Paediatrics Flashcards
Who can complete then routine examination of the newborn
Hospital paediatrician
Advanced neonatal nurse Practitioner
GP
Specially trained nurse/midwife
Routine examination of newborn
Head to toe
Completely undressed
- Skull shape, maximum circumference, fontanelles
- Face: any dysmorphisms, examine for cleft palate
- Ears: position, size, shape, patency
- Neck
- Chest: shape, symmetry, nipple position. RR 40-60, palpate precordium
- Abdomen: look at umbilical stump, inguinal hernias, palpate organs
- Genital: female inspect. male - urinary meatus, descended testes
- Femoral pulses
- Anus: patency
- Spine: deformity, dimple, naevi, hair
- Limbs: tone. Digit number. Clubbed foot, palmar creases
- DDH
- CNS: tone (should be flexed at hip and knee), pull baby to sitting by holding wrists. Ventral suspension
Moro reflex
Moro reflex
Act as if to drop the baby
Arms should extend and then flex
If bilateral absence then CNS damage
If unilateral then birth trauma e.g. Erb’s palsy
Define vernix
Normal cheesy white substance on the skin of baby at birth
Skull molding
Over riding skull bones
Palpable ridges
Normal
Resolves in 2-3 days
Caput succedaneum
Swelling or oedema on new born scalp
From prolonged pressure during delivery
Resolves in a few days
Chignon
Temporary swelling of infants head after ventouse suction cap
Increases rate of jaundice
Cephalhaematoma
Bruise on neonates head from prolonged stage 2 of labour or instrumental delivery
Subperisoteal
Boundaries are limited by bone margins
Subconjuctival haemorrhage in newborn
Can happen in precipitate delivery (<2 hours) or if cord around neck
Harmless
Will resolve in a few weeks
Be careful if later than newborn as can indicate abuse
Epstein’s peals
Self resolving white inclusion cysts on palate
Tongue tie
Shortened tongue frenulum
Ranula
Self resolving bluish mouth floor swelling
mucus retention cyst
Retracted testes
Due to exaggerated cremastus muscle
Palpate along to determine location of testes
Mongolian blue spot
Normal birth mark
Increased in Asian and Africans
Erythema toxicum
Normal neonatal rash
Erythematous base with small pustules
Unknown cause
Primitive reflexes
Rooting Grasping Moro Walking Sucking Asymmetrical tonic neck reflex - fencing posture Galant reflex Swimming reflex
Describe grasping reflex
Baby will grasp anything in palms
Disappears at 5-6 months
Describe asymmetrical tonic neck reflex
Fencing posture
Present from 1-4 months
When head is turned to the side, the arm on that side will straighten , opposite will bend
If >6months then UMN disorder
Characteristics of pathological heart murmur
All Diastolic All Pansystolic Late systolic murmurs Loud murmurs > 3/6 Continuous murmur Associated cardiac abnormalities Heard over upper L sternal border
Symptomatic:
SOB, easy fatigue, cyanosis, FTT, clubbing, hepatomegaly
Characteristic of innocent heart murmur
Always systolic Short duration Low intensity Increases with increased cardiac output Intensity can change with posture no thrill or heave No radiation No symptoms
Predisposing conditions for heart murmurs
Down's Noonan's Turner's Marfan's Foetal alcohol syndrome Foetal rubella infection
Still’s murmur
Innocent murmur Mid L sternal border Mid-systolic Grad 2-3 Twanging, musical, vibrating sound
Pulmonary flow murmur
Innocent murmur Upper L sternal border Mid systolic Grade 1-3 Grating
Acyanotic causes of congenital heart disease
Ventricular septal defect Atrial septal defect Patent Ductus Arteriosus Pulmonary valve stenosis Coarctation of the aorta Hypoplastic left heart syndrome Hypertrophic obstructive cardiomyopathy Dextrocardia
Cyanotic causes of congenital heart disease
Tetralogy of fallot Transposition of great arteries Tricuspid atresia Total anomalous pulmonary drainage Persistent truncus arteriosus Ebstein's abnormality
Epidemiology of congenital heart disease
8 per 1000 live births 1/3 of congenital abnormalities Increased if FHx Increased if parents are relatives Intrauterine - drugs, alcohol, rubella infection Down's syndrome DiGeorge's syndrome Williams syndrome Noonan's syndrome Turner's syndrome Maternal diabetes
Atrial septal defect
Left to Right shunt
Can be ostium secundum defect (foramen ovale) with normal valves or partial AVSD affecting valves
Usually asymptomatic
Tx - close ASD in early childhood
Ventricular septal defect
25% of all congenital heart disease Typically asymptomatic Pansystolic murmur at left lower sternal edge Most close spontaneously Can have heart failure
Patent ductus arteriosus
Common
Defined as patent ductus arteriosus if patent at 1 month
Connects pulmonary artery to aorta
Low diastolic pressure due to back flow through pulmonary artery
Wide pulse pressure
Bounding peripheral pulses
Continuous or machinery murmur in left infraclavicular area
Most close spontaneously
Tetralogy of Fallot
4 cardinal anatomical abnormalities
- VSD
- Over-riding aorta
- R ventricular outflow obstruction
- R ventricular hypertrophy
Cyanosis
Paroxysmal hypercyanotic spells - Tachypnoea, restlessness. Become white or floppy for minute-hours
Treated with prostaglandin E infusion
R to L shunt
Increased risk of cerebral ischaemia, endocarditis, HF, brain abscess, polycythaemia
Transposition of the great arteries
2 separate parallel circuits
Systemic venous blood returns to R heart and back to systemic flow
Not compatible with life unless mixing ASD or PDA
Severe hypoxia
No heart failure
Heart defect associated with Noonan’s syndrome
Pulmonary stenosis
Heart defect associated with Turner’s syndrome
Coarctation of aorta
Neonatal history
PREGNANCY
- parity
- any extra scans
- maternal problems in pregnancy
- medications
BIRTH
- gestation
- induced or spontaneous labour
- PROM?
