Paediatrics Flashcards
IV fluid choice in children
o Neonates = 10% glucose
o Older = 0.9% NaCl + 5% glucose (+/- KCl)
Fluid maintenance in neonates
o Day 1 = 60ml/kg/day
o Day 2 = 90ml/kg/day
o Day 3 = 120ml/kg/day
o Day 4 = 150ml/kg/day
Fluid maintenance in children
o (Age+4) x2 = weight in kg (approx)
o First 10kg = 100ml/kg
o Next 10kg = 50ml/kg
o Every other kg = 20ml/kg
Fluid deficit in children
- Dehydrated = 50ml/kg extra over 24/48 hrs
- Shocked = 100ml/kg extra over 24/48 hrs
Fluid bolus in children
20ml/kg of 0.9% NaCl
Presentation of bronchopulmonary dysplasia (chronic lung disease of prematurity)
- Low oxygen saturations
- Increased work of breathing
- Poor feeding and weight gain
- Crackles and wheezes on chest auscultation
- Increased susceptibility to infection
- Requires oxygen therapy after reaching 36 wks gestational age
Prevention of chronic lung disease of prematurity
- Corticosteroids to mothers that show signs of premature labour
- CPAP rather than intubation and ventilation
- Caffeine to stimulate respiratory effort
- Not over oxygenating with supplementary O2
- Surfactant
Causes of cleft lip and palate
- Benzodiazepines
- Antiepileptics
- Rubella
- Trisomy 18, 13-15
- Pierre robin short mandible = causes intermittent short airway obstruction
Management of cleft lip
- Feeding with special teats may be needed before plastic surgery
- Lip repair at 3m and palate at 6m
o Avoid NICU as decreased bonding
Risk factors for meconium aspiration syndrome
- Post-term deliveries (>42 wks)
- Maternal hypertension
- Pre-eclampsia
- Chorioamnionitis
- Smoking
- Substance abuse
Complications of meconium aspiration syndrome
- Airway obstruction
- Surfactant dysfunction
- Pulmonary vasoconstriction
- Infection
- Chemical pneumonitis
Causes of hypoxic-ischaemic encephalopathy
- Maternal shock
- Intrapartum haemorrhage
- Prolapsed cord = compression of cord during birth
- Nuchal cord = cord wrapped around neck of baby
Sarnat staging of hypoxic-ischaemic encephalopathy
- Mild = Poor feeding, general irritability and hyper-alert
- Moderate = Poor feeding, lethargic, hypotonic and seizures
- Severe = Reduced consciousness, apnoeas, flaccid and reduced/absent reflexes
Management of Hypoxic-ischaemic encephalopathy
Therapeutic hypothermia
Risk factors for necrotising enterocolitis
- Very LBW or very premature
- Formulae feeds
- Respiratory distress and assisted ventilation
- Sepsis
- Patent ductus arteriosus and other congenital heart disease
Presentation of necrotising enterocolitis
- Intolerance to feeds
- Vomiting (green bile)
- Generally unwell
- Distended tender abdomen
- Absent bowel sounds
- Blood in stools
AXR in necrotising enterocolitis
o Dilated loops of bowel
o Bowel wall oedema
o Pneumatosis intestinalis = gas in bowel wall
o Pneumoperitoneum = free gas in peritoneal cavity
o Gas in portal veins
o Rigler sign = air both inside and outside bowel wall
o Football sign = air outlining falciform ligament
Causes of neonatal hypoglycaemia
- Preterm birth
- Maternal DM
- IUGR
- Hypothermia
- Neonatal sepsis
- Inborn errors of metabolism
Management of neonatal hypoglycaemia
- Asymptomatic
o Encourage normal feeding
o Monitor blood glucose - Symptomatic or very low blood glucose
o Admit to neonatal unit
o IV 10% dextrose
Risk factors for neonatal jaundice
- Premature neonates = immature liver
- Low infant birth weight
- Male
- Visible bruising
- Maternal age >25
- Maternal DM
- Ethnicity = Asian, European, native American
- Sibling born with jaundice requiring phototherapy
- Dehydration
- Poor caloric intake/increased neonatal weight loss
Causes of neonatal jaundice
- Increased production
o Haemolytic disease of newborn
o ABO incompatibility (<24hrs)
o Haemorrhage
o Intraventricular haemorrhage
o Cephalo-haematoma
o Polycythaemia
o Sepsis and disseminated intravascular coagulation
o G6PD deficiency (<24 hrs) - Decreased clearance
o Prematurity
o Neonatal cholestasis
o Extrahepatic biliary atresia
o Endocrine disorders (hypothyroid and hypopituitary)
o Gilbert syndrome - Physiological (2-14 days)
o Breastfeeding (benign and self-limiting)
Criteria for admission of neonatal jaundice
- Emergency admission if signs of bilirubin encephalopathy
- Urgent admission (seen within 2 hrs) if jaundice appears <24hrs old
- Urgent admission (seen within 6 hrs)
o Jaundice first appeared >7 days old
o Neonate unwell (lethargy, fever, vomiting, irritability)
o Gestational age <35 wks
o Prolonged jaundice suspected = <37wks >21 days jaundice or >37 wks with >14 days jaundice
o Feeding problems or concerns about weight
o Pale stools and dark urine - Community care Record bilirubin level within 6 hrs and manage following local protocol
Treatment of neonatal jaundice
- None if bilirubin level below threshold
- Phototherapy
o Rebound bilirubin measured 12-18 hrs after - Exchange transfusions
- Early surgical treatment
Complications of neonatal jaundice
- Kernicterus = brain damage caused by excessive bilirubin levels
o Cerebral palsy
o Learning disability
o Deafness - Acute/chronic bilirubin encephalopathy (neurotoxicity)
o Atypical sleepiness
o Poor feeding
o Irritability
o Vomiting
o Hypotonia followed by hypertonia
Presentation of biliary atresia
- Persistent jaundice (>14 days if term or >21 days if preterm)
High conjugated bilirubin
Management of biliary atresia
Kasai protoenterostomy
Principles of neonatal resuscitation
- Warm the baby
o Get baby dry = vigorous drying helps stimulate breathing
o Warm delivery rooms
o Management under heat lamp
o Babies <28wks placed in plastic bag still wet and managed under heat lamp - Calculate APGAR score
o Done at 1, 5, 10 mins whilst resuscitation continues
o Used as indicator of progress over first minutes after birth
o Helps guide neonatal resuscitation efforts - Stimulate breathing
o Dry vigorously with towel
o Place baby’s head in neutral position to keep airway open
Towel under shoulders
o If gasping or unable to breath, check airway obstruction and consider aspiration under direct visualisation - Inflation breaths
o Given when neonate is gasping or not breathing despite adequate initial stimulation
o 2 cycles of 5 inflation breaths (lasting 3s each) can be given to stimulate breathing and heart rate
o If no response and HR low, 30s of ventilations breath can be used
o If still no response, chest compressions can be used, coordinated with ventilation breaths
o Maintain neutral head position and get good seal around mouth and nose
o Look for rise and fall in chest
o Air should be used in term/near term babies and mix air and oxygen should be used in pre-term babies
o O2 sats monitored throughout and aim for gradual rise to 95% - Chest compressions
o Start if HR remains below 60bpm despite resuscitation and inflation breaths
o Chest compressions performed at 3:1 ratio with ventilation breaths - Severe situations
o IV drugs and intubation should be considered
What is APGAR
Appearance
Pulse
Grimmace (response to stimulation)
Activity (muscle tone)
Respiration
Benefits of delayed cord clamping
o Improved haemoglobin
o Improved iron stores
o Improved BP
o Reduction in intraventricular haemorrhage
o Reduction in necrotising enterocolitis
Risk factors for neonatal sepsis
- Vaginal GBS colonisation
- GBS sepsis in previous baby
- Maternal sepsis, chorioamnionitis or fever >38
- Prematurity
- Early rupture of membranes
- Prolonged rupture of membranes
Red flags for neonatal sepsis
- Confirmed/suspected sepsis in mother
- Signs of shock
- Seizures
- Term baby needing mechanical ventilation
- Respiratory distress starting >4 hrs after birth
- Presumed sepsis in another baby in multiple pregnancy
Management of neonatal sepsis
- If 1+ risk factor/clinical feature = monitor obs and clinical condition for min 12 hrs
- Antibiotics if 2+ risk factors/clinical features or single red flag
- Abx given within 1 hrs of decision to start them
- 1st line = benzylpenicillin and gentamycin
o Stop Abx if clinically well, blood cultures neg 36 hrs after and CRP <10 - Check CRP again at 24 hrs
- Check blood culture results at 36 hrs
- Check CRP again at 5 days if still on Tx
Management of neonatal respiratory distress syndrome
- CXR = ground-glass appearance and indistinct heart border
- Antenatal steroids (dexamethasone) given with suspected/confirmed preterm labour
- Supplementary oxygen = keep sats between 91-95%
- Intubation and ventilation
- Endotracheal surfactant
- CPAP via nasal mask
Presentation of retinopathy of prematurity
- Scarring
- Retinal detachment
- Blindness
- Plus disease = tortuous vessels and hazy vitreous humour
Management of retinopathy of prematurity
- Transpupillary laser photocoagulation Halt and reverse neovascularisation
- Cryotherapy
- Injections of VEGF inhibitors
- Surgery (if retinal detachment)
Presentation of congenital varicella syndrome
o Fetal growth restriction
o Microcephaly, hydrocephalus, learning disability
o Scars and significant skin changes following dermatomes
o Limb hypoplasia (underdeveloped limbs)
o Cataracts and inflammation in eye = chorioretinitis
Presentation of congenital rubella syndrome
o Congenital cataracts
o Congenital heart disease (PDA and pulmonary stenosis)
o Learning disability
o Hearing loss (sensorineural deafness)
o Growth retardation
o Hepatosplenomegaly
o Purpuric skin lesions
o Salt and pepper chorioetinitis
o Microphthalmia
o Cerebral palsy
Presentation of ASD
- Childhood (can be asymptomatic)
o SoB
o Difficulty feeding
o Poor weight gain
o Lower resp tract infections - Adulthood Dyspnoea, HF, Stroke
- Mid-systolic crescendo-decrescendo murmur at upper left sternal border
- Fixed split second heart sound
Risk factors for VSD
- Down’s syndrome
- Turner’s syndrome
Presentation of VSD
- Poor feeding and failure to thrive
- Dyspnoea, Tachypnoea
- Pan-systolic murmur
- Systolic thrill
Presentation of PDA
- Shortness of breath
- Difficulty feeding and Poor weight gain
- Lower resp tract infections
- Murmur = continuous crescendo-decrescendo “machinery” sound
- Left subclavicular thrill
- Large volume, bounding, collapsing pulse
- Wide pulse pressure
- Heaving apex beat
Management of PDA
- Monitored until 1 year of age
- Indomethacin or ibuprofen
o Given to neonate
o Inhibits prostaglandin synthesis - After 1 year unlikely to close spontaneously = trans-catheter/surgical closure
Risk factors of coarctation of aorta
Turner’s syndrome
Presentation of coarctation of aorta
- Weak femoral pulses
- Systolic murmur
- Tachypnoea and increased work of breathing
- Poor feeding
- Grey and floppy baby
- LV heave
- Underdeveloped left arm
- Underdevelopment of legs
Presentation of aortic stenosis
- Mild = asymptomatic
- Fatigue
- Shortness of breath
- Dizziness
- Fainting
- Sx worse on exertion
- Ejection systolic murmur in aortic area
o Crescendo-decrescendo character
o Radiates to carotids - Ejection click before murmur
- Palpable thrill
- Slow rising pulse and narrow pulse pressure
Associations of pulmonary stenosis
- Tetralogy of Fallot
- William syndrome
- Noonan syndrome
- Congenital rubella syndrome
Presentation of pulmonary stenosis
- Mild = asymptomatic
- Fatigue on exertion
- Shortness of breath
- Dizziness
- Fainting
- Ejection systolic murmur over pulmonary area
- Palpable thrill
- Right ventricular heave
- Raised JVP with giant a waves
Management of pulmonary stenosis
- Asymptomatic = watching and waiting
- Symptomatic
o Balloon valvuloplasty via venous catheter
o Open heart surgery
Presentation of innocent murmurs
- Soft, short, systolic murmur
- Symptomless
- Situation dependent
Concerning features of mumrurs
- Murmur louder than 2/6
- Diastolic murmurs
- Louder on standing
- Failure to thrive
- Feeding difficulty
- Cyanosis
- Shortness of breath
Features of tetralogy of fallot
- Ventricular septal defect
- Right ventricular hypertrophy
- Pulmonary stenosis
- Overriding aorta
Triggers of tet spells
- Waking
- Physical exertion
- Crying
- Pain
- Fever
Presentation of TOF
- Cyanosis
- Ejection systolic murmur due to pulmonary stenosis
- Right sided aortic arch
- Severe episodes Reduced consciousness, Seizures, Death
CXR in TOF
Boot shaped heart
Associations of transposition of great arteries
- Ventricular septal defect
- Coarctation of aorta
- Pulmonary stenosis
Presentation of transposition of great arteries
- Cyanosis at or within few days of birth
- Respiratory distress
- Tachycardia
- Poor feeding
- Poor weight gain
- Sweating
- Single loud S2
- Prominent loud ventricular impulse
CXR in transposition of great arteries
Egg-on-side appearance of heart
What is Ebstein’s anomaly
Tricuspid valve set lower in right side of heart causing bigger right atrium and smaller right ventricle
Cause of rheumatic fever
Group A strep (strep pyogenes)
Jones diagnostic criteria for rheumatic fever
- 2 Major or 1 major and 2 minor plus evidence of preceding strep infection
o Scarlet fever
o Throat swab
o Serum ASO titre - Major criteria
o Carditis = changed murmur, CCF, cardiomegaly, friction rub, +ve echo
o Polyarthritis
o Erythema marginatum
o Subcutaneous nodules
o Sydenham’s chorea - Minor criteria
o Fever
o ESR >20mm or CRP increased
o Arthralgia (pain but no swelling)
o ECG: PR interval >0.2s
o Previous rheumatic fever or rheumatic heart disease - Joints Knees, ankles, elbows, wrists may be very tender but no sequelae
- Echo criteria
o Mitral regurg jet is: >1cm, holosytolic, visible in 2 planes, mosaic pattern - MacCallum plaque
o Base of posterior mitral leaflet
o Aortic, pulmonary, tricuspid valves are affected in descending order of frequency
Management of rheumatic fever
- Rest/immobilisation helps joints and heart
- NSAIDs
- Oral Phenoxymethylpenicillin (for pharyngitis) preceded by one dose of benzylpenicillin
- Sydenham’s chorea Unless mild consider prednisolone for 4wks then taper
What is PANDAS
Paediatric autoimmune neuropsychiatric disorders associated with strep infections
o Suspect this in those with tics/Tourettes and OCD
o Anorexia nervosa may also be feature
Causes of childhood obesity
- Imbalance between energy intake and expenditure
- Dietary and Exercise
- Sleep deprivation
- Socioeconomic background
- Genetics
- Ethnicity = Asian
- Female
- Taller children
- Medication = sodium valproate, carbamazepine, mirtazapine, steroids
- High/low birth weight
- Intrauterine exposure to gestational diabetes or maternal obesity
- Hypothyroidism
- Cushing’s syndrome
- Growth hormone deficiency
- Prader-Willi Syndrome
- Down’s syndrome
Complications of childhood obesity
- Insulin resistance
- Type 2 DM
- Sleep apnoea
- Orthopaedic problems
o Slipped upper femoral epiphyses
o Blout’s disease
o Musculoskeletal pains - Non-alcoholic fatty liver disease
- Psychosocial morbidity = poor self-esteem, bullying
- PCOS
- Vitamin D deficiency
- Atherosclerosis
- Early onset CVD
- Cancers = breast, bowel
- Subfertility
- Hypertension
Causes of hypogonadotropic hypogonadism
- Abnormal functioning of hypothalamus or pituitary gland
- Previous damage to hypothalamus or pituitary
- GH deficiency
- Hypothyroidism
- Hyperprolactinaemia
- Serious chronic conditions (cystic fibrosis, IBD)
- Excessive exercise or dieting (delay menstruation in girls)
- Constitutional delay in growth and development
- Kallmann syndrome
Presentation of Kallmann syndrome
- Failure to start puberty
- Reduced or absent sense of smell (anosmia)
- Hypogonadism, cryptorchidism
- Normal or above average height
- Cleft lip/palate and visual/hearing defects
Causes of hypergonadotropic hypogonadism
- Previous damage to gonads (testicular torsion, cancer, infections)
- Congenital absence of testes or ovaries
- Kleinfelter’s syndrome
- Turner’s syndrome
What is precocious puberty
Development of secondary sexual characteristics earlier than normal
Presentation of precocious puberty
- Girls
1. Thelarche = first stage of breast development
2. Adrenarche = first stage of pubic hair development
3. Menarche = onset of menstrual periods (2yrs after start) - Boys
o Bilateral testes enlargement
o Pubic hair growth
o Penis enlargement - Other symptoms
o Gynaecomastia in boys
o Short stature
o Disproportioned growth of one area compared to other
o Polyuria
o Polydipsia
o Sleep
o Temperature regulation
o Visual disturbance - Testes
o Small testes adrenal cause
o Bilateral enlargement gonadotrophin release from intracranial lesion
o Unilateral enlargement gonadal tumour
Puberty staging
Tanner
Congenital cause of testicular torsion
Belt-clapper deformity
PResentation of testicular torsion
- Abdominal pain
- Sudden severely painful, inflamed testis
o makes walking uncomfortable
o Pain often comes on during sport or physical activity
o With intermittent torsion the pain may have passed on presentation
o But if severe and lie is horizontal then prophylactic fixing may be wise
o Very tender, hot and swollen
o Testis may lie high and transversely - Nausea and vomiting
- Prehn’s sign = elevation of testes does not relief pain
- Cremasteric reflex lost
Management of testicular torsion
- Urgent surgical exploration
o If surgery performed in <6 hrs, salvage rate = 90-100%
o If >24 hours = 0-10% - Orchidectomy = removal of testis
- Bilateral fixation
Management of undescended testis
- Unilateral
o Referral from around 3m
o Urological surgeon before 6m
o Early (at 1yr) fixing within scrotum = Orchidopexy - Bilateral
o Review within 24 hrs
o May need urgent endocrine and genetic investigations
Congenital causes of deafness
o Maternal rubella or CMV infection in pregnancy
o Genetic deafness
o Down’s syndrome
Red flags for abdominal pain
- Persistent or bilious vomiting
- Severe chronic diarrhoea
- Fever
- Rectal bleeding
- Weight loss or faltering growth
- Dysphagia
- Night time pain
- Abdominal tenderness
What is intussusception
- Bowel telescopes into itself
- Thickens overall bowel and narrow lumen at folded area
- Obstruction to passage of faeces through bowel
- Proximal to or at level of ileo-caecal valve
Presentation of intussusception
- Severe, colicky abdo pain Draw knees up
- Pale, lethargic and unwell child
- Redcurrant jelly stool (late sign)
- Vomiting (bilious = green)
- Diarrhoea
- RUQ mass on palpation = sausage-shaped
- Intestinal obstruction
- Tender abdomen and guarding
Investigations of intussusception
Abdominal USS = Target or bull’s eye sign
Management of intussusception
- 1st line = reduction by air insufflation under radiological control
- Therapeutic enemas to try to reduce intussusception = contrast/water/air pumped into colon force folded bowel out
- Surgical reduction (if signs of peritonitis)
What is meckel’s diverticulum
Congenital diverticulum of small intestine
Red flags for constipation
- Not passing meconium within 48 hrs of birth
- Neurological signs/sx (lower limbs)
- Vomiting
- Ribbon stool
- Abnormal anus
- Abnormal lower back or buttocks
- Failure to thrive
- Acute severe abdominal pain and bloating/distension
Amber flags for constipation
- Faltering growth
- Disclosure or evidence that raises concerns over possibility of child maltreatment
Causes of constipation
- Functional constipation
- Hirschsprung’s disease
- Cystic fibrosis
- Hypothyroidism
- Spinal cord lesions
- Sexual abuse
- Intestinal obstruction
- Anal stenosis/fissure
- Cows milk intolerance
- Medication = opiates
- Hypercalcaemia
Mangement of idiopathic constipation
- Correct any reversible factors = high fibre diet and good hydration
- Faecal impaction present
o 1st line = polyethylene glycol 2250 + electrolytes (Movicol Paediatric plain)
o Add stimulant laxative (after 2 wks if no improvement)
o Substitute for lactulose
o Parent education = can increase Sx of soiling and abdo pain - Maintenance therapy
o Continue long term Movicol and slowly weaned off as child develops normal, regular bowel habit - Encourage and praise visiting toilet = scheduling visits, bowel diary and star charts
- Infants not yet weaned
o Bottle fed = give extra water in between feeds, gentle abdo massage, bicycling of legs
o Breast fed = consider organic causes - Infants have/being weaned
o Extra water, diluted fruit juice, fruits
o Consider adding lactulose
What is hirschsprung’s disease
Nerve cells of myenteric plexus are absent in distal bowel and rectum
- Nerve plexus responsible for stimulating peristalsis of large bowel
- Without stimulation bowel loses motility and stops being able to pass food along its length
Presentation of Hirschsprung’s disease
- Neonatal = Delay in passing meconium (more than 24 hrs)
- Chronic constipation since birth
- Abdominal pain and distention
- Vomiting
- Poor weight gain and failure to thrive
Investigations of hirschsprung’s disease
- Abdo XR = intestinal obstruction
- PR = stool ejection
- Full thickness Rectal biopsy (GS) = histology shows absence of ganglionic cells
Management of Hirschsprung’s disease
- Fluid resuscitation
- 1st line = Rectal washouts initially
- Anorectal pull through procedure
- Management of intestinal obstruction
- Definitive = Surgical removal of aganglionic section of bowel
Associations of congenital diaphragmatic hernia
- Other malformations (neural tube)
- Trisomy 18
- Chromosome deletions
- Pierre Robin
Presentation of congenital diaphragmatic hernia
- Impaired lung development (pulmonary hypoplasia and pulmonary hypertension)
- Difficult resuscitation at birth
- Respiratory distress shortly after birth
- Bowels sounds in one hemithorax
- pH <7.3
- Cyanosis augar badly = lung hypoplasia
- Heart sounds displaced medially
- Abdominal wall appears concave
Vomiting red flags
- Not keeping any feed down = pyloric stenosis/intestinal obstruction
- Projectile/forceful vomiting = pyloric stenosis/intestinal obstruction
- Bile stained vomit = obstruction
- Haematemesis/melaena = peptic ulcer, oesophagitis or varices
- Abdominal distention = obstruction
- Reduced consciousness/bulging fontanelles/neurological signs = meningitis/ raised ICP
- Respiratory sx = aspiration/ infection
- Blood in stools = gastroenteritis or cows milk protein allergy
- Signs of infection = pneumonia, UTI, tonsillitis, otitis or meningitis
- Rash, angioedema and other signs of allergy = cows milk
- Apnoeas = serious underlying pathology
Management of GORD
- Advise
o Small, frequent meals
o Burping regularly to help milk settle
o Not over-feeding
o Keep baby upright after feeding (not lying flat) - More problematic cases
o Thickened milk/formula
o Gaviscon mixed with feeds
o PPI = Omeprazole if unexplained feeding difficulties, distressed behaviour or faltering growth
o Metoclopramide - Rare severe cases Surgical fundoplication
Presentation of pyloric stenosis
- Presents in first few weeks of life (4-6 wks)
- Projectile vomiting (typically 30 mins after feed)
- Hungry baby
- Non bile stained
- Constipation and dehydration
- Thin, pale and failing to thrive
- See peristalsis of abdomen after feeding
- Firm, round, palpable mass felt in upper abdo
Investigations of pyloric stenosis
- Blood gas = metabolic alkalosis with low chloride and potassium
- Abdo USS = thickened pylorus
Management of pyloric stenosis
Laparoscopic pyloromyotomy (Ramstedt’s operation)
Presentation of Cow’s milk protein allergy
Colic symptoms = irritability, crying
Regurgitation and vomiting
Blood/mucus in stools
Faltering growth
Diarrhoea
Urticaria, atopic eczema
Rarely angioedema and anaphylaxis
Management of CMPA
Exclusively breastfed
* Continue breastfeeding
* Exclude cow’s milk protein from mothers diet
* Use eHF when breastfeeding stops until 12m and at least for 6m
Formula fed
* 1st line = change to hypoallergenic extensively hydrolysed formula
* amino acid formula
* 10% also intolerant to soya milk
Presentation of intestinal malrotation
If volvulus = bile stained vomiting in first day of life
Management of volvulus
Ladd’s procedure
Presentation of oesophageal atresia
Antenatal = polyhydramnios
Respiratory distress
Distended abdomen
Choking and problems with swallowing
Difficulty feeding and overflow saliva
Cyanotic spells Following aspiration
Association of duodenal atresia
Downs syndrome
Other intestinal atresia
VACTERL association
Presentation of duodenal atresia
Antenatal = polyhydramnios
Distended abdomen
Non-bilious/bilious vomiting
Investigations of duodenal atresia
XR = double bubble
Presentation of haemolytic disease of newborn
Jaundice (<24 hrs)
Infection
Yellow vernix
CCF (oedema, ascites)
Hepatosplenomegaly
Progressive anaemia
Bleeding
CNS signs (Kernicterus)
Hypoalbuminaemia
Maternal diabetes
Thalassaemia
Management of haemolytic disease of newborn
Exchange transfusion
* If Hb <7g/dL, give 1st volume of the exchange transfusion as packed cells
* Subsequent precise exchanges according to response
* Keep baby warm
Phototherapy
under phototherapy lights
Giving Rh negative mothers anti-D immunoglobulin
ABO incompatibility = Exchange transfusion may be needed
Complication of haemolytic disease of newborn
Hydrops fetalis
Infectivity of chickenpox
- Infectivity 4 days before rash and 5 days after rash appeared
- Incubation = 10-21 days
Groups at high risks of complications from chickenpox
- Immunocompromised
- Preterm babies
- Steroid use
- <1 yrs old
- Adults and adolescents >14
- Pregnant women
Presentation of chickenpox
- Fever initially
- Generalised itchy rash
o Erythematous, raised
o Starts on trunk/face and spreads outwards affecting whole body over 2-5 days
o Blistering lesions (macules papules vesicles) - General fatigue and malaise
- Mild systemic upset
- URTI symptoms
- Shingles Reactivated chicken pox
Mangement of chickenpox
- Supportive
o Keep cool, trim nails
o School exclusion and avoid high risk groups until all lesions crusted over (5 days)
o Itching = calamine lotion, chlorphenamine - Higher risk groups IV Acyclovir 5 days
Complications of chickenpox
- Secondary bacterial infection Necrotising fasciitis
o Increased with NSAID use - Rarely
o Conjunctival lesions
o Pneumonia
o Encephalitis
o Shingles
Cause of glandular fever
EBV
PResentation of glandular fever
- Classic triad = sore throat, lymphadenopathy, pyrexia
- Malaise, anorexia, headache
- Palatal peteciae
- Splenomegaly
- Hepatitis
- Lymphocytosis
- Haemolytic anaemia
- Maculopapular pruritic rash (if taking amoxicillin/ampicillin)
Investigations of glandular fever
Monospot test (in week 2)
Management of glandular fever
- Usually resolves in 2-4 wks
- Supportive
o Rest, fluids, avoid alcohol
o Simple analgesia
o Avoid playing contact sports for 4 wks (splenic rupture)
Cause of hand, foot and mouth disease
Coxsackie 16
Presentation of HFM disease
- Mild systemic upset (sore throat and fever)
- Oral ulcer
- Vesicles on palms and soles
Management of HFM disease
- Self-resolves 7-10 days
- Supportive Simple analgesia, Hydration, Reassurance
- Keep unwell children off school but no exclusion required
Cause of impetigo
- Staphylococcus aureus (bullous)
- Streptococcus pyogenes
Presentation of impetigo
- Non-bullous impetigo
o Typically occurs around nose or mouth
o Exudate from lesions dries to form golden crust - Bullous impetigo
o 1-2cm fluid filled vesicles to form on skin
o Vesicles grow in size then burst forming golden crust
o Heal without scarring
o Lesions are painful and itchy
o Feverish and generally unwell
Management of impetigo
- Contagious so children kept off school until lesions healed or treated with Abx for at least 48 hrs
- Advise not to touch or scratch lesions, hand hygiene, avoid sharing face towels and cutlery
- Non-bullous
o Antiseptic cream (hydrogen peroxide 1% cream)
o Topical fusidic acid - Bullous Flucloxacillin (oral or IV)
Complications of impetigo
- Cellulitis
- Sepsis
- Scarring
- Post streptococcal glomerulonephritis
- Staphylococcus scalded skin syndrome
- Scarlet fever
Cause of measles
RNA paramyxovirus
Presentation of measles
- Prodrome = cough, coryza, conjunctivitis, cranky
- High temp until 5 days after rash starts
- Koplik spots on palate (classic presentation)
o Spots often fade as rash appears
o behind ears, on day 3-5, spread down body, merging - Diarrhoea
Management of measles
- Isolate
- Ensure adequate nutrition
o Continue breastfeeding even during diarrhoea
o Pass nasogastric feeding tube if intake poor - Vitamin A
o Developing world
o CI = pregnancy, known not to be deficient - Treat secondary bacteria infection (otitis media/pneumonia)
- Admission considered in immunosuppressed or pregnant
- Notifiable disease
- Vaccinate contacts within 72 hrs if unvaccinated
Complications of measles
- More common if <5 yrs or >20yrs
- Otitis media
- Croup and tracheitis (infants)
- Pneumonia (cause of death)
- Encephalitis (older patients)
- Subacute sclerosing parencephalitis (chronic – develops 7-13 yrs after)
- Febrile convulsions
- Keratoconjunctivits, corneal ulceration
- Appendicitis
- Myocarditis
Presentation of mumps
- Fever
- Malaise
- Muscular pain
- Parotitis Ear ache, Pain on eating
Presentation of rubella
- Pink Maculopapular rash on face which spreads to whole body
- Suboccipital and post-auricular lymphadenopathy
Presentation of molluscum contagiosum
- Pinkish or pearly white papules with central umbilication (5mm diameter)
- Lesions appear in clusters in areas anywhere on body (except palms of hands and soles of feet)
Management of molluscum
- Self-care advice
o Reassure that self-limiting
o Spontaneous resolution within 18m
o Avoid sharing towels, clothing and baths with uninfected people
o Encourage not to scratch
o Exclusion from school not necessary - Treatment
o Not usually recommended
o Simple trauma
o Cryotherapy
o Emollient and mild topic corticosteroid
o Antibiotic if infected
Cause of 6th disease (roseola infantum)
HHV 6
Presentation of 6th disease
- High fever (precedes rash by few days)
- Maculopapular rash
- Nagayama spots
- Febrile convulsions
- Diarrhoea
- Cough
Presentation of scalded skin syndrome
- Generalised patches of erythema on skin similar appearance to burn or scalded
- Skin looks thin and wrinkled
- Formation of fluid filled blisters (bullae)
- Blisters burst and leave very sore, erythematous skin below
- Nikolsky sign = gentle rubbing of skin causes it to peel away
- Systemic: Fever, Irritability, Lethargy, Dehydration
Cause of scarlet fever
Group A strep
Presentation of scarlet fever
- Red-pink blotchy macular rash starting on trunk and spreads outwards
- Rough sandpaper skin
- Sore throat (tonsilitis)
- Strawberry tongue
- Fever (lasts 24-48 hrs)
- Red, flushed cheeks
- Cervical lymphadenopathy
- Systemic: Lethargy, Malaise, Headache, N+V
Management of scarlet fever
- Phenoxymethylpenicillin for 10 days immediately
o Azithromycin if penicillin allergy - Notifiable disease
- Keep children off school until 24 hrs after starting Abx
Complications of scarlet fever
- Otitis media
- Rheumatic fever
- Acute glomerulonephritis
- Invasive complications Bacteraemia, Meningitis, Necrotising fasciitis
Cause of slapped cheek syndrome
Parovirus B19
Cause of stevens Johnson syndrome
- Medications
o Anti-epileptics
o Antibiotics
o Allopurinol
o NSAIDs - Infections
o Herpes simplex
o Mycoplasma pneumonia
o Cytomegalovirus
o HIV
Presentation of stevens johnson syndrome
- Non-specific symptoms = fever, cough, sore throat, sore mouth, sore eyes, itchy skin
- Painful Purple/red rash with blistering
o Affects less than 10% body surface area
o Spreads across skin
o Shedding of top layer of skin
o Can happen to lips and mucous membranes
o Ulcerated - Inflamed eyes
- Affect urinary tract, lungs, internal organs
Risk factors for developmental dysplasia of hip
- 1st born (tighter, unstretched uterus)
- Breech position (incl CS)
- Sibling/ FH of DDH
- Swaddling
- Macrosomia
- Oligohydramnios
- Congenital calcaneovalgus foot deformity
Presentation of developmental dysplasia of hip
- Asymmetrical skin folds
- Limb length discrepancy
- Less mobility/flexibility
- Limping, toe walking, waddling
Investigations for developmental displasia fo hip
- Screening at 6-8wks
o Barlow’s test (dislocate)
o Ortolani’s test (relocate)
o Symmetry of leg length
o Level of knees when hips and knees are bilaterally flexed
o Restricted abduction of hip in flexion - US at 6w
o 1st degree relative with DDH
o Breech
o Other RF - 6m > US
- 6m < XR
Management of developmental dysplasia of hip
- Observation Most unstable hips spontaneously stabillise by 3-6 wks
- Pavlik harness (constant, few months)
o Children younger than 4-5m - Abduction brace (if harness fails/ineffective)
- Surgical reduction/fixation
Presentation of transient synovitis
Recent viral URTI (sx occur within few wks)
Limp
Refusal to weight bear
Groin or hip pain
Mild low grade temp
Management of transient synovitis
Simple analgesia
Exclude other pathology
Clear safety net advice to attend A&E if Sx worsen or develop fever
Follow up at 48 hrs and 1 wk
PResentation of juvenile idiopathic arthritis
Joint swelling/inflammation/pain/stiffness
Fever
Limp
Fatigue
Lymphadenopathy
Hepatosplenomegaly
Blurry/gritty eyes (uveitis)
Salmon-pink Rash
Appetite loss and weight loss
Differential of limping child
- Septic arthritis/osteomyelitis
- Juvenile idiopathic arthritis
- Trauma
- Development dysplasia of hip
- Perthes disease
- Slipped upper femoral epiphysis
What is Osgood-Schlatter’s disease
Inflammation at tibial tuberosity where patella ligament inserts
PResentation of osgood-schlatter
Gradual onset
Anterior knee pain
Usually unilateral (can be bilateral)
Pain exacerbated by physical activity, kneeling and on extension of knee
Visible or palpable hard and tender lump at tibial tuberosity
What is osteogeneis imperfecta
Brittle bone disease – group of disorders of collagen metabolism resulting in bone fragility and fractures
Presentation of osteogenesis imperfecta
Increased fragility
* Frequent fractures following minor trauma
* Abuse
* Crush fractures (vertebrae)
Bone deformity = bowed legs
Joint issues
Scoliosis
Short stature
Weak teeth/ dental caries
Blue sclera
Hearing loss (deafness secondary to otosclerosis)
What is perthes disease
Idiopathic avascular necrosis of proximal femoral epiphysis
Presentation of perthes disease
Insidious onset
Painless limp (worsens)
Intermittent hip, knee, groin or thigh pain
Gait disturbance
Hip stiffness and loss of int rot and abd
Reduced range of hip movement
Limb length discrepancy
Muscle wasting
Management of perthes disease
Keep femoral head within acetabulum: cast, braces
If <6 yrs = observation
Resolve symptoms
* NSAIDs
* Traction
* Crutches
Restore ROM
* Physio
* Muscle lengthening
Surgery (if older and with moderate results)
* Osteotomy
Presentation of rickets
Lethargy
Bone pain
Swollen wrists ‘ricket rosary’
Bone deformity
Poor growth
Dental problems
Muscle weakness
Pathological or abnormal fractures
Bowing of legs (curve outwards)
Knock knees (legs curve inwards)
Rachitic rosary (ends of ribs expand at costochondral junctions, causing lumps along chest)
Craniotabes (soft skull, with delayed closure of sutures and frontal bossing)
Delayed teeth (underdevelopment of enamel)
Harrison’s sulcus
Risk factors for slipper upper femoral epiphysis
Adolescence
Male
Obesity
History of radiotherapy to area
Puberty
Downs syndrome
Hypothyroidism
Hypopituitary
GH deficiency
Presentation of SUFE
Groin and thigh pain
Limp = antalgic gait, externally rotated foot
Loss of internal rotation of leg in flexion
Knee pain
Present for wks/mnths
Prefer to sit with affected leg crossed over other
Causes of global developmental delay
- Down’s syndrome
- Fragile X syndrome
- Fetal alcohol syndrome
- Rett syndrome
- Metabolic disorders
Causes of gross motor delay
- Cerebral palsy
- Ataxia
- Myopathy
- Spina bifida
- Visual impairment
Causes of fine motor delay
- Dyspraxia
- Cerebral palsy
- Muscular dystrophy
- Visual impairment
- Congenital ataxia
Causes of hearing, speech and language delay
- Specific social circumstances
- Hearing impairment
- Learning disability
- Neglect
- Autism
- Cerebral palsy
Presentation of ADHD
Inattention
* Does not follow through on instructions
* Reluctant to engage in mentally-intense tasks
* Easily distracted
* Finds it difficult to sustain tasks
* Finds it difficult to organise tasks or activities
* Often forgetful of daily activities
* Often loses things necessary for tasks or activities
* Often dose not seem to listen when spoken directly
Impulsivity/Hyperactivity
* Unable to play quietly
* Talks excessively
* Dose not wait their turn easily
* Will spontaneously leave their seat when expected to sit
* Is often ‘on the go’
* Often interruptive or intrusive to others
* Will answer prematurely before a question has been finished
* Will run and climb in situations where it is not appropriate
Different presentation in girls (underdiagnosis)
Medication for ADHD
Methylphenidate (Ritalin) = 6wk trial
* S/E = abdo pain, nausea, dyspepsia, stunted growth
* Monitor weight and height every 6m
2nd line - Lisdexamfetamine (Elvanse)
Atomoxetine (Strattera)
Guanfacine (Intuniv)
Clonidine
Severity of ADHD
Connor’s
Presentation of Autism Spectrum Disorder
Impaired reciprocal social interaction
* Children frequently play along (relatively uninterested in being with other children)
* Fail to regulate social interaction with nonverbal cues (eye gaze, facial expression, gestures)
* Fail to form and maintain appropriate relationships = become socially isolated
Repetitive behaviours, interests, activities
* Stereotyped and repetitive motor mannerisms, inflexible adherence to non-functional routines or rituals
* Children noted to have particular ways of going about everyday activities
Impaired communication and language
Spectrum (can be high functioning)
Higher head circumference to brain volume ratio
Red flags for child abuse
- Disclosure by child
- Odd story, incongruent with injuries, odd mode of injury, odd set of signs
- Delayed presentation to doctor, taken by someone other than parents
- History inconsistent with child’s development
- Efforts to avoid full examination
- Psychological sequelae from sexual/emotional abuse
- Unexplained fractures (forearm, rib)
- Rare for non-ambulant baby to sustain accidental fracture
- Buttock, perineum or face injury, intracranial bleeds, torn lingual frenulum, vitreous/retinal bleeds, hyphaemia, lens dislocation, bulging fontanelle, increased head circumference + xanthochromia
- Cigarette burns, whip marks, bruised non-mobile baby, signs of suffocation, fingermark bruising, perforated pharynx, bite marks
- Torn frenulum
- Failure to thrive
- STIs
Severity of AKI in children
Paediatric RIFLE criteria
* Risk
* Injury
* Failure
* Loss of kidney function
* End-stage renal failure
Types of nocturnal enuresis
Primary = never been continent through night (at least 2x per week for 3m)
Secondary = been continent for at least 6m before
Causes of nocturnal enuresis
Constipation
Abuse/emotional upset
UTI
Diabetes mellitus
Renal failure
Management of nocturnal enuresis
Parental advice
* diet, fluid intake, toilet patterns, lifting and waking
* Punishment and disapproval ineffective
Conservative measures
* Restricting fluid intake before bedtime and irritating fluids (orange juice)
* Double voiding at night
* Waking child to pass urine once in night
* Introduce reward system for agreed behaviours
* Clear constipation
Use bed-wetting (enuresis) alarm = trial for 4 wks
* 1st line for children <7
If all unsuccessful or >7
* Desmopressin 1-2 hrs before bed
* Do not drink after medication as increases risk of cerebral oedema
Cause of bronchiolitis
Respiratory syncytial virus
Presentation of bronchiolitis
- Coryzal sx = runny/snotty nose, sneezing, mucus in throat, watery eyes
- Dry cough
- Poor feeding with increasing dyspnoea
- Mild fever
- Apnoeas
- Wheeze and fine inspiratory crackles on auscultation
- Signs of respiratory distress
o Use of accessory muscles
o Intercostal and subcostal recessions
o Nasal flaring
o Head bobbing
o Tracheal tugging
o Cyanosis
o Abnormal airway noises
o Tachypnoea
Maangement of bronchiolitis
- Supportive management
o Ensuring adequate intake = NG tube/IV fluids
o Saline nasal drops and nasal suctioning = clear nasal secretions
o Supplementary oxygen = if sats below 92%
o Ventilatory support if required - Palivizumab (monoclonal antibody) = monthly injection as prevention
Cause of Croup
parainfluenza virus
Presentation of Croup
- Increased work of breathing
- “Barking” cough, occurring in clusters of coughing episodes
- Hoarse voice
- Stridor
- Low grade fever
- Respiratory distress
- Sx worse at night and increase with agitation
- Preceded by non-specific upper RTI (12-72 hrs) = coryzal Sx
- Usually resolves within 24hrs but may last up to 1wk
Management of croup
- All children with croup = Single dose oral dexamethasone
- Managed at home fluids and rest, Infection control, Simple Analgesia
- Safety-net parents
o Child very pale, grey or blue for more than few secs
o Unusually sleepy or unresponsive
o Having trouble breathing
o Upset while struggling to breath
o Unable to talk or drooling - Admission for
o >60 breaths/min or high fever or toxic appearance
o <6m age
o Known upper airway abnormalities (Laryngomalacia, Downs)
o Uncertainty about diagnosis - Severe croup
o Oxygen
o Nebulised budesonide
o Nebulised adrenalin
o Intubation and ventilation
CXR in epiglottis
Steeple sign = subglottic narrowing
Presentation of diptheria
- Sore throat
- Swollen tonsils bull neck
- Low grade fever
- Pseudomembrane formation
- Polyneuritis (starting with cranial nerves)
- Shock = myocarditis, toxaemia, cardiac conducting system involvement
- Dysphagia
- Muffled voice
- Bronchopneumonia
- Airway obstruction preceded by brassy cough
- Nasal discharge with excoriated upper lip
- Motor palatal paralysis also occurs causing fluids to escape from nose on swallowing
Management of diptheria
- IM penicillin
- Diphtheria antitoxin = 10 000-30 000 units IM
- Erythromycin
- Contacts <2 receive erythromycin syrup 7 days
- Keep away from pregnant women
Cause of whooping cough
Bordetella pertussis
Presentation of whooping cough
acute cough lasting >14 days without another apparent cause and 1+ of:
o Paroxysmal cough
o Inspiratory whoop
o Post-tussive vomiting
o Undiagnosed apnoeic attacks in young infants
Maangement of whooping cough
- Oral Clarithromycin if onset of cough within previous 21 days
- Admit if <6m
- Notifiable disease
- May need ventilating
- Household contacts offered antibiotic prophylaxis
- School exclusion: 48 hrs after commencing Abx
Cause of epiglottitis
Haemophilus influenza type B (HiB)
Presentation of epiglottitis
- Rapid onset
- Fever
- Stridor
- Pooling/drooling saliva
- Sore throat
- Muffled voice/cry
- Dysphagia
- Tripod stance: sitting and lean forward, extend neck
- NO COUGH
- Respiratory distress respiratory retractions and cyanosis
Management of epiglottitis
- Intubate (or tracheostomy)
- Antibiotics = cephalosporins
- Dexamethasone
- Fluid resuscitation
Presentation of viral induced wheeze
- Viral Sx = fever, cough, coryzal Sx 1-2 days before
- Shortness of breath
- Signs of respiratory distress
- Expiratory wheeze throughout chest
Management of viral induced wheeze
- Encourage smoking parents to stop
- Moderate
1. Short acting beta 2 agonist (salbutamol) via spacer
2. Intermittent leukotriene receptor antagonist (montelukast) and/or inhaled corticosteroids - Severe
o Oxygen if required
o Aminophylline infusion
o Consider IV salbutamol
Angelman syndrome
Fascination with water
Happy demeanour
Down’s syndrome
Hypotonia
Brachycephaly (small head with flat back)
Short neck
Short stature
Flattened face and nose
Prominent epicanthic folds
Upward sloping palpable fissures
Single palmar crease
Brushfield spots in iris
Protruding tongue
Small low-set ears
Antenatal screening for Down’s syndrome
- 1st line = combined USS and maternal blood test (11-14/40)
- Nuchal thickness >6mm
- Beta-HCG = higher is greater risk
- Pregnancy-associated plasma protein-A = lower is greater risk
Complication’s of Down’s syndrome
Learning disability
Recurrent otitis media
Deafness (Eustachian tube abnormalities)
Visual problems (myopia, strabismus, cataracts)
Hypothyroidism
Cardiac defects = endocardial cushion defect (ASD, VSD, PDA, ToF)
Atlantoaxial instability
Acute lymphoblastic Leukaemia
Dementia (Alzheimer’s)
Duodenal atresia
Hirschsprung’s disease
Subfertility
Repeated respiratory infections
Edward’s syndrome (trisomy 18)
Micrognathia
Low set ears
Rocker bottom feet
Overlapping of fingers
Patau syndrome (13)
Microcephalic small eyes
Cleft lip/palate
Polydactyly
Scalp lesions
Fragile X syndrome
Long, narrow face
Large ears
Large testicles after puberty
Hypermobile joints
Klinefelter’s syndrome (47XXY)
Appear normal until puberty
Taller height
Wider hips
Gynaecomastia
Weaker muscles
Small testicles
Reduced libido
Shyness
Infertility
Subtle learning difficulties (speech and language)
Marfan syndrome
Tall stature
Long neck
Long limbs
Long fingers (arachnodactyly)
High arch palate
Hypermobility
Pectus carinatum or pectus excavatum
Downward sloping palpable fissures
Noonan syndrome
Short stature
Broad forehead
Downward sloping eyes with ptosis
Hypertelorism (wide space between eyes)
Prominent nasolabial folds
Low set ears
Webbed neck
Widely spaced nipples
Prader-Willli syndrome
Constant insatiable hunger that leads to obesity
Neonatal hypotonia
Turner syndrome (45X0)
Short stature
Webbed neck
High arching palate
Downward sloping eyes with ptosis
Broad chest with widely spaced nipples
Cubitus valgus
Underdeveloped ovaries with reduced function
Late or incomplete puberty
William syndrome
Broad forehead
Starburst eyes
Flattened nasal bridge
Long philtrum
Wide mouth with widely spaced teeth
Small chin
Very sociable trusting personality
