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Rapid Review Paediatrics Angelica Lindsey-CLydia Roberts Presentation adapted from original by Isabelle Williams and Natasha Thomas • Emergency Paeds • Cardiology • Respiratory • Gastro What we will • Neuro cover • MSK • Infectious diseases • Endocrinology • Neonatology I Emergency paeds1-year-old Zane presents to the ED with swollen lips and noisy breathing for the last 2 hours. https://dftbskindeep.com/ I Anaphylaxis • What? Severe type of allergic reaction • Management: • Drugs (penicillin), sting venom (bees), food (peanuts) • Acutely • A to E approach • Presentation: sudden onset and rapid • Remove trigger if possible (e.g. stop any infusion) progression of generalized pruritis, • Lie patient flat (with or without legs elevated) widespread erythema/ urticarial rash, • IM Adrenaline at 1 mg/mL (1:1000) concentration hypotension, tachycardiaheeze, SoB, • Establish airway, give high flow oxygen • Apply monitoring: pulse oximetry, ECG, blood pressure • Diagnosis – look for: • If no response repeat IM adrenaline after 5 minutes + IV • Sudden onset of Airway and/or Breathing fluid bolus and/or Circulation problems Note chlorphenamine and hydrocortisone no longer part of the anaphylaxis algorithm • And usually skin changes (e.g. itchy rash) • Admit for at least 6-12 hours (biphasic reaction) • Investigations: • Refer to allergy clinic • Bloods for mast cell serum tryptase (3x) • Education (Epipen, allergen avoidance)I Burn Appearance Referral? Burns classification Superficial Red and painful Primary care •Burns and scalds are relatively common Epidermal (1st •!consider NAI degree) •Make a rapid assessment: A to E Partial thickness Pale, pink, >2% TBSA in a (2 degree) painful child → burns •Burns first aid: Superficial facility • Cool area with running water (20 min) • Plastic wraps after cooling dermal • Pain relief Partial thickness White, reduced All deep dermal (2 degree) sensation burns in a child •Estimate burn size: • Lund and Browder chart Deep → burns facility dermal •All burns to face, ears, eyes, hands, feet, genitalia, perineum or major joint need to be referred to burn’s facility Full thickness White / Burns facility •Fluid resus: Parkland formula rd • Volume of fluid = total body surface area of the burn % x (3 degree) necrotic, weight (kg) x4 painless st • Give half in 1 8hCommon poisonings •General Management: • A&E: TOXBASE • Within 1h? Activated charcoal • Antidote? • Circumstance? •Paracetamol: • Presentation: • Early: abdo pain, vomiting • Later: acute liver failure • Mechanism: • Accumulation of NAPQI (toxic metabolite) w/ saturation of liver metabolism • Management: • Treat with NAC if levels above treatment line • Staggered OD/ ingestion time unknown = treat • Urticaria common with NAC infusions: stop, re-start at slower rate; chlorphenamineCont … •Salicylates: •Presentation: •Early: vomiting, tinnitus •Later: resp alkalosis → metabolic acidosis •Me•Stimulation of resp centre → hyperventilation → resp alkalosis •Uncouples oxidative phosphorylation → metabolic acidosis •Management: •NaHCO •HaemodialysisHead injury – NICE CT head guidelines • Are any of the following present? • If no → are any of the following present? • Suspicion of NAI • Witnessed LOC >5 min • Post-traumatic seizure • GCS <14 initially or <15 2h post • Abnormal drowsiness injury • 3 or more discrete eps of vomiting • Dangerous mechanism of injury – e.g., • fractured open/depressed skull high-speed road traffic collision, or fall from height >3m • Sign of basal skull fracture – panda • Amnesia >5 min eyes, battle sign, CSF leak from • If yes for more than 1 → urgent CT within an hour nose/ears • Focal neurological signs • If only 1 → admit and observe for at least 4h; CT if • Less than 1 year old with concerned bruise/swelling >5cm on head • No symptoms/ signs and benign mechanism of • If yes → urgent CT within an hour injury → discharge home with written adviceAcute appendicitis • Most common cause of • Lab: acute surgical abdomen in children • Raised WCC • Anatomy: McBurney’s point • Urine dip: mild leukocytosis • Pathology • Imaging: • Obstruction of st appendix lumen by • 1 line = USS faecolith, lymphoid • eCXR if ?perforation hyperplasia • (differential = torsion) • Symptoms: • Periumbilical pain → • Girls → pregnancy test (if of localized to RIF child-bearing age; ask if she • Anorexia has started her periods) • Low-grade fever • Management • Vomiting (once) • Laparoscopic • Signs: prior abxstomy w/ • Rigidity/ guarding • Rovsing’s sign • Non-operative management is only • Peritonism if rupture recommended in the appendicolith IM BenPen → Blue light to hospital Courtesy of Skin Deep https://dftbskindeep.com/Meningococcal sepsis Mx • Management: •Community → blue light, IM ben-pen •Secondary care → IV ceftriaxone •Prophylactic abxs for contacts (ciprofloxacin) •Vaccination → MEN-B, MEN-ACWY •Bacterial meningitis notifiable diseases • Complications: •Septic shock •DIC •Multi-organ failure and death Blue = Gram positive Red = Gram negative Bacterial meningitis • Can be part of a bacteraemia or occur via direct spread e.g., from ear infections, skull or sinus fractures • 50-75% neonates have some developmental disorder post-meningitis Newborn (Baby BEL) • IV cefotaxime + • Group B strep, E. coli, Listeriaamoxicillin (covers • Cerebral palsy, blindness, deafness, Listeria) learning difficulties <6yrs (NHS) • IV ceftriaxone (good BBB • Use dexamethasone to prevent SNHL • N. meningitidis (diplococcus) penetration; not in unless septicaemia or <3mo • Strep pneumoniae neonates as increased • HiB bilirubin - use cefotaxime • Consider TB in <5yrs instead) • No LP if: • IV dexamethasone for >3mo • ?meningoccocal septicaemia (DIC) >6yrs • N. meningitidis • IV ceftriaxone + IV dex • ?raised ICP (do CT head if any focal • Strep pneumoniae neurology, papilloedema) • If will significantly delay giving abxsCardiologyA 6-year-old boy presents to his GP with a cold. On examination the GP notices a soft systolic murmur at the left sternal edge. Are you worried?Innocent murmur • Sensitive to position • Short duration • Sternal edge (left) • Soft, blowing murmur • Sweet • Systolic • No Symptoms • Increased CO during illness or anaemia • Reassure and monitor • Refer for echo if unsure A 5-week-old baby was referred to hospital because of wheezing, poor feeding and poor weight gain. On examination there is a thrill and a pansystolic murmur at the lower left sternal edge. What is the diagnosis?VSD •Most common congenital heart defect (30% of defects) •edgeds to a pan-systolic murmur loudest at the left sternal Features: •Small VSDs can be asymptomatic, large VSDs can cause: • Breathlessness • Failure to thrive • Recurrent chest infections • Enlarged liver (heart failure) Management: • Conservative - monitor small VSD, may close spontaneously • Medical - diuretics and ACE-i for heart failure • Surgical - at 3-6 monthsAcyanotic defects L → R shunts Causes: • ASD • VSD • PDA • Coarctation of the aorta • are picked up antenatallyheart defects • factor for infective endocarditiss a riskASD Presentation • Usually only noticed in adulthood • SOB, reduced exercise tolerance • May be no murmur • May be ejection systolic at upper left sternal border due to increased flow across pulmonary valve Management: • Medical - anticoagulation to reduce risk of stroke in adults • Surgical - 3-5 years if symptomatic/ RV overload Complications • Eisenmenger’s • Paradoxical emboli → stroke I PDA • Failure of DA closure at 1 month, causes pulmonary hypertension Presentation: • Can cause feeding difficulties, failure to thrive, LRTIsl • Continuous “machinery” murmur beneath the left clavicle • Collapsing pulse and wide pulse pressure • Seen commonly in premature babies Management: • If associated with another CHD, give PGE1to maintain ductus • Medical - NSAIDs (ibuprofen, indomethacin) • Surgical - ligation, coils 16-year-old girl presents with dizziness. On examination she has a systolic murmur heard loudest at the back between her scapulae. She is short for her age with a broad chest and wide neck. Which syndrome do you suspect?Coarctation of the aorta • Coarctation of the aorta may occur due to the remnant of the ductus arteriosus acting as a fibrous constrictive band of the aorta • Can lead to CCF overtime • Associated with Turner’s syndrome Features: • Can be asymptomatic • Hypertension • Radiofemoral delay • Ejection systolic murmur interscapular area • Absent or weak femoral pulses Investigations: • CXR – rib notching (late) • CT angiography Management: • Corrective surgery/ stentingEisenmenger’s syndrome •Large left to right shunt (e.g., VSD, ASD, PDA) •Over time, right ventricular overload leads to pulmonary artery hypertension, increased right heart pressures and reversal of shunt (right to left) → cyanosis Management: • Prevention! • Treat right heart failure – what are some signs of right heart failure? • Transplant Parents bring their 4-week-old baby to the GP as they have noticed his lips getting blue when he cries, and he has not been breastfeeding well. On examination the GP can hear an ejection systolic murmur at the left sternal edge. What is the diagnosis? A) Tetralogy of Fallot B) VSD C) Transposition of the Great Vessels D) Eisenmenger’s E) Flow murmur secondary to sepsisRespiratoryUpper/ lower respiratory tract infectionURTI vs LRTI • Upper respiratory tract = the airway above the glottis (vocal chords) → larynx, pharynx, sinuses and nose • Lower respiratory tract = the airway below the glottis → trachea, bronchi, bronchioles and alveoli • Generally URTIs are less severe → characterised by cough, fever, a fluctuating level of unwellness but absence of respiratory distress • Pneumonia = LRTI specifically involving the alveoli Pneumonia ● Pneumonia should be considered if the child has: ○ A high fever (over 39°C) and/or ■ Cyanosis. ■ Raised respiratory rate (greater than 60 breaths per minute, age 0–5 months; greater than 50 breaths per minute, age 6–12 months; greater than 40 breaths per minute, age older than 12 months). ■ Signs of increased work of breathing, such as chest indrawing and nasal flaring. ■ Persistently focal crackles. ■ Oxygen saturation of 95% or less in air. ■ Absent breath sounds with a dull percussion note (possibility of pneumonia complicated by an effusion). ● Pneumonia is a clinical diagnosis - CXR is not recommended as a way of diagnosing uncomplicated community acquired pneumonia ● All children with a clinical diagnosis of pneumonia should receive antibiotics, as bacterial and viral pneumonia cannot reliably be distinguished from each other Stridor URT obstruction InspiratoryCroup • URTI - Parainfluenza virus • Management: • Presentation: 6mo to 6yo in autumn • For ALL: single dose of all • Stridor Dex • Increased WoB • Barking cough, worse at night • Mild: manage at home, • Low-grade fever parental obs • Coryza • Severe: hospital treatment, • Grading: CKS high-flow O 2 nebulised • Mild → seal-like barking cough, no stridor or adrenaline, close obs sternal/intercostal recession at rest • Moderate → seal-like barking cough with stridor and sternal recession at rest; no agitation/lethargy • Severe → seal-like barking cough with stridor and sternal/intercostal recession associated with agitation or lethargy I … bacterial tracheitis •= pseudomembranous croup •Rare but dangerous •Usually follows a viral URTI •Similar to severe epiglottitis - acute airway obstruction with thick airway secretions •High-grade fever •Cause: S. aureus •Management: IV abx ± intubation and ventilationAcute epiglottitis •Intense swelling of the epiglottis and •Management surrounding tissues associated with septicaemia • DO NOT examine child •Life threatening due to high risk of airway • Urgent hospital admission – obstruction ITU •Cause: HiB infection • Ask for senior help – ENT • Check vaccination history • Intubate and GA: once •The 4 D’s secure, cultures, IV abxs • Dysphagia • Prophylactic rifampicin of • Dysphonia – ‘hot potato’ voice household contacts • Drooling • Distress I Other causes •Acute stridor • FB inhalation • Anaphylaxis •Chronic stridor – usually due to a structural problem • Laryngomalacia – floppy larynx • Subglottic stenosis (hx of neonatal ventilation) • Papillomatosis (HSV infection in mother) • Subglottic haemangiomaThe wheezy childBronchiolitis •Most common serious respiratory infection of infancy •Features: • Coryza •2-3% of all infants are admitted to • Feeding difficulties with hospital with the disease each year dyspnoea during winter epidemics • Dry, wheezy cough •90% are 1-9 months • Cyanosis or pallor •Cause: RSV (80%), parainfluenza virus, • Hyperinflation of the chest rhinovirus, adenovirus, influenza virus • Subcostal and intercostal and human metapneumovirus recession •‘Gets worse before it gets better’ • Fine end-inspiratory cracklesCont … •Investigations: Pulse oximetry •Management is supportive • Sats determine when admission is needed • Humidified oxygen/ CPAP • CXR & blood gases only if atypical • Fluids (NG or IV) • Infection control, as RSV is very •Hospital admission if any of: contagious • Apnoea (observed or reported) •Discharge: when infant is stable, • Persistent oxygen sats <90% on air maintaining sats o/a >92% for 4h, • Inadequate oral fluid intake incl period of sleep for 12hrsormal) or no wet nappies • Severe respiratory distress •Prevention: monoclonal RSV • NICE traffic light antibody is given to high-risk preterm infants (pavilizumab) I Viral-induced wheeze •Consider in those 6 months - 5 years •Episodic – only wheeze when viral URTI and is symptom free between episodes • Infective exacerbations of asthma and viral-induced wheeze are often indistinguishable in children under 5 years of age who present with wheeze and a respiratory tract infection, unless there is a history of wheeze in the absence reliably for definitive asthma diagnosis)cannot perform lung function tests •Multiple trigger wheeze – other factors appear to trigger wheeze • Exercise, allergens, smoke •Acute management: • Determine severity: as acute asthma • Severe: nebulised salbutamol / Oxygen • Mild-to-mod: SABA via MDI w/ large volume spacer •Long-term management: • Episodic: SABA via spacer • MTW: inhaled steroids or trial of montelukast • Increased risk of asthma Asthma • Reversible (lower) airway • Signs: obstruction • Raised HR/RR • Aetiology: • Widespread, • Airway (type I) polyphonic wheeze hypersensitivity • Ask about FHx of • Prolonged exp phase atopy, parental • Chronic: Hyperinflated smoking, sleep/ school chest, Harrison’s sulcus • Presentation: • Atopy: Polyps/eczema • Dry cough, worse at • Diagnosis: night • Noisy breathing: • <5: clinical dx wheeze • 5-16: spirometry w/ • Hx of precipitants, e.g., BDR, FeNO cold, exercise Asthma Management • Management (NICE): • 0-2: MDI + spacer + face mask • Step 2: SABA + ICS • Step 3: SABA + ICS + LTRA• 3-5: MDI + spacer • Step 4: SABA + ICS + LABAAcute asthma management •immediate transfer to hospitala attack → Severe Life-threatening SpO2 < 92% SpO2 < 92% •Mild-to-mod: PEF 33-50% best or PEF < 33% best or • SABA via spacer predicted predicted • Oral pred Can't complete full Silent chest •Severe / Life-threat: sentences Poor respiratory effort • High-flow oxygen (sats <92%) HR > 125/min Altered consciousness • SABA via spacer/ neb (back-to-back) RR > 30/min Cyanosis • Oral pred Accessory muscle use • Consider: ip brom, aminophylline, Mg2+ • Discuss w/ PICUDischarge • Criteria for discharge • Been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours • Inhaler technique checked and recorded • PEF >75% of best or predicted • Also need to arrange • Weaning plan for steroids/ inhalers • Review previous meds/ triggers and adapt doses: NICE/BTS guidelines • Review by GP in 48h • Review in asthma clinic in 2 weeks What investigation is likely A 10-year-old child presents with to be diagnostic? enlarged tonsils that meet in the midline, first noticed 4 days ago. A. Throat swab B. Bone marrow aspirate Throat examination confirms this + trephine finding, and you also notice C. FBC petechial haemorrhages affecting the oropharynx. On systemic D. testm heterophile ab examination he is noted to have E. ASOT titre splenomegaly. • Acute tonsillitis = inflammation of the tonsils ± inflammation of pharynx (pharyngitis) • Terms used interchangeable • Cause: mostly viral or GABHS • Strep pyogenes (predominant GABHS species) Sore throat • Px: fever, sore throat, painful swallowing • Use the Centor criteria to determine likelihood that sore throat is due to GABHS Investigations •DO NOT routinely take throat swabs •ASOT - no role in dx but helps confirm hx of GABHS in kids with GN / rheumatic fever Management Sore throat •Self-limiting cont … •Abx of choice - Pen V or erythromycin for 7-10 days •AVOID AMOXICILLIN – in context of acute glandular fever can lead to generalised rash •If on DMARDs/ carbimazole - do FBC urgently •?neutropenic sepsis Scarlet fever • Scarlet fever: reaction to erythrogenic toxins produced by GABHS • Strawberry tongue • Sandpaper rash • Circumoral pallor • Desquamation occurs later • Management: • Pen-V for 10 days • (Droplet spread)hool 24h after commencing abxs • Complications: • AOM = most common • Rh fever • Acute GN • Invasive infection – bacteremia, meningitis, nec fasc https://dontforgetthebubbles.com/scarlet-f ever/Acute otitis media •Middle ear inflammation • Abxs should be prescribed if •Common GP presentation • Symptoms lasting more than 4d, or worsening • Systemically unwell (<3 mo with T 38º or •Presentation: more, or 3-6 mo with T 39º or more) • Otalgia, fever ± discharge • Follows viral URTI • Immunocompromised • Child may be crying/ pulling at affected • <2yo with bilateral OM ear • OM with perforation ± discharge in canal • otorrhoea (if perforation)m ± purulent • 1 line = amoxicillin •Management: • Complications • (return if symptoms worsen/do notnet advice • C(S)OM improve after 3 days) • Mastoiditis • MeningitisOther resp • Cystic fibrosis disorders to • Pertussis look upGastroDifferentials to know ● Abdominal pain ● Vomiting ● Constipation ● Diarrhoea ● Abdominal mass • Inadequate intake → poor feeding • Malabsorption → coeliac disease, CF • Excess loss → vomiting (GORD), pyloric stenosis, protein-losing enteropathy Failure to (CMPA) • Increased demand → CCF, recurrent thrive infection (UTI) chronic infection (HIV), malignancy, inborn error of metabolism • Metabolic/endocrine → diabetes mellitus, thryoid disease • Social → child abuse/ neglect I Very common Constipation Red flags: • Failure to pass meconium in 1 48h Differentials: • FTT • Abdominal distension ● Non-pathological (dehydration, •above natal cleft, hairy patch/ deformity, sacral dimple low-fibre diet) • Perianal bruising/ fissures/ fistulae ● Hirschsprung’s disease ● Cystic fibrosis Should not routinely perform DRE in children ● Medications Can result in overflow diarrhoea ● Hypercalcaemia ● Hypothyroidism Management: ● CMPA • Conservative: Fluids, behavioural, dietary fibre • Disimpaction regimen with Movicol Paediatric Plain (polyethylene glycol 3350 + electrolytes) • Followed by maintenance treatmentHirschsprung’s disease Pathophysiology: • Failure of NCC migration from top → Investigations: bottom of GIT → developmental • AXR +/- contrast failure of parasympathetic Auerbach/ • Suction rectal biopsy 3x >2.5cm above dentate line Meissner’s plexuses → aganglionic distal bowel → no peristalisis Management: • a/w Down’s syndrome, MEN-2 • Initially: rectal washouts to reduce risk of Complications: enterocolitis • For enterocolitis: stoma to decompress distal • Bowel perforation bowel • HD enterocolitis • Surgery: pull-through procedure, Soave procedure Presentation: • Failure to pass meconium in 1 48h st • Abdominal distension, explosive diarrhoea, bile-stained vomit CMPA • Very common - affects 3-6% of infants in 1 3 months of life Management • Systemic symptoms w/ angioedema? Suspect • More commonly seen in bottle-fed infants anaphylaxis • Types: • Immediate (IgE-mediated) • Consider referral to • Delayed (non-IgE-mediated) • Allergy clinic if FTT Presentation: • Paediatric dietician • Cow’s milk protein elimination/ home • Irritability (colic) • Reflux & vomiting reintroduction • Loose/ frequent stooleing fed • Formula: eHF/ AAF • Constipation (straining to pass soft stool) • iMAP guidelines for parents • Abdominal pain • Blood/ mucus in stool Note: CMPA usually resolves in most children • Iching/ redness of skin, eczema (non-IgE > IgE) Investigations: • Diagnosis is often clinical (improvement with cow’s milk protein elimination) • Skin prick/ patch testing • Total IgE/ specific IgE (RAST) for cow’s milk proteinGastroenteritis – acute diarrhoea • Most common cause in kids: rotavirus Investigations: • Live vaccine available • Clinical diagnosis usually • Bacterial causes less common • Stool culture if septic, blood/ mucus in stool • Bloody → campylobacter, shigella, salmonella, • Consider culture if recent travel, not improving EHEC • U&Es, Cr, glucose • Non-bloody → cholera, ETEC Management: • Infants are at risk of severe dehydration/ shock • No evidence of dehydration: encourage fluid due to increased SA:VR, higher basal fluid intake, discourage fruit juices/ fizzy drinks requirements and immature renal anatomy • Dehydration: oral fluid challenge / ORS • Red flags: • Red flags: IV fluids, or child is vomiting ORS • Unwell/ deteriorating • DO NOT use anti-diarrhoeal medications • Irritable, lethargy (loperamide) • SAFETY NET • Eyes sunken • Tachycardia/ tachypnoea • Reduced skin turgor I Coeliac disease Gluten-sensitive enteropathy Investigations: •Clinical features • Serum tTG IgA levels • FTT • Check total IgA alongside • Buttock wastingnsion • Abs become negative on strict • Anaemia gluten-free diet • Dermatitis herpetiformis (older adults) • Genotyping •Screen those at risk: • Small bowel biopsy • T1DM • Must be eating gluten for 6 • Autoimmune thyroid disease weeks prior • Downs syndrome I Duodenal biopsy • Villous atrophy (reduced absorptive surface) • Crypt hyperplasia (increased cellular proliferation) • Inflammatory infiltration (increased IEL, influx of immune cells into lamina propria) I • Life-long adherence to gluten-free diet • Correct dehydration • Correct anaemia (mixed IDA/ folate; increased RCDW) • Vaccinations due to hyposplenism • Annual influenza • One-off pneumococcal Management • if indicated (osteoporosis/ with DEXA osteomalacia) Rare complication = EATL (night sweats, fever)Vomiting Diffe tials Red flags Diff nti ls • Pyloric stenosis • Bile-stained vomit • GORD • weeks of lifemiting in first few Vomiting • Gastroenteritis • Vomiting at the end of a paroxysmal cough • Obstruction • Abdominal tenderness/ pain (intussusception, • Abdominal distension atesia) • Hepatosplenomegaly • Whooping cough • Blood in stool • Strangulated hernia • Severe dehydration, shock • Bulging fontanelle or seizures • Faltering growthGastro-oesophageal reflux • Very common in infants • Complications: • Faltering growth • Inappropriate relaxation of the LOS bc • Oesophagitis of functional immaturity • Recurrent pneumonia • Exacerbating factors: • Sandifer syndrome • Fluid-based diet • Investigations: • Horizontal feeding posture • Clinical diagnosis • Anatomy • 24h oesophageal pH/ impedance monitoring • Nearly all resolve by 12 mo of age • Management: • Infant gains weight! • Reassure parents • Feed position → 30 degree head-up • Feed thickeners • Acid suppression • Failure to response to treatment, consider alternative diagnosis, e.g., CMPAPyloric stenosis “olive-shaped mass” • Hypertrophy of pyloric muscle causing gastric outlet obstruction • Presents at 2-8 weeks of life • Diagnosis: • M > F • (Test feed) • 5-10% have a positive family history • Abdominal USS • Presentation: projectile non-bilious vomiting, failure to gain weight, hungry • Management: baby (early) • NBM and NG tube for decompression + IV • Labs: fluids (rehydration and replacement of electrolytes) • metabolic alkalosisokalaemic • Check glucose • Surgical – Ramstedt’s pyloromyotomy • Children 6 mo to 2 years • In children, most common cause is hypertrophic lymphoid tissue following an infection • Lead points (more common in adults) include • GI malignancy – CRC, mets, small bowel lymphoma/ Burkitt lymphoma • Congenital – Meckel’s • Inflammatory – appendicitis • Presentation: • Lethargy is early sign • Redcurrant jelly stool – late sign Intussusception • Sausage-shaped mass in RUQ and emptiness in RLQ (Dance’s sign) • Investigations: • USS – target sign • Management: • Air enema reduction • Surgical reduction/ resection is usually required • Red flags • Older child (over 2yrs) • Enlarged liver • Atypical presentationINeurology • Definition = umbrella term for permanent disorder of movement and/ or posture and of motor function due to a non-progressive abnormality in the developing brain • Affects 2 in 1000 LBs • 80% antenatal due to haemorrhage or ischaemia, cortical migration disorders or structural malformations • 10% perinatal due to HIE • 10% postnatal due to acquired brain injury, e.g. • Meningitis Cerebral palsy • Head trauma • NAI • Kernicterus • Consider CP… • Hand dominance before 1 yo age in boys • Abnormal gait • Delayed motor milestones • Feeding difficultiesHeadache – red flags •Developmental regression in a child •Raised ICP •Headache worse when lying down / in the morning •a/w confusion, vomiting •CN VI palsy •Papilloedema • Visual field defects (think craniopharyngioma = pituitary tumour) • Also growth failure • Neck stiffness, signs of infection • MeningitisMigraine • Migraine w/o aura is most common cause of primary headache in children • Management: • 1 line = ibuprofen • To diagnose, must have 5 or more episodes with: •Headache lasting 4-72h, and • If >12 yo age: sumatriptan nasal •2/4 key features: spray (oral not licensed if <18) • Prophylaxis: • bilateral or unilateral (frontal/temporal) location • Pulsatile • Pizotifen, propranolol • Moderate/severe intensity • Worsened by routine physical activity •And at least one of: • Nausea +/- vomiting • Photophobia and phonophobia Most paediatric brain tumours are primary (in contrast to secondary in adults) Most common benign brain tumour in children: pilocytic astrocytoma Most common malignant brain tumour in Brain tumour children: medulloblastoma As a general rule … in children, most primary brain tumours arise infratentorially Important exception – craniopharyngioma (see appendix)Neurofibromatosis NF-1 NF-2 • AD inheritance • AD inheritance • Café au lait • 18-24yrs, tumours by 30yrs • Axillary freckling • Bilateral vestibular schwannomas • Fibromas → SNHL • Iris harmatomas (Lisch nodules) • Meningiomas • Skeletal anomalies (scoliosis, sphenoid dysplasia, leg b• Ependymomas • Pheochromocytomas • Optic glioma - may cause visual impairment • Astrocytomas • Other tumours e.g. malignant peripheral nerve sheath tumour Febrile seizures Breath-holding spells Epileptic Anoxic seizures Reflex anoxic seizure Seizure Non-epileptic Infection Seizure mimics Head trauma Toxins Other Metabolic Febrile convulsion • 6 months to 6 years • Generalised tonic-clonic seizure associated with fever Simple Complex Status • 25% have FHx <15mins 15-30mins 30+mins • 30% have further episodes • Must exclude underlying causes such as infections e.g., Generalised: tonic Focal meningitis clonic Complete recovery May have second • Advice to parents: within 1hr within 24hrs • Short lasting seizures are not harmful • Reducing the fever does not prevent recurrence • Normal intellect and behaviour Increased risk of • Usually don’t develop epilepsy (2% risk) epilepsyAnoxic seizures Breath holding attack Reflex anoxic seizure • Usually having a tantrum/crying and • Unexpected pain before convulsions they hold their breath (not seen intentionally) • Child went “deadly white” then • Child went “blue” then “collapsed” “collapsed” • Holds breath → cyanosis and cerebral • Pain → vagus nerve stimulation → anoxia bradycardia/brief asystole → cerebral anoxia • Grow out of this I Absence seizure Myoclonic Generalised Tonic-clonic Tonic Atonic Frontal Epileptic Temporal Focal Seizure Non-epileptic Parietal Seizure mimics Occipital West syndrome Epilepsy syndromes LGS Janz syndrome I Generalised epilepsy • Absence Seizures • ‘petit-mal’ • During typical absence, person becomes blank or unresponsive for a few seconds • ‘daydreaming’, look blank/ stare or eyelids begin to blink or flutter • They do