- RF for infection
- Vaginal or C-section
SINCE BIRTH
- Feeeding, meconium, urine, vomiting
- Receive Vit K
- Any problems or concerns
Fhx and social
- genetic conditions
- RF for DDH
- SIDS
- Social set up
Causes of sick newborn
Sepsis Hypoxic Ischaemia Encephalopathy Transient Tachypnoea of newborn RDS Hypoglycaemia Jaundice Necrotising enterocolitis Cardiac murmur Neonatal abstinence syndrome Seizures
Changes in foetal circulation at birth
In utero - blood vessels that supply and drain lungs are constricted
Increased pulmonary vascular resistance
Blood bypasses lungs through ductus arteriosus
Pulmonary vessels dilate due to increased O2
Encourages blood flow to lungs
Closure of ductus arteriosus
Pulmonary expansion Increased O2 tension Decreased pulmonary vascular resistance Increased pulmonary blood flow Increased LA filling Closure of foramen ovale
Apgar score
HR - 0-absent, 1-<100, 2>100
Respiration - 0-absent, 1-gasping, 2-regular
Muscle tone - 0-flaccid, 1=some flexion, 2=well flexed
Reflex irritability 0-none, 1-grimace, 2-cry/cough
Colour - 0-pale/blue, 1-body pink, blue limbs, 2-pink
Cleft palate/lip
1 in 1000 children
Tends to run in families
Problems
- Difficulty feeding
- Milk aspiration
- Speech difficulties
- Conductive hearing loss due to Eustacian tube dysfunction
- Dental problems
Surgically corrected at 9 months
Give specialist advice on managing baby
Neural tube defects
Failure of neural tube to close in early pregnancy - incidence decreased with folic acid supplements
Screening with US and alpha fetoprotein
Anencephaly - most severe. complete failure of development of cranial nerve tube
Myelomeningocoele - open lesion with malformed and exposed spinal cord covered by meninges. Severe neurological abnormality of lower limbs
Meningocoele - spinal cord intact, exposed meninges. High risk of meningitis and hydrocephalus
Spina bifida occulta - hidden abnormality. Develop bladder dysfunction and pyramidal tract signs in legs as child grows
- Deep pit, tuft of hair, naevus, lipoma in midline
US offers diagnosis
Hypospadias
Urethra abnormally placed
1 in 500 boys
Most commonly ventrally on glans up to perineum
Increased severity with increased penile curve
Severe cases require repair before 2 years
DO NOT CIRCUMCISE as foreskin used in reconstruction
Bowel obstruction
1 in 1000 babies
Can be anatomical or functional
Clinical features:
- Bile stained vomiting
- Failure to pass meconium
- Abdominal distension
- Visible peristalsis
Oesophageal atresia: mucus, chokes on first feed
Duodenal atresia - bile stained vomit, double bubble on AXR
Jejunal atresia = most common. distension. bile stained vomit
Hirschsprung’s disease
Absence of myenteric nerve plexus in the rectum
may extend along the colon
abdomen distends
15% present with acute enterocolitis
Exomphalos
Often diagnosed Antenatally
Also called omphalocele
Abdominal contents protrude through umbilical ring, covered by transparent sac.
Gastroschsis
Bowel protrudes through defect in anterior abdominal wall adjacent to umbilicus
no sac covering
Cover with cling film
Increased risk of dehydration
Hypoxic ischaemic encephalopathy
Hypoxia. Hypercapnia. Metabolic acidosis.
Decrease tissue perfusion.
Brain damage, disability or death
Causes:
- prolonged uterine contractions
- placental abruption
- ruptured uterus
- cord compression
- shoulder dystocia
- cord prolapse
- maternal hypotension
- anaemia
- IUGR
MILD - infant irritable, responds excessively to stimulation
MODERATE - marked abnormalities in tone and movement
SEVERE - no normal spontaneous movements or response to pain. prolonged seizures. 30-40% mortality
Brachial nerve palsies
Occurs if breech birth or shoulder dystocia
Upper nerve root C5-6 = ERB’s palsy
Lower nerve root = KLUMPKEYS palsy
Facial nerve palsy
Via compression of facial nerve on ischial spine Unilateral Facial weakness on crying Eye remains open Usually transient
Define pre-term infant
Under 34 weeks
Medical problems in pre-term infants
Resuscitation at birth RDS Hypotension PDA Temperature control issues Hypoglycaemia, hypocalcaemia, electrolyte imbalance Nutrition Infection Jaundice Necrotising entercolitis Retinopathy of prematurity Anaemia of prematurity Brocnhopulmonary dysplasia Inguinal hernias
Respiratory distress syndrome
Deficiency of surfactant from type II pneumocytes
Widespread alveolar collapse and inadequate gas exchange
Steroids given Antenatally stimulate surfactant production
Tachypnoea >60
Laboured breathing, chest wall recession, nasal flaring
Expiratory grunting
Cyanosis if severe
CXR - diffuse granular or ground glass appearance
Treat with CPAP and O2
Necrotising enterocolitis
Affects pre-term babies in first few weeks
Bacterial invasion of ischaemia bowel wall
increased if cows milk fed
Infant stops tolerating feeds, milk aspirated from stomach
Vomiting +/- bile staining
Distended abdomen
Fresh blood in stools
Distended loops of bowel
Thickening of bowel wall
Can cause perforation
Stop feeding
Start broad spec Abx
Retinopathy of prematurity
Affects developing blood vessels at the junction of vascular and non-vascularised retina
Vascular proliferation
Retinal detachment
Fibrosis
Blindness
Bronchopulmonary dysplasia
Infants who still require O2 at 36 weeks
Lung damage from pressure and volume trauma from ventilation
CXR - widespread opacification and cystic changes
Jaundice in neonates
Over 50% of newborns are visibly jaundiced
- Marked physiological release of Hb from breakdown of Hb at birth
- RBC lifespan is only 70 days
- Hepatic bilirubin metabolism if less efficient in first few days
May be a sign of:
- Haemolytic anaemia
- Infection
- metabolic or liver disease
Kernicterus
Encephalopathy resulting from deposition of unconjugated bilirubin in basal ganglia and brainstem nuclei
- lethargy and poor feeding
- irritability
- Increased muscle tone
- Seizures, coma
- Survivors can develop choreoathetoid CP - learning disability and sensorineural deafness
Causes of jaundice in neonate
Haemolytic disorders: Rhesus/ABO incompatability. G6PD deficiency. Spherocytosis.
Physiological. Breast milk jaundice Infection Haemolysis Bruising Polycythaemia Hypothyroid High GI obstruction
Management of jaundice
Phototherapy
- blue/green band converts unconjugated bilirubin to water soluble pigment
Exchange transfusion
- if dangerously high levels. Remove baby blood and replace with donor blood
Causes of infection in neonate
Group B Strep
- Pneumonia or meningitis
- Give prophylactic Abc intrapartum
Listeria monocytogenes
- from unpasteurised milk, soft cheese, undercooked poultry
- Bacteraemia with mild flu like illness
- Meconium staining of licquor
- Widespread rash, septicaemia
Conjunctivitis
- sticky eye on day 3 or 4
- Chlamydia, gonorrhoea,
- Can be staph or strep
Epidemiology of sudden infant death syndrome
Most common aged 2-4 months
Incidence is decreasing with Back to Sleep campaign
RFs
- Low birth weight and pre-term
- Increased in males
- Multiple births
- Increasing maternal parity
- Parental low income
- Poor or overcrowded housing
- Maternal age under 20
- Single unsupported mother
- Maternal smoking during pregnancy or in the same room post birth
- Sleeping prone
Prevention of SIDS
Back to Sleep Campaign
Lie infant on back
Feet to foot position
Do not smoke in same room
Avoid overheating
Baby should sleep in same room for first 6 months
Avoid sleeping with the infant e.g. sofa, chair
Investigations and management for SIDS
Detailed clinical exam
Remove any ET tubes and needles but retain venous lines
Retain child clothes, bedding and nappy for police
Nasopharyngeal aspirate Blood for toxicology, metabolic screen Chromosomal anomalies Blood cultures Urine LP for virology and culture
PM and coroners review Give parents opportunity to see and hold child Social review Case discussion Bereavement counselling
Causes of shock in child
Hypovolaemia
- Dehydration from gastroenteritis
- DKA
- Blood loss from trauma
Maldistribution of fluid
- anaphylaxis
- Septicaemia
Cardiogenic
- Arrhythmia
- Heart failure
Causes of respiratory distress in children
Croup Epiglottitis Foreign body Congenital malformations Trauma Asthma Bronchiolitis Pneumonia pneumothorax
Causes of drowsiness in children
Post-ictal Status epilepticus Meningitis Encephalitis DKA Hypoglycaemia Electrolyte disturbance Inborn metabolism error Head injury Drug/ poison ingestion Intracranial haemorrhage
Paediatric BLS
Open airway
- Infants: neutral position
- Children: sniffing position
5 rescue breaths
Check pulses
- < 1 year = brachial and femoral
- > 1 year = carotid and femoral
If no pulse or pulse <60 then chest compressions
15:1
Adrenaline every 3-5 minutes
10 micrograms per kg IV
Apparent life-threatening events
Combination of apnoea, colour change, alteration in muscle tone, choking
Most common in under 10 weeks
Most are brief with rapid recovery
Causes
- Infections (RSV, pertussis)
- Seizures
- Upper airway obstruction
- GORD
Clinical manifestations of Down’s syndrome
Round face, flat nasal bridge Upslanted palpebral fissures Epicanthic folds Brushfield spots in iris Small mouth, protruding tongue Small low set ears Short neck Flat occiput Single palmar crease Incurved 5th finger Hypotonia Congenital heart defects Duodenal atresia Hirschsprung's disease
Later medical problems in Down’s syndromes
Delayed motor milestones
Moderate-severe LD
Small stature
Increased susceptibility to infection
hearing impairment from secretory otitis media
Visual impairment - cataracts, squint, myopia
Increased risk of leukaemia and solid tumour
Hypothyroidism
Coeliac disease
Epilepsy
Alzheimer’s disease
Genetics of Down’s
TRISOMY 21
94% meiotic non-disjunction (increases with maternal edge)
Edward’s syndrome
TRISOMY 18 1 in 8000 Multiple severe abnormality Low birth weight Prominent occiput Small mouth and chin Short sternum Fixed overlapping fingers Rocker bottom feet Cardiac and renal malformations
Patau’s syndrome
TRIMSOMY 13 1 in 14,000 Structural defect in the brain Scalp defects Small eyes (microphthalmia) Cleft palate and lip Polydactyly Cardiac and renal malformations
Turner’s syndrome
45 XO 95% are spontaneously miscarried Often diagnosed on US - cystic hygroma and foetal neck oedema Lymphoedema of hands and feet Spoon shaped nails Short stature Neck webbing Wide carrying angle Widely spaced nipples Congenital heart defects Delayed puberty Infertile Hypothyroidism Renal anomalies Pigmented moles Recurrent otitis media
Klienfelter’s syndrome
47 XXY 1-2 per 1000 males Infertility Hypogonadism Small testes Pubertal development, may appear normal Gynaecomastia
Autosomal dominant conditions
Achondroplasia Ehler's Danlos syndrome Familial hypercholesterolaemia Huntington's disease Noonan's syndrome Otosclerosis Tuberous Sclerosis Marfan's syndrome Myotonic dystrophy Neurofibromatosis Osteogenesis imperfect Polyposis coli
Describe autosomal dominant inheritance
Chromosomes 1-22
Children of someone affected
50% affected
50% normal
Autosomal recessive conditions
Cystic fibrosis Congenital adrenal hyperplasia Galactosaemia Freidreich ataxia Glycogen storage disease Phenylketonuria Hurler syndrome Tay-Sachs disease Sickle cell disease Thalassaemia
X linked inheritance & diseases
Can be dominant or recessive
males affected, females usually healthy but carriers
- Colour blindness
- Duchenne’s and Becker’s muscular dystrophy
- Fragile X syndrome
- G6PD
- Haemophilia A and B
- Hunter’s syndrome
Fragile X syndrome
Moderate-severe LD Macrocephaly Macro-orchidism Long face Large everted ears Prominent mandible Broad forehead mitral valve prolapse Joint laxity and scoliosis Autism Hyperactivity
Imprinting
Normally in a gene - mothers and fathers acts equally
In imprinting, one is more functional that the other
Chromosome 15
- If mothers unfunctional: Angelman’s syndrome
- If fathers unfunctional: Prader-Willi syndrome
Prader-Willi Syndrome
Chromosome 15 - parental gene unfunctional
Hypotonia Neonatal feeding difficulties Failure to thrive Obesity in later childhood with hyperphagia Hypogonadism Developmental delay and LD
Angelman’s syndrome
Chromosome 15 - maternal gene non-functional
Severe intellectual and developmental disability
Sleep disturbance
Seizures and jerky movements (hand flapping)
Frequent laughter and smiling
William’s syndrome
Short stature
Transient neonatal hypercalcaemia
Congenital heart disease - aortic stenosis
Mild-moderate LD
Newborn screening
Hearing
Blood spot test
Newborn hearing screening
Within 4-5 weeks usually prior to discharge
1st test: Automated Oto-Acoustic Emission (AOAE)
- play sound in ear, try to detect echo response from baby’s cochlea
2nd test: Automated Auditory Brainstem Response (AABR)
- play sound, detect response from brain stem via electrodes. assesses integrity from inner ear
AABR if no clear response on AOAE or >48 hours in SCBU or NICU
Newborn Blood Spot Test
Blood spot/heel prick/Guthrie test
Ideally on day 5 (day 5-8)
Tests for:
- Phenylketonuria
- Cystic fibrosis
- Congenital hypothyroidism
- Maple syrup urine disease
- Sickle cell disease
- MCAD deficiency
- Homocysteinuria
- Glutaric aciduria type 1
- Isoraleric acidaemia
Phenylketonuria
Testing looks for total biopterin and dihydropteridine reducates
allows for early implementation of phenylalanine restricted diet
Early diagnosis and treatment decreases handicap
Inborn error of amino acid metabolism
Absent phenylalanine hydroxylase - important in formation of catecholamine’s, neurotransmitters and melanine
Musty or mousey odour
Developmental delay
Recurrent vomiting
Homocysteinuria
Rare inherited metabolic disorder Raised blood and urine concentration of homocysteine Autosomal recessive Normal at birth Complications in childhood Tall stature (Marfanoid habitus) Fine brittle hair High arched palate Pectus excavatum Limited joint mobility Dislocation of lens Increased risk of VTE,MI, osteoporosis, mitral valve prolapse
Maple syrup urine disease
1 in 185,000 Autosomal recessive Maple syrup odour in cerumen Poor feeding Vomiting Poor weight gain Lethargy Dystonia Seizures
Clinical features of foetal alcohol syndrome
Failure of growth
- Never catch up
Facial abnormalities
- Microcephaly
- Flat philtrum
- Thin upper lip
- Retrognathia, micrognathia
- Microphalamia
- Cleft palate/lip
- posterior rotation of ears
Neurodevelopement
- Low IQ, memory problems
- Hyperactivity, attention deficits
- Poor judgement
- Immature behaviour
- Speech and language delay
- Sucking and feeding problems
Also
- Congenital heart disease (ASD and VSD)
- Partial deafness
- Significant visual disability
Stages of growth
FOETAL
- fastest period of growth, accounting for 30% of eventual height
- Size at birth depends on size of mother and placental nutrient supply
- IGF-2, insulin and human placental lactogen control growth
INFANTILE
- growth dependent on adequate nutrition
- good health and normal thyroid function necessary
- rapid but decelerating growth rate
- inadequate weight gain = FTT
CHILDHOOD
- slow and steady
- role of pituitary growth hormone. GH is secreted to produce insulin life growth factor 1 - IGF-1
- profound unhappiness can decrease GH and causes psychological short stature
PUBERTY
- sex hormones (testosterone and estradiol) causes back lengthening and increased GH secretion
- Adds 15% to final height
Define short stature
Height below the 2nd centile (2SD below the mean)
Many will be normal, just short with short parents
The further under the centile, the high risk of pathological cause
Height will fall through centile lines
Can be plotted on height velocity chart
Calculating genetic height
Mothers height + fathers height /2
If female -7cm
If male +7cm
Aetiology of short stature
- Familial
- IUGR and extreme prematurity
- Constitutional delay of growth and puberty
- Hypothyroidism
- Growth hormone deficiency
- Corticosteroid excess, Cushing’s
- Nutritional / chronic illness
- Psychosocial deprivation
- Chromosomal disorders/syndromes
- Achondroplasia
Extreme short stature
- Laron syndrome
- Primordial dwarfism
- idiopathic
- SHOX gene abnormality
Constitutional delay of growth and puberty
Increased in males
Variation in normal puberty timings
Not pathological
Can be induced by dieting or excessive physical training
Long legs in comparison to back
Onset of puberty can be induced with androgens/oestrogens
Hypothyroidism causing short stature
Usually caused by autoimmune thyroiditis in childhood
Growth failure
Excessive weight gain
When treated = catch up, can limit final height
Congenital hypothyroidism is often diagnosed at birth and therefore does not cause short stature
Causes of growth hormone deficiency
Craniopharyngioma - bitemporal hemianopia, papilloedema, optic atrophy
- hypothalamic tumour
- head injury
- meningitis
- cranial irradiation
- Laron syndrome
Chromosomal syndromes causing short stature
Laron's syndrome Down's syndrome Noonan's syndrome Russell-Silver syndrome Turner's syndrome
Investigations for short stature
FBC U&Es LFTs TFTs ESR and CRP Urinalysis Karyotyping Bone age - radiograph of L hand and wrist If pathological short stature then delay in bone age
Growth hormone provocation tests
MRI scan if neurological symptoms
Management of short stature
Somatotropin
used in growth hormone deficiency
Stop when final height attained or adherence poor
Noonan’s syndrome
Autosomal dominant Congenital heart defects - pulmonary vascular stenosis Short stature Learning problems Pectus excavatum Impaired blood clotting Webbed neck Flat nose
Silver Russell Syndrome
Primordial dwarfism SGA Feeding problems Hypoglycaemia Excessive sweating Blue tinge to sclera Triangular face, small jaw, pointed chin Wide and late closing fontanelle Decreased subcut fat
Laron syndrome
Autosomal recessive Insensitivity to growth hormone Abnormally short stature Prominent forehead, depressed nasal bride, underdeveloped mandible Truncal obesity Micropenis in males
William’s syndrome
Deletion of sections of chromosome 7 Developmental disorder Broad forehead, short nose, full cheeks Elfin face Intellectual disability Short stature Aortic stenosis Hypercalcaemia
Advantages of breast feeding
Ideal nutrition for infants during first 6 months
Life saving in developing countries
Decreases GI infection risk
Decreased necrotising enterocolitis
Increased mother child bond
Decreased diabetes, HTN and obesity in later life
Disadvantages of breast feeding
Unknown volume intake
Transmission of infection
Transmission of drugs
Vit K deficiency as not in breast milk (but in formula)
Less flexibility - other family can’t help
Colostrum
Produced for first few days
Increased protein and immunoglobulin component
Decreased volume
First breast feed should take place as soon as possible after birth
Physiology of breast feeding
Baby roots and sucks
Tactile receptors in nipple activated
Hypothalamus sends efferent impulses to pituitary
Anterior pituitary produces PROLACTIN which stimulates milk production by cuboidal cells in acini of breast
Posterior pituitary produces OXYTOCIN to contract myoepithelial cells in alveoli into large ducts (let down reflex)
Prolactin = increased milk production Oxytoxin = contraction of breast
Describe nutritional requirements of the baby
Breast of formula feeding for first 12 months
Cow’s milk may be given from 1 year
Introduce solid foods after 6 months
Done gradually
If starting food before 6 months - avoid wheat, eggs and fish
No honey in under 1s due to infantile botulinism
Define failure to thrive
Suboptimal weight gain in children (infants and toddlers)
Below 5th percentile or fall across centiles
- Mild: fall across 2 centile lines
- Severe: fall across 3 centile lines
Hard to distinguish TT from a normal but small baby
They will be asymptomatic
Aetiology of failure to thrive
70% inorganic (under feeding/psychosocial)
30% organic (secondary to disease)
- Decreased intake (social/economic/education)
- Decreased ability
CNS: CP, tumour, suck/swallow reflex
GI; GORD, pyloric stenosis
Cleft palate
Micrognathia - Decreased absorption:
Lactose allergy, CF, IBD, Coeliac
Biliary atresia, cirrhosis
Obstruction: hernia, malrotation, intussusception
Neonatal: NEC, short bowel syndrome - Increased requirement
Storage disease, inborn error
CHD
CF, bronchopulmonary dysplasia
Hypo/hyperthyroid disease
Malignancy
Investigations in failure to thrive
FBC, ESR, CRP, U&Es Glucose TFTs Sweat chloride Coeliac - tissue transglutaminase
2nd line
- Lead levels
- Abdominal US
- CXR
- Head US
- ECG/ echo
Management of failure to thrive
Health visitor involvement 3 meals a day + snacks Increased energy density foods Regular meal times Praise when food eaten Never force feed a child
MDT: health visitor, paediatrician, dietician, social worker
Marasmus
Weight for height > 3SD
Wasted, wizened appearance
No oedema
Withdrawn and apathetic
Kwashorkor
Generalised oedema and severe wasting Flaky pain skin Hyperkeratosis Distended abdomen Hepatomegaly angular stomitis Diarrhoea, hypothermia, bradycardia, hypotension
Types of abuse
Physical Emotional Neglect Sexual Fabricated or induced illness
Risk factors for abuse
Child
- Failure to meet parental expectation e.g. wrong gender or disabled
- Resulted from forced, coercive or commercial sex
Parent
- Mental health problems
- Parental indifference, intolerance or over anxious
- Alcohol or drug use
Family
- Step parents
- Domestic violence
- Social isolation
- Young parental age
Environment
- Poverty, poor housing
Injuries more likely to indicate physical abuse
Fractures: in non-mobile child, rib fractures, multiple fractures, fractures of different ages, skull fractures
Bruises: shape of hand or object, on the neck (e.g. strangulation), Wrists and ankles, buttocks in under 2s
Burns: in non-mobile child, in shape of implement e.g. iron or cigarette, glove and stocking from forced immersion
Emotional abuse
Persistent emotional maltreatment resulting in severe adverse effects on child’s emotional development
Inappropriate expectations / over protection / made to feel worthless, unloved or inadequate
Presentation of emotional abuse
Hardest to identify
Babies – apathetic, delayed development
Toddlers: violent, apathetic, fearful
School age: wetting, soiling, non-attendance
Adolescents: self-harm, depression, aggressive
Neglect
Persistent failure to meet a child’s physical or psychological needs. Failure of:
Adequate food and clothing
Shelter
Protection from physical and emotional harm or danger
Inadequate supervision
Presentation of neglect
Consistently misses important medical appointment Lacks needed medical and dental care Dirty Inadequate clothing in cold weather Using alcohol or drugs Child mentions no one at home
Sexual abuse
Forcing or enticing a child to take part in sexual activity
Includes: physical contact (rape, oral sex), non-contact (watching sexual activities, looking at pornographic material, encouraging them to behave inappropriately
Presentation of sexual abuse
Child may tell someone STI with no cause Vaginal bleeding, discharge, itching Rectal bleeding Self harm, aggressive or sexualised behaviours
Fabricated or induced illness
Behaviour of parents (usually mother >80%) which causes harm to children
Verbal fabrication: parents invent signs and symptoms. Abuse is done through tests and treatments
Induction of illness:
- Suffocation of child presenting as acute life threatening event
- Administration of noxious substance or poison
- Excessive administration of normal substance e.g. salt
- Excessive or unnecessary use of medication
Only happens when a parent/guardian around
Effects of alcohol abuse on the child
Severe congential abnormalities
Imapired growth and leaning and behavioural impairment
Foetal alcohol syndrome
Effects of heroin abuse on the child
Withdrawal syndrome
Advise methadone
Decreased birth weight
Effects of cocaine abuse in the child
Powerful vasoconstrictor Increased miscarriage Increased placental abruption Premature labour Foetal death in utero
Effects of alcohol/drug misuse on child
Physical harm
- access to drugs or paraphernalia
- increased violence due to decreased inhibition
- Increased strangers in home
- Chemical dependence
Not meeting child's physical needs Inadequate supervision Disruption to education or poor school attendance Child assuming parental role Decreased boundaries and routine Frightening Emotional stresses - fear of abandonment/parents dying/not loving child Feeling responsible for parents drug use
Describe meconium
Black colour First stool GI cells Filled with bilirubin If not expelled quickly, increased risk of jaundice Should be expelled in <24 hours
Palpable posterior fontanelle indicates what?
hypothyroidism or Down’s syndrome
Describe presentation of metabolic conditions
If problem with fat/protein/carbohydrate metabolism
Presents after first 1-2 days
Have a good first feed
Then start to get unwell, minimal further feeds
Ill due to build up of toxic metabolites from failed metabolism
Fields of development
Gross motor
Vision and fine motor
Hearing, speech and language
Social, emotional and behavioural
How are developmental milestones judged?
Median age - when half of the population at that level
Limit age - 2SD above mean. Age at which it should have been achieved
If a baby is pre-term should be calculated from expected date of delivery to allow to catch up. Only up to 2 year.
Gross Motor Developmental milestones
6-8 weeks: raises head to 45 degrees when prone
6-8 months: sits without support. At 6m = round back, 8m = straight back (limit 9 months)
8-9 months: crawling
10 months: cruising around furniture
12 months: walking unsteady (limit 18m)
15 months: walks steadily
Vision and fine motor milestones
6 weeks: follows object by moving head (limit 3 months)
4 months: reaches for toys
4-6 months: palmar grasp
7 months: Transfers objects between hands
10 months: pincer grip (limit 12 months)
16-18 months: makes marks with crayons
18 months: 3 blocks 2 years: 6 blocks 2.5 years: 8 blocks 3 years: 3 block bridge 4 years: steps
2 years - line 3 years - circle 3.5 years - cross 4 years - square 5 years - triangle
Hearing, speech and language milestones
Newborn - startles to loud noise
3-4 months: vocalises alone or when spoken too. Coos and laughs
7 months: turns to soft sounds out of sight. Uses should indiscriminately
10 months: sounds used discriminately to parents
12 months: 2-3 words (other than mama and dada)
18 months: 6-10 words. Shows 2 parts of body.
20-24 months: uses 2+ words to make simple phrases
2.5-3 years: talks constantly in 3-4 word sentences
Social, emotional and behavioural normal milestones
6 weeks: smile
6-8 months: puts food in mouth
10-12 months: waves bye. peek a boo.
12 months: drinks from a cup 2 handed
18 months: self feeds with spoon
18-24 months: symbolic play
2 years: dry by day. pulls off some clothing
2.5-3 years: parallel play, starting interactive play. taking turns
Standardised testing of milestones
Screening
- schedule of growing skills
- Denver development screening test
Assessment
- Griffith’s/ Bailey Infant Development scales
Formal IQ testing
Define developmental delay
Slow acquisition of all skills (global delay) or one of specific delay particularly in relation to developmental problems in 0-5 years
Define learning difficulty
Used in relation to children of school age and may be cognitive, physical or both
Define impairment
Loss or abnormality of physiological function or anatomical structure
Define disability
Restriction or lack of ability due to impairment
Features suggestive of neurodevelopmental concerns
Positive FHx Antenatal screening positive Neonatal encephalopathy Birth asphyxia Dysmorphic features Pre-term infants Abnormal neurological behaviour Global delay
Conditions that cause abnormal development and learning difficulty
PRE NATAL
PRE-NATAL
- Genetic: Down’s, Fragile X
- Cerebral dysgenesis: microcephaly, absent corpus collosum, hydrocephalus
- Vascular: occlusions, haemorrhage
- Metabolic: hypothyroid, phenylketonuria
- Teratogens: alcohol, drugs
- Infection: rubella, CMV, toxoplasmosis, HIV
- Tuberosclerosis, neurofibromatosis
Conditions that cause abnormal development and learning difficulty
PERINATAL
Extreme prematurity
Birth asphyxia - hypoxic ischaemic encephalopathy
Metabolic - hypoglycaemia, hyperbilirubinaemia
Conditions that cause abnormal development and learning difficulty
POSTNATAL
Infection: meningitis, encephalitis
Anoxia: suffocation, near drowning, seizures
Trauma: head injury
Vascular: stroke
Investigations for developmental delay
Cytogenic
- chromosome karyotyping
- Fragile X analysis
Metabolic: TFTs, LFTs, U&Es, plasma amino acids
CK, blood lactate, ammonia
ABG
Urate, ferritin
Congenital infection screen Cranial US in newborn CT/MRI Skeletal survey - bone age EEG Nerve conduction studies hearing. vision.
Global developmental delay
All fields
Usually apparent in the first 2 years
Always investigate for cause
Gets clearer to define as child gets older
Abnormal motor development symptoms
Delay in acquisition of motor skills Balance problems Abnormal gait Asymmetry of hand use - hand dominance not acquired until 1-2 years Involuntary movements Loss of motor skills (rare)
usually presents between 3months-2years
Causes of abnormal motor development
Central motor deficit - cerebral palsy Congenital myopathy Primary muscle disease Spinal cord lesions - spina bifida Global developmental delay
Define cerebral palsy
Abnormality of movement and posture causing activity limitation attributed to non-progressive disturbances that occurred in developing foetal or infant brain
Often accompanied by distrubances in cognition, communication, perception, sensation or behavioural problems.
Causes of cerebral palsy
80% antenatal
- Vascular occlusion
- cortical migration disorders
- structural maldevelopment
- genetic syndromes
- congenital infections
10% hypoxic ischaemic injury during delivery
10% post natal
- meningitis/encephalitis
- encephalopathy
- head trauma
- hypoglycaemia
- hydrocephalus
- hyperbilirubinaemia
Presentation of cerebral plasy
Abnormal limb and/or trunk posture Abnormal tone in infancy Delayed motor milestones Feeding difficulties - slow feeding, gagging, vomiting Abnormal gait once walking Asymmetric hand function <12 months Primitive reflexes may persist
Types of cerebral palsy
Spastic - can be split into hemiplegia, quadriplegia or diplegia
Dyskinetic
Ataxic
Spastic CP
Damage to upper motor neurone limb tone increases (spasticity) Brisk reflexes, extensor plantars Tone is velocity dependent (faster movement = increased tone) Presents early
Spastic CP - hemiplegia
Arms > Legs
Unilateral
Face spared
presents at 4-12 months
Fisting of hand, flexed arm, pronated forearm
Then tiptoe walking
If large brain lesion may have hemianopia
Spastic CP - quadriplegia
All 4 limbs
Severe
Extensor posturing
Poro head control
Low central tone
Seizures, microcephaly, moderate-severe LD
May have history of hypoxic ischaemic injury
Spastic CP - diplegia
Legs >> arms All 4 limbs Walking abnormal Can appear normal arm movements Assocaited with pre-term births due to periventricular haemorrhage
Dyskinetic CP
Movements which are involuntary, uncontrolled, occasionally stereotypes Often more evident on movement - Muscle tone variable - primitive reflexes predominate - Can have: chorea, athetosis, dystonia - Intellect usually intact - Usually presents with floppiness and poor trunk control Movements appear ~ 1 year
Most commonly caused by hypoxic ischaemic brain injury
Ataxic CP
Hypotonic Most are genetic Early trunk and limb hypotonia Poor balance Delayed motor development Inco-ordinate movements Intention tremor Ataxic gait
Causes of speech and language delay
Hearing loss
Global developmental delay
Difficulty in speech production - cleft palate, CP
Environmental deprivation - lack of opportunity for social interaction
Normal variant / familial pattern
Speech and language disorders
Disorders in
- Language comprehension
- Language expression
- Phonation and speech production e.g. stammer (dysfluency), dysarthria, dyspraxia
- Pragmatics
- Social and communication disorders
Testing language development
Symbolic Toy Test - for early language development
Reynell test - for expressive/receptive language in pre-school children
Dyspraxia
Disorder of motor planning or execution
No findings in neurological exam
Disorder of higher cortical function
Problems with: - Hand writing - Dressing - Cutting up food - Poorly established laterality - Copying and drawing - Difficulty co-ordinating biting and chewing. Drooling common. Achieves normal gross motor milestones
Dyslexia
Disorder of reading skills disproportionate to IQ
Reading age > 2 years behind chronological age
Causes of sensorineural hearing impairment
Antenatal: congenital infection, pre-term, hyperbilirubinaemia, hypoxic ischaemic brain injury
Post-natal: meningitis, encephalitis, trauma, drugs, neurodegenerative disease
Sensorineural hearing loss in child
1 in 1000 May be profound Does not improve May progress Manage with amplification and cochlear implant if required
Conductive hearing loss
Causes: otitis media + effusion, Eustachian tube dysfunction (Down’s, cleft palate, mid facial hypoplasia), wax
Intermittent or resolves
Max 60dB hearing loss
Stabismus
Squint - misalignment of visual axes
- Refer after 3m to ophthalmology
- Usually caused by failure to develop binocular vision due to refractive errors
- Concomitant: common, refractive error. generally convergent squint eye
- paralytic: varies with gaze direction due to paralysis of motor nerves: SINISTER ? space occ lesion
Aetiology of visual impairment in child
Genetic - cataracts, albinism, retinal dystrophy, retinoblastoma
Antenatal: congenital infection, retinopathy of immaturity, hypoxic ischaemic encephalopathy, trauma, optic nerve hypoplasia
Postnatal - trauma, infection, juvenile idiopathic arthritis
Gross motor function classification
Level 1 - walks without limitations
Level 2 - walks with limitations
Level 3 - walks with handheld mobility device
Level 4 - self-mobility without limitations (can be powered mobility)
Level 5 - transported in manual wheelchair
Common medical problems in those with developmental delay
Hearing
Vision
Orthopaedic (fixed contractures, spasms, spinal deformity, osteoporosis, fractures)
GI - GORD, constipation, aspiration
GU - UTI, delay in continence, neuropathic bladder
Resp - infections, aspiration, chronic lung disease, sleep apnoea
Neuro - epilepsy, CP, microcephaly, hydrocephalus
Failure to thrive
Poor weight gain
Causes of vomiting in infants
GORD Feeding problems Infection (gastroenteritis, meningitis, UTI, pertussis, Otitis media) Dietary protein intolerances Obstruction - Pyloric stenosis - Atresia - Intussusception - Malrotation - Volvulus - Strangulated inguinal hernia - Hirschsprung's disease Inborn errors of metabolism Congenital adrenal hyperplasia Renal failure
Causes of vomiting in Pre-school children
Gastroenteritis infection Appendicitis Obstruction - