluses if shocked
Consider ITU if hypotensive or age when glucose falls to 14mmol/L give 0.9% saline, 5% glucose and 20mmol KCl/500ml
Start insulin only after 1 hour of IV fluids – cerebral oedema is more likely if insulin is started early
Avoid bicarbonate: can increase risk of cerebral oedema
Female Puberty Order:
1) Breast development (8.5-12.5)
2) Pubic hair/growth spurt - immediately after
3) Menarche - usually 2.5yrs after start. Signals end of growth
Male Puberty Order:
1) Testicular enlargement to >4ml volume
2) Pubic hair growth
3) Height spurt - when testicular volume is 12-15ml
Delayed/Precocious Puberty Definition
Delayed: Absence of pubertal development by 14 (female)/ 15 (male)
Precocious puberty: before age 8 (girls), 9 (boys)
Delayed puberty causes
Constitutional delay of growth and puberty – most common
Low gonadotropin secretion: systemic disease, CF, severe asthma, Crohn’s disease, organ failure, anorexia nervosa, starvation, excess physical training, hypothalamopituitary disorders, panhypopituitarism, isolated gonadotropin or GH deficiency, intracranial tumours (including craniopharyngioma), Kallman syndrome (LHRH deficiency and anosmia), acquired hypothyroidism
High gonadotropin secretion: chromosomal abnormalities, Klinefelters (47XXY), Turner’s syndrome (45XO), steroid hormone enzyme deficiencies, acquired gonadal damage
Assessment:
Male: pubertal staging (testicular volume), identification of chronic systemic disorders
Female: karyotyping, thyroid and sex hormones
Precocious puberty: Causes, investigation and management
Causes:
Central: gonadotrophin dependent e.g. craniopharyngioma or pituitary tumour
Peripheral: testis/adrenal problem; increased hCG from rare tumours
Rare: stress, thyroid disorders, choriocarcinoma, meningoencephalitis, McCune-Albright syndrome, lack of 21-hydroxylase, rare genetic defects
Ix: growth charts, puberty staging, CNS CT/MRI, bone age, urinary 17-ketosteroids, karyotyping, adrenal, testis and pelvic ultrasound, thyroid function, LH/FSH, hCG, AFP, GH, pituitary tests, oestrogen/testosterone
Complications: gynaecomastia in boys; short stature caused by early fusion of epiphyses, insulin resistance
Mx:
GnRH analogues
Anti-androgens e.g. flutamide
Spironolactone
Transient synovitis Sx:
Most common cause of acute hip pain in children
Age: 2-12 years
Often follows or is accompanied by a viral infection
Sx: sudden onset of pain in hip or limp, no pain at rest, decreased range of movement (particularly external rotation), pain may be referred to knee, patient may or may not have a mild fever
Ix: normal/slightly raised neutrophils and CRP/ESR; negative blood cultures; hip x-ray is normal, ultrasound may show a small effusion
Mx: bed rest
Osteogenesis imperfect features
Range of disorders of collagen metabolism
Causes bone fragility, bowing and frequent fractures
Type I is the most common form
Autosomal dominant
Features: blue sclerae, fractures during childhood, hearing loss
Type II can be lethal and may result in stillbirth
Commonest childhood Leukaemia?
Acute Lymphoblastic Leukaemia
ALL presentation?
Sx: pancytopenia (pallor, infection, bleeding), fatigue, anorexia, fever, bone pain, painless lumps in neck, axilla & groin; cranial infiltration can lead to CNS effects e.g. cranial palsies; testicular infiltration can lead to orchidomegaly
Ix:
Bloods: deranged WCC; normochromic, normocytic anaemia; low platelets; raised urate; raised LDH
Marrow: 50-98% of nucleated cells will be blasts
CSF: pleocytosis, raised protein, low glucose
CXR: mediastinal mass
Cytogenetic analysis: 80% will have genetic abnormalities
G6PD triggers + presentation
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency
Commonest red cell enzymopathy
X-linked
Red cells lacking G6PD are susceptible to oxidant induced haemolysis
Sx:
Neonatal jaundice within first 3 days of life
Acute haemolysis precipitated by infection, drugs (e.g. antimalarials, sulphonamides, quinolones, aspirin), fava beans, naphthalene (moth balls) – fever, malaise, dark urine
Ix: measure G6PD activity in RBCs when well (may be misleadingly elevated during a haemolytic crisis)
Mx: avoid triggers
PC: Dark urine (Haemolysis), yellow stools (non-obstructive) , Med origin
What is hereditary spherocytosis?
Hereditary spherocytosis
Main cause of haemolysis in north European children
Often mild
Caused by mutations in genes for skeletal proteins of red cell membrane
Red cell loses part of its membrane when it passes through the spleen causing a reduction in surface to volume ratio leading to the cells becoming spheroidal
Spheroidal cells are less deformable than normal red cells and are destroyed in the microvasculature of the spleen
Sx: jaundice, anaemia, splenomegaly
Parvovirus B19 infection can trigger transient severe anaemia or an aplastic crisis
Mx: oral folic acid; splenectomy
Causes of Purpura
Meningococcal sepsis HSP (well & normal platelets) ITP (well and low platelets) Leukaemia DIC HUS Viruses (measles/enteroviruses) Other Vasculities SBE Wiskott-Aldrich Syndrome Aplastic Anaemia
HSP? What is the classic triad?
Acute immune complex mediated vasculitis
Most patients have an antecedent URTI
Sx:
Classic triad: purpura, arthritis/arthralgias and abdominal pain
Renal involvement, scrotal oedema and intussuscption
Ix:
Raised ESR, raised IgA, raised ASO titres
Proteinuria
Mx: steroids; most recover in
ITP?
Chief acquired bleeding disorder in childhood
Can be acute or chronic
Recent history of URTI/gastroenteritis
May follow CMV, EBV, parvovirus, VZV or live virus vaccine
Sx: acute bruising, purpura, petechiae
Ix: isolated thrombocytopaenia, abnormal cells on file, lymphadenopathy; CT head if signs of intracranial haemorrhage
Mx:
Steroids or immunoglobulin may be needed
Admit if excessive bleeding
Platelet transfusion for life threatening bleeding
Splenectomy for chronic ITP and failure of treatment
Prognosis:
Gradual resolution over 3 months in 80% with or without therapy
20% become chronic – normal life can be lived but avoid contact sports
What is the most common Primary immunodeficiency in kids and how do they present?
IgA deficiency
Many are asymptomatic, but may tend to develop resp infections which may lead to bronchiestasis.
Also associated with GI infections eg. giardia, malabsorption, coeliac disease & UC
nb. Complications: blood products and IV immunoglobulin infusion can lead to anaphylaxis due to the presence of IgA; if needed, blood products should be obtained from a IgA-deficient individual—or washed red cells given
What is the commonest INHERITED antibody deficiency?
Bruton x-linked agammaglobulinaemia
Tyrosine kinase gene mutation (xq21) causes low immunoglobulins and low mature b cells hence increased susceptibility to bacterial (but not viral) infections
Lymphocytes are unable to synthesize immunoglobulin.
Age: 3months–3years
Sx: arthropathy + absent Peyer’s patches, tonsils and appendix.
Prevalence: 1 in 250,000 (the commonest inherited antibody deficiency)
Complications: septicaemia and CNS infections (may require interferon-α and high-dose iv immunoglobulin)
Mx: marrow transplantation; serum immunoglobin should rise to normal levels over 3 months
Most common muscular dystrophy? What is the inheritance?
Duchenne’s Muscular Dystrophy
Affects 1 in 4000 male infants
X linked inheritance
Loss of dystrophin protein which is responsible for maintaining integrity of muscle cell wall
Influx of calcium ions into muscle cells leads to destruction of muscle cells
Presentation and Mx of DMD
Sx: waddling gait, language delay, selective atophy of muscles e.g. pectoralis major and brachioradialis, no longer ambulant by age 10-14, death in late teens/twenties from respiratory failure or associated cardiomyopathy
Ix: raised serum CK; muscle biopsy staining
Mx:
Exercise helps to maintain muscle power and mobility and delays scoliosis
Passive stretching and night splints to prevent contractures
Orthoses
Lengthening of Achilles tendon
CPAP/NIPPV overnight to prevent hypoxia due to weakness of intercostal muscles
Ambulant children – prednisolone for 10 days per month to preserve mobility
Differences between DMD and Becker’s Muscular dystrophy?
Some functional dystrophin is produced
Similar features to Duchenne’s but progresses more slowly i.e. onset at age 11, inability to walk in twenties and death in forties
Neurofibromatosis: inheritance?
Types?
Autosomal dominant inheritance
Affects 1 in 3000 births
One third are de novo mutations
Type 1 more common (classic type)
Neurofibromatosis Diagnostic Criteria?
Diagnostic criteria – two or more of the following:
Six or more café-au-lait spots >5mm in size before puberty; >15mm in size after puberty
More than one neurofibroma: dermal - small nodules which appear at puberty and may become papillomatous
nodular - arise from nerve trunks; can give rise to paraesthesiae if pressed
Freckling in skin folds e.g. axilla
Optic glioma – may cause visual impairment
One Lisch nodule: tiny harmless hamartomas on the iris
Bony lesions from sphenoid dysplasia which can cause eye protrusion
1st degree relative with NF1
Neurofibromatosis complication and management?
Complications:
Mild learning disability
Megalencephaly with learning difficulties and epilepsy is sometimes seen
Cutaneous features become more evident after puberty
Nerve root compressions - visual/auditory impairment can occur if CN II or CN VIII are compressed
GI bleeds & obstruction
Bone – cystic lesions, scoliosis, pseudoarthrosis
Renal artery stenosis/phaeochromocytoma – hypertension; malignancy
Management:
Most people with NF1 carry no other features other than the cutaneous stigmata
MDT care; monitoring of BP; excision of some dermal neurofibromas if troublesome; genetic counselling
Neurofibromatosis type 2?
Autosomal dominant inheritance
50% are do novo
Less common than NF1
Presents in adolescence
Features:
Few café-au-lait spots
Bilateral vestibular Schwannomas (acoustic neuromas): cause sensorineural hearing loss at age 20
Cerebellopontine angle syndrome with CN VII paresis and cerebellar ataxia
Juvenile posterior subcapsular lenticular opacity: form of cataract
Complications: tender Schwannomas of cranial and peripheral nerves and spinal nerve roots; meningiomas
Management: hearing tests; MRI brain; neurosurgical treatment of Schwannomas
TS Inheritance and associations?
Aut-Dom, but up to 70% are new mutations.
Associated with learning difficulties and epilepsy, as well as involvement of any organ including skin:
CNS: - Giant cell astrocytoma (associated with epilepsy and behavioural problems), may have focal neurological deficits, raised ICP
Retinal astrocytomas
Cardiac Rhabdomyomas - Detect by echo, may cause heart failure.
Arrhythmias (WPW), thromboembolism or sudden cardiac death
Renal Angiomyolipomas & cysts
Pulmonar lymphangioleiomyomatosis
Bone cysts and new periosteal bone formation
TS: Features
Cutaneous:
- Ash leaf patches
- Shagreen patches (roughened patches of skin usually over lumbar spine)
- Adenoma sebaceum (angiofibromata) in a butterfly distribution over bridge of nose/cheeks
Neurological:
- Infantile spasms & developmental delay
- Epilepsy (often focal)
- Intellectual impairment
Other:
- subungal fibromata
- Dense white areas on retina (phakomata) from local degeneration
- Rhabdomyomata of heart
- PCKD
Sturge-Weber?
Sporadic disorder
Port-wine stain in trigeminal distribution associated with similar lesion intracranially
Ophthalmic (v3) of V always involved
Features: Epilepsy, learning disability & hemiplegia
Ix: Calcification of gyri causes characteristic rail road track calcification on skull X-ray
Causes of raised ICP
- meningoencephalitis
- Head injury
- Subdural/extradural bleeds (NAI?)
- hypoxia
- Ketoacidosis
- Tumours
- Thrombosis
- Reye’s syndrome
Raised ICP symptoms? What is Cushing’s triad?
Listless, irritable, drowsy, headache, diplopia, vomiting, tense fontanelle, decreased GCS, pupil changes, abnormal posturing
Cushing’s triad: Slow pulse, raised BP and breathing pattern abnormalities - warns of imminent coning.
Papilloedema and hydrocephalus are signs of chronic raised ICP
Mx of raised ICP?
Aim to prevent ischaemia
Keep head in midline and elevate to 25° to help venous drainage
Give O2
Treat hypoglycaemia
Control seizures
Do not do an LP
If severe take to ITU and monitor ICP and cerebral perfusion pressure (if CPP
Herpes Simplex Encephalitis?
Most treatable encephalitis
Sx: fever, focal/general seizures, CNS signs, decreased consciousness
Ix: CT, EEG and CSF often non-specific; PCR; MRI
Mx: acyclovir
CNS sequelae: Kluver-Bucy syndrome (hypersexuality, rage, visual agnosia), aphasia, amnesia, auditory agnosia, autism
Types of Paediatric Brain Tumours?
Brain tumours
Sx: unexplained headache, focal symptoms e.g. progressive weakness/numbness, unsteadiness, difficulty speaking, vision changes, CN VI nerve palsy
Consider in children with lethargy, behavioural change, visual disturbances, diabetes insipidus, growth disturbances, nausea and vomiting
Medulloblastoma
Midline cerebellar embryonal tumour
Age: peak at 4 years
Sx: raised ICP, speech difficulty, truncal ataxia, falls
Mx: surgical resection and radio/chemotherapy
Brainstem astrocytoma
Most common brain tumour in children
Associated with neurofibromatosis and prior radiation
Sx: CN palsies, pyramidal tract signs, cerebellar ataxia, signs of raised ICP
Midbrain and third ventricle tumours
Astrocytomas, pinealomas or colloid cysts
Sx: behaviour change, pyramidal tract and cerebellar signs; upward gaze defect
Suprasellar gliomas
Sx: visual field defects, optic atrophy, pituitary disorders (growth arrest, hypothyroidism, delayed puberty), diabetes insipidus
Ix: MRI/CT and EEG
Mx: excision if possible, CSF shunting, radiotherapy, chemotherapy
Rheumatic fever criteria?
Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) Streptococcus pyogenes infection. 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 ASOT > 200iu/mL history of scarlet fever positive throat swab increase in DNase B titre
Major criteria erythema marginatum Sydenham's chorea polyarthritis carditis (endo-, myo- or peri-) subcutaneous nodules
Minor criteria raised ESR or CRP pyrexia arthralgia (not if arthritis a major criteria) prolonged PR interval
Hereditary haemorrhagic telangiectasia diagnostic criteria?
AKA Osler-weber-Rendu (Aut dom)
IF they have 2/4, possible HHT, 3/4 - definite HHT:
1) Epistaxis - spontaneous/recurrent
2) Telangiectasia - multiple at characteristic sites (lips, oral cavity, fingers, nose)
3) Visceral lesions - GI telangiectasia, pulmonary AVM, hepatic AVM, cerebral AVM, spinal AVM
4) FH - 1st deg relative with HHT
Paediatric DKA protocol
1) Work out daily requirements (100ml/kg for first 10kg, 50ml/kg for subsequent kg)
eg. 20kg child = 1500ml/day
therefore for 48 hrs = 3000ml
Work out level of dehydration based on pH;
Gas pH 7.1 = 5% depleted.
add this onto 2 day to give total
eg. 10% = 3300ml
put this as an infusion over 2 days and add potassium to every bag
Add insulin after 1hr
Migraine Mx
Prophylaxis:
- Encourage regular sleep
- Propanolol and pizotifen (5-HT2a antagonist)
Acute attack:
- Paracetamol/ibuprofen
- If fails, try sumatriptan (5-HT agonist)
- If vomiting, use rectal/nasal routes or IV chlorpromazine
Causes of encephalitis?
Infective: HSV, mumps, VZV, rabies, parvovirus, immunocompromised, influenza, toxoplasmosis, TB, mycoplasma, malaria, dengue, Rickettsia
Non-infective: hypogly, DKA, kernicterus, hepatic encephalopathy , poisoning (lead) , SAH, malignancy, lupus
Meningitis: Infective causes
Neonatal to 3 months GBS (especially in LBW babies, following Prolonged rupture of membranes) E. coli and other Gram -ve organisms Listeria monocytogenes Staph
1 month to 6 years
Neisseria meningitidis
Strep pneumoniae
Haemophilus influenzae
Greater than 6 years
Neisseria meningitidis
Streptococcus pneumoniae
Signs & complications of meningitis
Sx: may be subtle in infants – irritability, abnormal cry, lethargy, difficulty feeding; fever, seizures, apnoea, bulging fontanelle
Signs of sepsis: fever, cold peripheries, limb/joint pain, abnormal skin colour, odd behaviour, rash, DIC, tachycardia, hypotension, tachypnoea, raised WCC
Signs of meningism: present after signs of sepsis; stiff neck, Kernig’s sign (resistance to extending knee with hip flexed), Brudzinski’s sign (hips flex on bending head forward), photophobia, opisthotonus
Ix: LP (if not contraindicated) followed by: FBC, U&Es, blood cultures, urine, nose swabs, stool virology, CXR, fluid balance, TPR & BP hourly
Complications: disseminated sepsis, subdural effusion, hydrocephalus, ataxia, paralysis, deafness (use steroids after), low IQ, epilepsy, brain abscess
Mx meningitis
In community: IM benpen
A - protect airways
B - High flow O2
C - 0.9% saline 20ml/kg bolus if in shock. IF shock beyond 3 boluses, consider intubation + inotropic support (dobutamine/dopamine)
Abx:
Up to 3/12: Ceftriaxone + ampicillin/amoxicillin (listeria cover)
3/12 up : Ceftriaxone 40mg/kg
(aged 50 and up: Ceftriaxone + ampicillin/amoxacillin)
Ix:
–> FBC, CRP, coag, blood cultures, whole blood PCR, blood glucose, blood gas
+ LP if no sign of raised ICP
Partial seizure?
Fits confined to one hemisphere
Complex features eg. decreased consciousness, automatism, fits of pure pleasure
Generalised seizure
Not confined with loss of consciousness
- Tonic/clonic (Grand mal)
- Absence (petit mal)
Infantile spasms/West syndrome
Myoclonic seizures
West syndrome?
Aka infantile spasms:
Peak age 5 months
Sx: clusters of head nodding (salaam attack) and arm jerks, every 3-30secs
low IQ in 70%
- EEG is characteristic (hypsarrythmia - chaortic and disorganised brain activity with no recognisable pattern)
Mx: Vigabatrin (SE. visual field defects)
Myoclonic seizures?
Type of generalised seizure
Age: 1-4yrs
Sx: ‘thrown’ suddenly to the ground
Mx: Valproate
Causes of seizures
Often none Infection Raised U+Es Hypoglycaemia Low Calcium Low Mg2_ Deranged sodium Toxins Trauma Metabolic defects TS CNS tumours/malformation Flickering lights Exercise
Febrile convulsions:
Age
Sx
Mx:
Age: 6 months to 5 years
Prevalence: 3% of children have at least one febrile convulsion
Sx: single tonic-clonic symmetrical generalised seizure lasting 15 mins or more than 1 attack in 24h; consider meningo-encephalitis, CNS lesion, epilepsy, trauma, hypoglycaemia, hypocalcaemia or hypomagnesaemia
Mx:
Put in recovery position
Tepid sponging
Paracetamol
If fits last >5 mins: lorazepam IV or diazepam PR
Educate parents:
Reassure
Febrile convulsions do not necessarily mean epilepsy (
Children’s coma scale
Best motor response: 6 - Obey command. Move to request 5 - Localise Pain 4 - Withdraws to pain 3 - Flexor response to pain (decorticate) 2 - Extensor to pain (decerebrate) 1- No response
Best verbal: 5 - Orientated/smiles 4 - Crying but consolable 3 - Moaning/ inconsistently consoble 2 - Inconsolable crying 1 - No response
Eye opening: 4 - spontaneous 3 - To speech 2 - To pain 1 - None
Cerebral palsy : definiton
Chronic disorders of posture and movement caused by non-progressive CNS lesions sustained before 2 years old resulting in delayed motor development, evolving CNS signs, learning disability and epilepsy
Cerebral Palsy: causes
Prenatal: APH with hypoxia
X-rays, alcohol
TORCH , rhesus disease
Perinatal: Birth trauma, fetal distress, hypoglycaemia, hyperbilirubinaemia
Postnatal: Trauma/ IVH, hypoxia, meningoencephalitis, Cerebral vein thrombosis.
cerebral palsy symptoms:
paralysis/stiff muscles/contractures
delayed milestones
seizures
speech/language problems
Cerebral palsy types
Types: spastic, dyskinetic, ataxic and mixed CP
Spasticity: pyramidal lesions (motor cortex)
Dystonia (uncoordinated involuntary movements and postures): basal ganglia involvement
Spastic:
Hemiplegia: arm > leg; early development of hand preference (before 12 months), delay in walking, increased deep reflexes of affected limb
Diplegia: both legs affected worse than arms; child looks normal until he is picked up – legs scissor (hip flexion, adduction and internal rotation with knee extension and feet plantar flexed)
Quadriplegia: most severe form; associated with seizures and low IQ; swallowing difficulties (retrobulbar palsy) can lead to aspiration pneumonia
Dyskinetic (athetoid): unwanted actions, poor movement flow/posture control, spasticity, hypotononia, reduced hearing, dysarthria; associated with kernicterus
Ataxic palsies: hypo/hypertonia; uncommon
Antidotes for:
1) Beta blockers
2) CO
3) Digoxin
4) Opiods
5) Methanol
6) Sulphonylureas
7) Iron
1) Beta blockers –atropine for bradycardia then glucagon; consider adrenaline or dopamine infusions
2) Carbon monoxide – high flow O2 and mannitol for cerebral oedema; hyperbaric oxygen therapy if severe
3) Digoxin – atropine for bradycardia; Digibind (digoxin specific antibody) for severe dysrhythmias/hyperkalaemia
4) Opioids – IV naloxone
5) Methanol/ethylene glycol – fomepizole; contact poisons unit
6) Sulphonylureas - ?octreotide
7) IV fluids + sodium bicarb to counteract metabolic acidosis
- IV desferroxamine chelation
Salicylate poisoning: Sx and Mx
Sx: tinnitus, hearing loss, tachypnoea, respiratory alkalosis, metabolic acidosis, GI irritation (nausea, vomiting, abdominal pain), agitation, delirium, seizures; rhabdomyolysis, pulmonary oedema and electrolyte disturbances may also occur
Ix: ABG, FBC, U&E, glucose, salicylate levels at 6 hours
Mx:
0.9% saline boluses
Correct hypoglycaemia
Potassium if hypokalaemic
Urinary alkalinisation with IV sodium bicarbonate for serious poisoning
Activated charcoal can be given
Haemodialysis if evidence of end organ injury e.g. seizures, severe acidosis, rhabdomyolysis, renal failure, pulmonary oedema
Paracetamol poisoning: Sx and Mx
Sx: Nausea + pallor initially, Jaundice + tender hepatomegaly after 48h. Also hypoglycaemia, hypotension, encephalopathy, coagulopathy and coma
Mx:Admit if presenting within 8h of ingesting >150mg/kg/24h
Serum paracetamol levels at 4h
If presenting 150mg/kg of tablets ingested and no contraindication give activated charcoal
Consult nomogram; if plasma paracetamol level is above the appropriate line treat with N-acetylcysteine
Patients with delayed presentation or in whom a level cannot be obtained within 8h should have N-acetylcysteine started immediately if dose >150mg/kg/24h or unknown
Psychiatric evaluation
Gross Motor development?
3mo: little head lag, head sitting, lumbar curve
6mo: lying abdo, arms extended. Lying on back, lifts and grasps feet. Pulls self to sitting. Held sitting, back straight. Rolls front to back
7-8mo: sits without support (refer at 12)
9 mo: Pulls to stand, crawls
12 mo: Cruises, Walks with 1 hand head
13-15mo: Walks unsupported (refer at 18)
18: Squats to pick up toys
2 yrs: runs, stairs holding rail
3yrs: Tricycle. Stairs without rail
4yrs: Hops on 1 leg
Fine motor and vision General
3mo: Reaches, holds rattle, visually alert, fixes + follows to 180deg
6mo: Palmar grasp, pass from hand to hand, visually insatiable
9mo: Points. Early pinceer
12mo: Good pincer. Bangs toys together
Bricks (fine motor)
Tower of 2: 15mo
Tower of 3 : 18mo
Tower of 6: 24mo (2yrs)
Tower of 9: 36 months (3 yrs)
Fine motor: drawing
18mo: Circular scribble 2 yrs: copies vertical line (2 points) 3 yrs: circle (360) 4 yrs: cross (4 points) 5 yrs: square + triangle
development: speech & hearing
3mo: Quieten to parent voice, turns to sound, squeals
6mo: double syllables ‘adah’ ‘erleh’
9 mo: Mama/Dada. Understands No
12mo: Knows + responds to own name
12-15mo: 2-6 words (refer at 18). Understands simple commands ‘give it to mummy’
2yrs: combines 2 words. Points to parts of body
2. 5yrs: 200 word vocab
3yrs: 3-5 word sentences. Asks what and who. Identifies colours. Counts to 10
4yrs: asks ‘why’ , ‘when’ and ‘how’ questions
Social behaviour: development
6 weeks: Smiles (refer at 10)
3mo: Laughs. Enjoys friendly handling
6mo: Not shy
9mo: Shy, takes everything to mouth
Social behaviour: feeding
6mo: hand on bottle when fed
12-15mo: drinks from cup + uses spoon
2yrs: competent with spoon, doesn’t spill cup
3yrs: uses spoon and fork
5yrs: uses knife and fork
Social behaviour: dressing
12-15mo: helps getting undressed/dressed
18mo: takes of shoes + hat, unable to replace
2yrs: puts on hat and shoes
4 yrs: can dress/undress independently except laces/buttons
Social behaviour: Play
9mo: peek boo
12mo: waves ‘bye-bye’. Plays pat a cake
18mo: plays contentedly alone
2yrs: plays nears others, not with them
4 yrs: plays with other children
Causes of delay in walking?
Chronic illness Global delay benign immaturiy Generalised joint hypermobility DMD Exclude cerebral palsy
APLS: Intraosseos transfusion
Intraosseous transfusion:
In emergencies if rapid IV access is not available within 60-90s of trying -> intraosseous infusion is a rapid, safe, easy and effective means of obtaining vascular access
Safe to administer all IV medicines via IO
Bloods can be taken – inform haematology that they will see blasts
CI: osteoporosis, osteogenesis imperfecta and infection/fracture at the site of insertion
Devices: bone injection gun or EZ-IO
Site: proximal tibia is the best (1-2cm medial to and below the tibial tuberosity); others: proximal humerus, distal femur or distal tibia
Complications: extravasation of fluid, cellulitis, fractures, osteomyelitis, pan and fat/bone microemboli
Anaphylaxis APLS doses:
Repeat adren after 5 min if no improve
Salbutamol for bronchospasm
Paediatric BLS
1) Unresponsible
- -> Shout for help
2) Open air (neutral)
- Not breathing normally?
3) 5 rescue breaths
- -> No signs of life?
4) 15 chest compressions
2: 15
do for 1 min, go get help
Paediatric BLS: Choking
If coughing, encourage to cough
If unconscious or an ineffective cough remove any obvious obstructions
Recheck that there is adequate head tilt and chin lift, but do not overextend the neck
Do up to 5 back blows between the scapulae to dislodge hidden obstructions (hold on your lap whilst seated, positioning the head lower than chest)
If this fails, do 5 chest thrusts: turn to supine; over 12sec, give 5 sternal thrusts (same position as for compressions, but be sharper and more vigorous)
Remove any foreign bodies which have become visible
Tilt head upwards; lift chin to reopen the airway, and assess breathing
If not breathing; do 5 more rescue breaths: does the chest move now?
If not, for a child >1 year, give 5 abdominal thrusts (directed towards diaphragm); use the upright position if the child is conscious; supine if not
Repeat these sequences until breathing is ok, alternating chest and abdominal thrusts
Do not give abdominal thrusts to infants (risk of internal injury)
Depression Dx in kids:
Core features: low mood, anhedonia and reduced energy
Others: poor concentration, disturbed sleep, poor appetite, low self-esteem & confidence, guilt, thoughts of self-harm or suicide, psychomotor retardation/agitation
Diagnosis:
Mild: 2 core symptoms and total of 4 symptoms
Moderate: 2 core and total of 6 symptoms
Severe: 3 core and total of 8 symptoms; psychotic symptoms
Children and adolescents present differently to adults:
Mood
Sleep
Irritability
Somatic symptoms
Anxiety
Depression Tx
Psychoeducation: explain what is happening and what the patient will experience
Self help
First line: psychological therapies (3 months) e.g. CBT, interpersonal therapy, family therapy
Antidepressant if no response – fluoxetine
Ideally in conjunction with psychological therapies
Monitor carefully for first 4 weeks (risk of suicide)
For at least 6 months after remission (8 weeks of no symptoms)
Can also use citalopram
If mild depression: psychoeducation, self-help, therapy – may not need antidepressant
If severe depression consider starting antidepressant first
Prescribing SSRIs explanation
Prescribing SSRIs – explanation to parents/patient:
Mechanism of action
Delayed benefit onset
Side effects on starting: headaches, nausea, GI symptoms (cramping/diarrhoea), fidgety agitation/anxiety, increased suicidality/DSH(do not full understand why it happens but if depression is untreated then could still result in suicide/self-harm; could be due to increases anxiety), sleep disturbance, serotonin syndrome, mania
Discontinuation symptoms
Why it might not be working: too early (can take up to 2-3 weeks to start feeling better), dose, ineffective
Plan for stopping (tentative; gradual)
See patient weekly for first 2-3 weeks, then fortnightly and then monthly
Depression: prognosis
Episodes last 6-9 months
Recurrence is common (>50% within 5 years)
Increased risk of depression/suicide in adult life
20% will develop bipolar disorder
Higher risk of conduct disorder and drug abuse
Anxiety disorder: Diagnosis and Tx:
ICD-10
Child specific: separation anxiety disorders, phobic disorders of childhood, social anxiety disorder of childhood
Seen in children and adults: panic disorder, generalised anxiety when disorder, agoraphobia, social phobia
Treatment
Psychoeducation: child and family
Normal responses
Understating how avoidance can be harmful
Recognising anxious responses/symptoms (especially physical symptoms in children)
Reduce unnecessary stressors
Psychosocial situations that can be altered without resulting in avoidance
Psychotherapeutic
Individual: CBT, anxiety management strategies
Family therapy: avoiding avoidance/collusion
Managing anxious responses in parents
Pharmacology
SSRIs (effective in adult anxiety disorders)
ADHD triad
Hyperactivity: fidgeting, difficulty remaining seated, running, climbing
Impulsivity: answering questions before they’re finished, interrupting
Inattention: difficulty concentrating on details, failure to sustain attention, often appears to not be listening, difficulty following instructions, poor organisation
ADHD diagnostic features
Diagnostic features Symptoms of all three aspects must: Be present for at least 6 months Have started before age seven Be pervasive Cause clinically significant distress or impairment in social, academic Assessment: Teacher, parent and child Connors questionnaire
ADHD Mx
Diagnosis and drug treatment should be initiated by a specialist
Advise parents on positive parenting and behavioural techniques
Psychoeducation
1st line for pre-school and school age children: parent training and education programmes (8-12 sessions)
Older children: CBT
If non-drug treatments fail or if very severe (e.g. suspension from school or parents want to kick child out of the house): methylphenidate (Ritalin) or atomoxetine
SE: appetite suppression, growth retardation, insomnia, increased heart rate, headaches, GI upset, increased risk of seizures if epileptic
Chronic fatigue syndrome: Sx and Mx
Persisting levels of subjective fatigue leading to rapid exhaustion on minimal physical or mental exertion
Sometimes serological evidence of recent infection with coxsackie B virus, EBV or hepatitis virus
Cause: physical and psychological
Sx: myalgia, migratory arthralgia, headache, difficulty getting off to sleep, poor concentration, irritability, depressive symptoms are common; others – abdominal pain, scalp tenderness, eye pain, photophobia, tender cervical lymphadenopathy
Mx:
Self-limiting – can take months or years
Gentle rehabilitation
Support to maintain normal life as much as possible
Autistic spectrum disorder: Features
Symptoms need to be present before age 3
Features:
Poor or odd non-verbal communication
Difficulty seeing things from another person’s perspective/ascribing mental states to others
Relating to others as objects rather than as people
Difficulty understanding unwritten social rules
Hard to form friendships
Not knowing how to interact
Other common problem: hyperactivity, sleep difficulties, food fads, self-injurious behaviours, epilepsy, visual and/or hearing difficulties, motor clumsiness, explosive aggression/eruptions
Autistic spectrum disorder Mx
Multidisciplinary
Clinical observation of the child’s social and communication abilities
In clinic with and without parents present
At school
Professional
Speech and language assessment
Psychology assessment (cognitive/educational)
Physical examination and investigations
Structured assessment tools
ADOS (autism diagnostic observation schedule)
ADi-R (autism diagnostic interview or 3Di)
Commonest cause of non-blanching petechial/purpuric rash?
Non-specific Viral exanthem
Suspected encephalitis Mx?
1) Aciclovir (viral causes - HSV)
2) Third gen cephalosporin (bacterial causes)
3) macrolide (mycoplasma cover)
benefits of LP in suspected Meningitis?
1) Can confirm if they have meningitis or not
2) Easiest source of organism - If bacterial meningitis, can give early steroids to prevent later complications, particularly sensorineural hearing loss
Plasma osmolality formula
2(Na+ + K+) + Glucose + Urea
Viral exantham causes:
Measles
Rubella
Chickenpox
Glandular fever
Erythema infectiosum
Roseola Infantum
Measles : Paramyxovirus
Rubella: Togavirus
Chickenpox: HHV-3 / VZV
Glandular fever: HHV-4 / EBV
Erythema infectiosum: Parvovirus B19 (slapped cheek)
Roseola infantum: HHV-6
Parvovirus b19 - pts with important sequale?
1) Pregnancy - risk of hydrops
2) Chronic haemolytic anaemia - SCD, haemoglobinopathies, G6PD, PKD, HS etc:
- -> Aplastic anaemia (reduced reticulocytes)
Glandular fever presentation
Fever
Prolonged malaise
Lymphadenopathy
Mac/pap - Petechial rash
Jaundice
mild hepatosplenomegaly
Glandular fever Ix:
FBC: - Increased WCC - particularly monocytes
- Monospot (heterophile antibody test)
Nec- fasciitis organism?
Group A haemolytic strep
Well described association with chickenpox
Pyelonephritis choice of IV ABx?
- pick an antibiotic excreted urinarily
- -> Ceftriaxone
Oral - Augmentin (as trimethoprim resistance is so high)
Hydronephrosis?
Indicates obstruction
- If just hydronephrosis, suggests obstruction at renal pelvis eg. pelvic-urethro-junction syndrome
- If also ureteral dilatation - VUR
Bladder hypertrophy and dilatation +- dilated ureters –> Think posterior urethral valve
Nephrotic syndrome triad and common causes?
1) Proteinuria
2) hypoalbuminaemia
3) Oedema
–> Minimal change glomerulonephritis
(steroid responsive)
Bilateral peripheral oedema ddx
1) Nephrotic syndrome
2) Right sided heart failure
3) Oncological disease
4) Orbital cellulitis
5) Anaphylaxis
6) Kwashiorkor
7) Protein-losing enteropathy
Nephrotic syndrome - fluid choice?
Albumin infusion (+ diuretic shortly after to prevent overload)
- restrict oral fluid intake + advice low salt diet
Seizure vs convulsion
Seizure - sudden disturbance of neuro function
–> Convulsion implies abnormal motor activity
Febrile convulsion triad
Seizure + fever + age (6mo-6yrs)
–> In absence of another cause and not due to intra-cranial infection from meningitis or encephalitis
Febrile convulsion Mx
Do: Paracetamol, ibuprofen, no excessive clothing, advise to drink lots of fluids + eat as much ice cream as they want (reduce core body temperature)
Don’t: Cool peripheries down too much (eg. with tepid sponging/ice bath) as may actually cause increase core-temp
Coma causes?
Acute development of dimished level of consciousness that persists
Trauma: Head injury Infection: meningitis/encephalitis Poisoning: Barbiturates/opiates/alcohol Seizures: post-ictal state Metabolic: Hypoglycaemia/hyperglycaemia/hepatic Vascular: Intracranial haemorrhage
DiGeorge syndrome?
CATCH 22
Cardiac abnormalities Athymia Thymic aplasia Cleft palate Hypocalcaemia/hypoPTH
Microdeletion in 22q (long arm)
- Auto.dom
Kartagener’s triad?
1) PCD
2) Situs invertus
3) Recurrent sinusitis
Autosomal recessive
Paediatric Vital signs: HR
12: 60 - 100
Paediatric vital signs: RR
12: 15-20
DR ABCDE: Treatment for Breathing?
Oxygen Bronchodilators Respiratory support Steroids Antibiotics
Hypoglycaemia management?
Buccal hypostop
Treat: 2ml/kg 10% dextose bolus as required
Acute asthma: Initial drugs
1) salbutamol nebulisers 5mg
2) Ipratropium bromide (Atrovent) nebulisers: 250 micrograms
3) Prednisolone 1-2mg/Kg (40mg max) (will start working in the first 4 hours) Usually given for 3 days
Factors that determine a child’s peak flow
Age (need to be >6 to use reliably) Gender BMI Practice Height
Moderate asthma ?
Sp02 >92
PEF > 50 best or predicted
Able to talk
HR
Severe asthma?
SpO2 125
RR > 30
Use of accessory neck muscles
Life threatening asthma ?
SpO2
CXR: Assess quality?
Patient details – “This is a chest radiograph of Alice Smith, a 10 year old girl”
Film details – “this AP film was taken on XX date at 9am”
Rotation – “it does not appear rotated” (check that the medial ends of the clavicles are equidistant from the spinous processes)
Penetration – “it appears adequately penetrated” (this is basically an assessment of how white or dark the X-ray is. If it is over-penetrated, all of the x-rays will have penetrated through to the plate, making the lung fields very dark and you may miss fine detail. If it is under-penetrated it means all the x-rays have been stopped by the tissue and the film appears very white. In this case you may see excessive lung markings or miss details behind the heart of diaphragm. To assess penetrance you should be able to make out the vertebral shadows behind the heart shadows. If you can’t see them, the film is underpenetrated (it’s all white); if you can see them very clearly through a pale heart shadow the film is over-penetrated.
Inspiratory effort – “there is a good inspiratory effort”. Chest X-rays are taken during inspiration to force the diaphragm down and see as much of the lung fields as possible. You should be able to see at least 6 anterior ribs and ideally the 6th rib should intersect the diaphragm in the mid-clavicular line.
Fields – can you see everything you want to see? You should be able to see the apices and the costo-phrenic angles. If any part of the lung fields are missed, it is an inadequate chest X-ray.
Asthma control history?
MAILS IT
Meds
Atopy
Inpatient admissions
Life affects (eg. school)
Smoking
Interval symptoms
Triggers
Asthma discharge?
1) Check inhaler technique
2) Advice/organise GP review within 48hrs
3) Give a written asthma plan for both home and school
4) Give a peak flow meter and diary and check they know how to use it
5) Start regular preventer
6) Organise follow up in asthma clinic
7) Consider visit by community childrens nursing team on D/C
A 12 y/o boy collapses while running at school. Prior to collapsing, he was completely well. He is unconscious for 1 min, with no abnormal movements. He rapidly recovers completely to normal. What is the single most important investigation? A) CT Head B) ECG C EEG D FBC No investigation necessary
ECG - rule out cardiac causes first
Sickle cell chest crisis
1) Hypoxia
2) Chest pain
3) SOB
Which situations in sickle cell require exchange transfusion?
- Priapism
- Cerebral crisis
- Chest crisis
Sickle cell crisis general mx?
1) Hydration
2) oxygen
3) Analgesia
4) Infection - Abx