NOT response to what is happening around them • Tonic clonic • ‘grand-mal’ • Stiff, then jerking • LoC, tongue biting, incontinence Investigations • EEG (3Hz) • Video telemetry • MRI Management • Advice Epilepsy • Avoid baths and swimming in the sea • Abseiling is the safest sport work-up • Alcohol, drugs and sleep deprivation may trigger an episode • Medical • Generalised: Valproate (teratogenic) or Keppra first line • Absence: Ethosuximide • Atonic: Valproate or Lamotrigine first line • Focal: Carbamazepine or lamotrigine • Infantile spasms: Vigabatrin Regular follow upWest syndrome • Triad of • “Jackknife” Flexion of head, trunk, limbs → extension of arms (Salaam attack); last 1-2 secs, repeat up to 50 times • Developmental regression • EEG: hypsarrhythmia • 90% begin before 1st birthday https://www.youtube.com/watch?v=yAY P8r-MBcgMSK •Infection • Septic arthritis • Osteomyelitis • Post-strep (reactive) •Malignancy • ALL Painful limbs • Bone tumour (osteosarcoma, Ewing’s sarcoma) • Mets •Trauma • Bone fracture / NAI •Kawasaki disease (CRASH and BURN) •JIA Septic arthritis Organisms Most common pathogen causing septic arthritis Staph aureus Most common pathogen causing septic arthritis in Salmonellae an individual with sickle cell Gram negative diplococcus in knee aspirate N. gonorrhea Bone tumours Ewing’s Osteosarcoma Lytic Osteoid producing 10-20yrs 15-30yrs • Uncommon before puberty Diaphysis of long bones, Metaphysis of long bones • Male predominance pelvis, patella and spine • Px: localized bone pain, severe Sx following minor injury Tumour of neuroectoderm Mesenchymal cells with (small round blue cell) osteoblastic differentiation • Investigations: Stain for CD99 • XR/ MRI/ bone scan Radiology: onion skin Radiology: Codman’s • OS → destruction, new bone appearance triangle, sunburst formation appearance • ES → soft tissue involvement 95% have Translocation • Management: surgery + chemo-RT involving EWS gene on Chr 22 I Definition: arthritis in 1 or more joint(s) for more than 6 weeks in under 16-year-olds Presentation: •5x more common in girls •Stiffness in morning, ‘gelling’ after periods of rest •Limp •Anterior uveitis – BUT WHITE EYE NOT RED Types: •Systemic (high daily spiking fever, salmon pink rash, lymphadenopathy, serositis) JIA •Polyarticular (RhF+/-) •Oligoarticular (most common) Investigations: •gonococcus film, ESR/CRP/ferritin, ANA/RhF, slit lamp examination, XR, NAAT for Management: •1 line = NSAIDs •2 line = DMARDs •Physio to maintain joint function and ophthalmology reviews •Aim to avoid systemic steroids as much as possible Acute Chronic / intermittent 1-3yrs Transient synovitis DDH Neuromuscular (CP) 3-10yrs Transient synovitis Perthes disease Perthes disease NM disorders (Muscular JIA dystrophy) Complex regional pain syndrome 11-16yr Slipped upper femoral Slipped upper femoral Limp epiphysis epiphysis Reactive arthritis JIA Complex regional pain syndrome Osgood-Schlatter disease All ages Trauma JIA Infection: septic arthritis, osteomyelitis Malignancy: leukaemia, neuroblastoma, bone tumour • Acute joint pain associated with viral infection • Most commonly affects the hip and is the most common cause of hip pain in children • Age 2-10 • May have low grade fever Transient • If high, suspect septic arthritis • Investigations: synovitis • Normal XR, FBC, CRP, ESR • USS – may see effusion • Management: • Self-limiting • Rest + analgesia • Should recover in 6 weeksPerthe’s disease • Avascular necrosis of the femoral head • Boys 4-8 • Presentation: • Progressively worsening hip pain + limp • Reduced range of movement - especially abduction • Antalgic gait, leg length discrepancy • Investigations • Bilateral hip XR - flattening of femoral head • MRI • Management • Conservative - casts and braces to keep femoral head within the acetabulum, physiotherapy • Surgical - THR if severe • Complications • Osteoarthritis • Premature fusion of growth plates • Early diagnosis key to prognosisSUFE • headerior inferior displacement of femoral Right Left • Obese boys 10-15 • Presentation: • Loss of internal rotation • Externally rotated, shortened leg • 20% bilateral • Investigations: • Bilateral hip XR: AP and frog-leg views • Klein’s line • Southwick angle • Severity of SCFE • Management: • Admit and refer to orthopods • Surgery – internal fixation to stabilize growth plate I DDH • Affects up to 3% of newborns, 20% • Screening: bilateral • For ALL → newborn baby check, 6w baby • What happens? check (Barlow, Ortolani) • Femoral head dislocates • USS within 6 weeks if • 1 degree affected relative • Ball and socket grow out of proportion to each other • Breech • Risk factors: the F’s → feet first, female, • Multiple pregnancy fluid low, fat (maternal T2DM), • If >4.5mo, bilateral hip XR first-born, FHx • Signs: leg length discrepancy, • Management: asymmetric skin folds • Pavlik harness if <4-5mo • If >6mo, surgical correction • If not detected at birth → waddling gait, OA in adultsIA 6-year-old boy is brought to surgery by his mother. For the past 2 months he has been complaining of pain in his shins and ankles at night-time. His symptoms are bilateral; he is otherwise well. There is no family history of note. Clinical examination is unremarkable. I Pain in the legs, no obvious cause M=F Growing pains The rules of growing pains: • Age 3-12 • Symmetrical, lower limb • Never at start of day after waking • No limp • Examination normal, incl pGALSInfectious diseasesSpot diagnosis • 17-month-old previously healthy but unimmunised child develops fever, malaise, cough, runny nose, and conjunctivitis, that worsen over several days. • Fever increases gradually up to 39-40°C over several days and the cough worsens. Photophobia and whitish lesions on erythematous buccal mucosa. • Two days later, an erythematous, maculopapular rash appears on the head and spreads from head to toe over the next 3 days. MeaslesMeasles • Highly infectious disease caused by measles virus • Characterised by a maculopapular rash, cough, coryza, conjunctivitis, and a pathognomonic enanthem (Koplik's spots) • Incubation period ~10 days. • Preventable by immunisation but high levels of coverage are required to prevent outbreaks of disease from occurring. • No specific treatment for measles is available except for supportive care. • Notifiable disease. • School exclusion for 4 days from onset of rash. • Complications include pneumonia, laryngotracheitis, otitis media, and encephalitis → more common in immunocompromised and poorly nourished individualsMumps • Acute systemic infectious disease caused by an RNA paramyxovirus • Spread by droplets. Infects respiratory tract epithelial cells → parotid glands → other tissues • Infective 7 days before and 9 days after parotid swelling starts. Incubation period = 14-21 days • Clinical features = fever, malaise, muscular pain, parotitis ('earache', 'pain on eating') → unilateral initially then becomes bilateral in 70% • Prevention through vaccination (MMR) • Management is supportive. Notifiable disease. • Complications • Orchitis - more common post-puberty • Hearing loss - usually unilateral and transient • Meningoencephalitis • PancreatitisParvovirus B19 •Causes erythema infectiosum (also known as fifth disease or 'slapped-cheek syndrome') •Features: mild feverish illness, rose-red rash over cheeks (may spread) •Mx: supportive care •Complications: • Aplastic crisis if child has haemolytic anaemia (sickle cell, HS, G6PD) • Disaster in pregnancy • Most common viral cause of fetal hydrops •high output cardiac failure → non-immune fetal hydropsmia → • Mx: intrauterine blood transfusionRoseola infantum Hand, foot and mouth disease • Caused by HHV6 • Caused by the intestinal viruses • Features: (most commonly coxsackie A16 • Initial high fever lasting a few and enterovirus 71) days • Very contagious - nursery • Maculopapular rash after fever outbreaks common • Nagayama spots → papular • Features: enanthem on the uvula and soft • Mild systemic upset: sore throat, palate fever • Febrile convulsions occur in around 10-15% • Oral ulcers • Followed later by vesicles on the • Diarrhoea and cough are also palms and soles of the feet commonly seen For both - symptomatic treatment only, no school exclusion requiredEndocrine Presentation: weight loss, FTT, polyuria/ polydipsia, secondary nocturnal enuresis, candida infection/balanitis, DKA Diagnosis: •Symptoms + RG ≥ 11.1 mmol/L or FG ≥7.0 mmol/L, •OR asymptomatic with 2 RGs/FGs of ≥11.1/ 7.0, respectively Management: T1DM •Subcut insulin: 0.5 units/kg/day •MDII as basal bolus regimen •Admit for education/ stabilization •Discharge when able to check BM with telephone follow-up Review: eyes, renal function, BMI, HbA1c, thyroid/coeliac abs, feet, BP and imms NOTE T2DM is rare in children, but becoming more common as obesity increases •Triad of: • Hyperglycaemia (>11) • Acidosis (pH <7.30 or3HCO <15 mmol/L) • Ketonaemia (>3.0 mmol/L) Quick note on •Cerebral oedema is most common cause of death in children! DKA •Headache, behavioural change, low GCS •Too rapid lowering of serum Na+ •Neuro obs every 30 mins Puberty(too early, too late) Other things to Growth failure (craniopharyngioma) cover CAH (neonatal px) Congenital hypothyroidismNeonatology Physiological • More common in breastfed infants Neonatal jaundice • Reduced RBC lifespan • Immature bilirubin metabolism / enterohepatic circulation Differentials: Unconjugated Jaundice in the first 24 hrs is always pathological ● Haemolytic disorders ○ Blood group incompatibility - Causes of jaundice in the first 24h rhesus haemolytic disease, • Rhesus haemolytic disease ABO haemolytic disease) • ABO haemolytic disease ○ Red cell enzyme deficiency - • Hereditary spherocytosis G6PD deficiency • G6PD ● Meconium retention Conjugated After 14d = prolonged jaundice screen ● Biliary atresia ● breast milk jaundice • Features of obstruction (pale stool, dark urine) ● Infections • Conjugated bilirubin levels (biliary atresia) ● Hypothyroidism • LFTs • FBC • Urine culture • Metabolic screenNeonatal jaundice • Unconjugated bilirubin is toxic to neural tissue (crosses BBB) • Kernicterus: yellow staining of cerebral tissue (basal ganglia) • Bilirubin encephalopathy • Acute: lethargy, irritability, abnormal muscle tone/ posture, apnoea, convulsions • Chronic: CP (diplegic), SNHL, gaze palsy, dental dysplasia • Investigations: confirm jaundice by measuring serum bilirubin levels • Management: • Depends on tx threshold graph/table • Includes • Phototherapy • Exchange transfusionRespiratory distress in the newborn Premature Term RDS: Respiratory Distress Syndrome TTN - Transient Tachypnoea of the Newborn • Presentation: tachypnoea >60 shortly after birth • Delayed lung liquid resorption at birth (fluid seen in horizontal • Grunting on expiration to help maintain airways open fissure on CXR) • Nasal flaring and chest wall recession • More common after C-section • CXR: diffuse ground glass appearance (may lose Heart border) • Usually resolves within a day but must exclude infection • Mx: oxygen / CPAP / ventilation + surfactant • Reduce risk with antenatal steroids (which also reduce the risk of BPD and IVH) • May occur in term infants from diabetic mothers BPD: Bronchopulmonary Dysplasia PPHN - persistent pulmonary hypertension of the newborn • Persistent oxygen requirement after 36 weeks • ECHO to rule out CHD • Attributed to delay in lung maturation but also likely related to • Life-threatening may lead to cyanosis after birth mechanical trauma etc. • Associated with birth asphyxia, meconium aspiration, • CXR: widespread opacification septicaemia and RDS • Risk of pulmonary HTN and pneumonia • Often requires long term oxygen therapy and gradual weaning • Likely to have more severe disease course with subsequent chest infections Meconium aspiration Lung irritant → chemical pneumonitis, mechanical obstruction, increased risk of infection May require ventilation Usually, post-term deliveries RFs: Maternal HTN, Pre-eclampsia, Chorioamnionitis, smoking, substance abuse Pneumothorax - spontaneous in 2% or as a result of ventilation Congenital Diaphragmatic Hernia - usually on left side - bowel displacing heart Consider in infants who fail to respond to resus Confirmed with XR of chest and abdo Mx: NG tube to stop overdistension of the bowel and urgent repair of defect Long term → hypoplastic lung Pneumonia RFs: prolonged rupture of membranes, low birth weight and chorioamnionitis What is the definitive A 6-day-old baby was born prematurely management? at 33 weeks. He has been suffering from A. IV ceftriaxone and respiratory distress syndrome and has vancomycin been receiving ventilatory support on NICU. He has developed abdominal B. IV fluids distension and is increasingly septic. C. Repeat AXR Ultrasound of the abdomen shows free D. Urgent laparotomy fluid and evidence of small bowel E. Increase target oxygen dilatation. His blood pressure has sats remained labile despite inotropic support. NEC • The premature gut is at risk of ischaemia/ bacterial invasion bc of immature immunity • Breast milk protective (IgA) • Signs: abdominal distension, passage of bloody stools • Investigations: • AXR: pneumatosis intestinalis • Treatment: • Total gut rest and TPN • IV abxs • Perforation → laparotomy and resection of necrotic bowel • Complications: Crescents of intramural gas = pathognomonic • Short gut syndrome • Strictures I Abdominal wall defects Omphalocele Gastroschisis • Central defect of anterior abdominal wall • Defect to right of an intact umbilical cord • Failure of midgut rotation and return to allowing extrusion of abdominal content abdomen • RFs: young parents, smoking, maternal • Abdominal cavity may be too small infection (= socioeconomic deprivation) • Bowel covered by sac (amnion, Wharton’s jelly + peritoneum) • Bowel is not covered • Associated anomalies • Baby at risk of fluid, electrolytes and heat loss • Management: • Management • Staged closure • Surgery immediately following delivery I … and breathe that was A LOTTIPS and TRICKS SAQ • Give a full differential • Bullet point answers & diagrams • Always consider NAI and safeguarding • Don’t forget the basics SBA • Don’t forget General Medicine • Common is common • Read the question! (immediate vs definitive vs rule out)Feedback I Appendix I Dermatology I A 2-month-old baby comes into the GP with a dry, scaly rash on his face and chest. Baby is alert and smiling. FHx of asthma. https://dftbskindeep.com/Eczema • Inflammatory skin condition characterised by dry, pruritic skin with a chronic relapsing course • Most commonly diagnosed before 5 years of age and affects 10% to 20% of children • Presentation: • Infants: on cheeks/ face, dry, scaly • Toddlers: extensors (wrists, ankles, knees) • School-age: flexors (joint creases), lichenification • Management: • Educate parents • Avoid irritants (synthetic clothing) • Use soap substitutes • Keep nails short • Emollients - large amounts needed (250g/week) • Mild topical steroid e.g., 1% hydrocortisone for acute flare of eczema I Very potent • Clobetasol propionate Potent 0.05% (Dermovate) • Fluticasone propionate Moderate 0.05% (Cutivate) • Betamethasone • Betamethasone valerate 0.1% valerate 0.025% (Betnovate) Mild (Betnovate RD) • Hydrocortisone • Clobetasone butyrate 0.5-2.5% 0.05% (Eumovate) A 6-month-old boy presents with a severe exacerbation of eczema. His skin is markedly inflamed all over. He has been breast-fed from birth. His mother has a sore on her lip. His temperature is 37.8°C. Courtesy of Skin Deep https://dftbskindeep.com/ Ask: has anyone in the family currently got cold sores? What? HSV infection of eczematous skin Presentation: • Grouped vesicles and punched-out erosions Eczema • Lesions can become widespread and coalesce • 2º bacterial infection (golden crust) herpeticum • Unwell looking child Management • Admit child for urgent dermatology review, swabs and IV aciclovir • May also give concurrest Abxs if cannot distinguish between viral vs bacterial infection (1 line = flucloxacillin) Kawasaki disease • Vasculitis • Presentation: • Fever >5 days & resistant to paracetamol • Conjunctival ‘injection’ • Rash • Cervical lymphAdenopathy • Strawberry tongue & Red cracked lips • Hands and feet - Red palms and soles of feet – later, peeling • Investigations: • High CRP and ESR • Delayed rise in platelets (week 2) • Management: aspirin + IVIg • Follow up: echo (risk of coronary artery aneurysms) I Oncology I • 2mo presents to ED with widespread purpuric rash and abdominal distension • Urgent referral to paeds made and BM aspirate + trephine Neuroblastoma • Origin: neural crest of SNS (adrenal medulla) • Prognosis: • Median age of onset: 20 mo • Age and stage are important • Presentation: • Better differentiation = better prognosis • 60% present w/ metastatic disease → LNs, BM, liver, skin (blueberry muffin baby), orbits, • Poor if dura • >1 • Abdominal mass • Amplification of MYC-N • Hepatosplenomegaly • Management: • Pallor, weight loss • Bone pain, limp • Some resolve spontaneously • Localised disease: surgery alone • Investigations: FBC, urinary catecholamines • Metastatic disease: chemo chest, MRI heaf, MIBG, BM trephine primary site/ • Many patients with high-risk disease will relapse or be refractory to primary treatment Cont … Neuroblasts: small round Neuropil: eosinophilic Ganglion cells: mature Schwannian stroma: blue cells fibrillary acellular material neuroblasts, with abundant cellular wavy stroma pink cytoplasm and a large formed from Schwann nucleolus with a prominent cells nucleolus May be arranged in Homer-Wright Neuroblastoma = most immature, pseudo-rosettes with a centre of <50% Schwannian stroma neuropil Undifferentiated form: no neuropil Poorly differentiated form: some neuropil, <5% ganglion cells Differentiated form: neuropil, >5% ganglion cells Neuroblastoma 🡪 ganglioneuroblastoma 🡪 ganglioneuroma Which feature of A 4 yo girl, Jane, is seen in the urgent the history led to paediatrics clinic after being referred by her urgent referral? her GP yday who felt a mass in her R A. Abdominal mass side. She is complaining of pain on the B. High BP same side. She has no other GI/ urinary C. Abdominal pain Sx, but GP did find her BP higher than D. Absence of the normal range for her age on 3 urinary readings. symptoms E. <5yrs • Origin: undifferentiated mesodermal tumour of intermediate cell mass • Classic triad of painless haematuria, loin pain, abdominal pass • Less common cause of renal mass mesoblastic nephroma (benign) in infancy (reversed incidence after infancy) • Normally affects <6 yo • Commonly unilateral, can be bilateral Wilms’ tumour = • Mutated WT1 gene on Chr 11 → nephrogenic rests (precursor lesion) nephroblastoma • a/w BWS, WAGR syndrome • Histology: • SRBCT • Triphasic: metanephric blastema, stromal cells, epithelial cells • Anaplastic Wilms’: nuclei 3x normal size, hyperchromatic and abnormal mitosesCont … Investigations: • Check BP • Basic bloods • Imaging: USS, CT+- MRI abdo, CXR/ CT chest for staging Management: • Chemo & total nephrectomy • RT if advanced • Prognosis is goodHydrocephalus • Sutures have not yet fused → disproportionate increase in head circumference • Secondary to either • Obstruction within ventricles (Chiari malformation, posterior fossa tumour), or • Obstruction at arachnoid villi (meningitis) • Setting sun sign • Management: VP shunt YUM! These rosettes are Medulloblastoma delicious. • Precursor: primitive neuroectodermal tissue • Arises from cerebellar vermis • Presentation: • Cerebellar syndrome: clumsiness (ataxia), poor coordination, difficulty walking • Features of raised ICP: morning headaches, bulging anterior fontanelle, N&V, diplopia … from which CN defect? • Diagnosis: cranial MRI w/ contrast Small round blue cells • Treatment: resection; exquisitely Homer-Wright rosettes radiosensitiveCraniopharyngioma • Origin: remnants of Rathke’s pouch (ectoderm) • Supratentorial (suprasellar space) • Bimodal age distribution: 5-14 yo age, 50-70 yo age • Clinical features: • Bitemporal hemianopia • Disconnection hyperprolactinemia • Hyperphagia, obesity Adamantinomatous • Hypopituitarism type: • Workup: cysts/ nodules of • Visual field testing lamellated, calcified • Labs: pituitary/ endocrine profile wet keratin • Brain imaging (MRI, CT) Cholesterol crystals • Biopsy I Cardiology Tetralogy of Fallot Transposition of the great arteries Cyanotic Persistent truncus arteriosus heart disease Total anomalous pulmonary venous drainage Tricuspid atresia •Defects: • VSD • Pulm stenosis (RVOT obstruction) • RVH • Overriding aorta •Presentation: • At 1-2 months • ‘tet spells’ T etralogy of •Examination: • Clubbing • Ejection systolic murmur at left sternal edge - what defect causes the Fallot murmur? •Investigations: • CXR - “boot-shaped” heart • Echo •Management: • Surgical - intermediary shunts (Blalock-Taussig shunt), balloon dilatation, definitive surgery at 6 monthsTGA • Two parallel circulations • Most occur with VSD, ASD or PDA • Usually presents around day 2 of life when DA closes • Management: • Medical - prostaglandins • SurgeryHaematology • IDA • Haemoglobinopathy • HS • Thalassaemia Pallor • Haemolytic anaemia • G6DP • Sickle cell • ALL ALL • Accounts for 80% of leukaemia in children • Management: chemo • 2-5 years • Poor prognostic indicators: • a/w T21, Klinefelter’s syndrome • WCC >100 x 109/L • General features: malaise, anorexia • <2 or >10 • Bone marrow infiltration:- pancytopenia • Male • Anaemia: pallor, lethargy • Neutropenia: infection • T-cell origin • Thrombocytopenia: bruising, petechiae, • Philadelphia chromosome nose bleeds • Slow response to Rx: more than 5% • Bone pain blasts persisting on d28 • Reticulo-endothelial infiltration: • Investigations: • FBC, BM aspirate + trephine, coag screen, LP, CXR • Low platelets • ITP • Abnormal clotting • Haemophilia Excessive • DIC • Meningococcal bruising • Vasculitis • HSP • Bone marrow disorder • ALL • NAI • Concerning features: • Injury to immobile child • Mechanism inconsistent with injury • Vague hx • Delayed px to ED • Parent/ carer aggressive/ unconcerned • Recurrent px to ED/ previous injury (different coloured bruises) NAI • Background of RFs – low BW, mother <30, unwanted pregnancy, stress, poverty • Concerning injuries: • Triangle of safety • Bruising in shape of hand, teeth, implement Full history and examination Investigate both for medical cause of bruising and NAI • Height and weight + head circumference in infants (increased size -> bleed?) • Bloods: FBC, blood film, clotting screen • If bony tenderness or strong suspicion of NAI 🡪 skeletal survey • CT head if head injury <1yr Document, document & document again • Use a body map to document all bruising / injuries and get consent from parents to take photos if needed. • Fully document any concerns and discussions with parents / NAI actions child Escalate if concerned • Keep parents informed – be open and honest about the process (this is usually done by a senior paediatrician) • Talk to senior / child safeguarding lead • intervention form) or call directlylling out a SIF (statutory • Admit to paediatric ward as a place of safety if needed. • If parents try to leave against medical advice, then contact police (in preference to security) • Consider siblings / other children potentially at riskRenal A 4-year-old boy presented to the GP with a 7-day history of swollen eyelids. He is generally well. Urine dip: WCC -, blood-, nitrites-, protein++. Podocyte pathology Clinical features • Proteinuria (>3.5g/ 24 hrs) • Oedema: periorbital, scrotal, leg and ankle • Hypoalbuminaemia (<30g/L) • +/- hyperlipidaemia, thrombophilia, clotting risk Nephrotic Most common cause in children: minimal change disease • Steroid sensitive → give pred po for 8 weeks • If no response → renal biopsy necessary syndrome • Biopsy •Normal glomeruli on light microscopy •EM → fusion of podocytes/ effacement of foot processes Prognosis: rule of 3 • 1/3 never recur • 1/3 have infrequent recurrence • 1/3 have frequent relapsesAcute nephritis • Acute GN: immune-mediated damage to glomerulus • Urinalysis: active urinary sediment (blood++, protein++, red cell casts) • Post-infectious: GABHS • 1-2 weeks after URTI • ASOT titre • Mx: 10d course of Pen-V • IgA nephropathy • 2-3 days after URTI • HSP (systemic form of IgA nephropathy) Most common cause of acute paediatric renal failure Triad : 1. Microangiopathic haemolytic anaemia Haemolytic 3. AKI w/ haematuria and proteinuria uraemic Cause: E. coli O157:H7 → haemorrhagic colitis syndrome DO NOT give abxsChild psychiatry M > F Onset before age of 3 and can occur in first few months Triad of •Difficulties with social relationships •Problems with communication •Absorbing and narrowing interests Autistic Presentation •Attachment to unusual objects spectrum •Insistence on sameness (only eats white things) •Restricted range of interests/ activities •Stereotypies disorder •Sensory hypersensitivity Management •Parental support and education •MDT: GP, paediatrician, CAMHS, charities and support groups, SEN coordinator, applied behavioural analysis, environmental modifications Asperger’s → relatively unimpaired language & intelligence A 6-year-old boy is brought to see you by his mother who is concerned with his school performance. She reports he is unable to pay attention in his classes for more than a few minutes, as a result of which he is falling behind his peers and getting in trouble a lot due to getting distracted and making impulsive decisions. Furthermore, in the last 6 months he has also been having similar problems at home, switching rapidly between activities. • DSM-5 = ADHD is a condition incorporating features relating to inattention and/or hyperactivity/impulsivity that are persistent • Triad of • Inattention • Hyperactivity • Impulsivity • Symptoms normally present by age 7, and in at least 2 ADHD settings (home AND school) • Management • NICE – 10 week watch and wait period • Classroom intervention/ parental education • Drug therapy • If 5 yo or older → methylphenidate • Give on 6-week trial basis • SEs: abdo pain, nausea → monitor height/ weightMiscellaneous •Rule of 3 (Wessel criteria) • Resolves by 3 (to 4) months of age • Lasts more than 3 hours per day Infantile colic • Occurs more than 3d/week • Persists longer than 3 weeks •Infant is otherwise wellOligoarthritis (persistent) F: 1-6yrs 1-4 joints (knee, ankle, wrist common) Chronic anterior uveitis, leg length discrepancy Oligoarthritis (extended) F: 1-6yrs >4 joints after 6mo Chronic anterior uveitis Polyarthritis (RF negative) F: 1-6yrs Symmetrical large and small joints often with finger Low-grade fever involvement Polyarthritis (RF positive) F: Symmetrical large and small joints often with finger Rheumatoid nodules 10-16yrs involvement Systemic arthritis 1-10yrs Oligo or polyarthritis Acute illness, malaise, high daily fever May have muscle aches and pains but initially no Salmon pink macular rash arthritis Lymphadenopathy Anaemia Raised ESR, neutrophils etc. Psoriatic arthritis 1-16yrs Usually asymmetrical large and small joints, dactylitis Psoriasis, nail pitting, chronic anterior uveitis Enthesitis-related arthritis M: Lower limb, large joints initially, spinal / sacroiliac Enthesitis (localised inflammation of insertion of tendon / 6-16yrs involvement later ligaments e.g., achilles tendonitis) HLA-B27 Undifferentiated M: Overlapping 1-16yrs Inguinal hernia Hydrocele Patent processus vaginalis Fluid collecting in a patent processus vaginalis (young boys) Neonates → risk of strangulation R/O testicular ca in older men Does not transilluminate Transilluminates 6/2 rule Reassure (resolves by 2 yo age) Lump in the groinLump in groin cont. • Testicular torsion • Urological emergency! • High-riding testicle, N&V, negative Prehn’s sign • Surgery → bilateral fixation • Consent for orchidectomy • Lymph nodes → lymphadenopathy • Infection – TB • Malignancy • Systemic inflammatory conditions – JIABedwetting (nocturnal enuresis) • Dry by day + night at 3-4 years •Plot height and weight on • Primary or secondary to chart, perform urinalysis, • Diabetestion inspect genitalia/ spine, do • UTI lower limb neurology • Psychosocial •Management • 2ry if dry for 6 mo previously • Advice on fluid intake, diet, • Assess fluid intake/ toileting habits toileting • Keep diary for 2 weeks • Reward systems • Ask about constipation/ soiling, • Enuresis alarm if <7 yo development/ behaviour, weight, • >7 yo, consider desmopressin- polydipsia trial for 4 weeks.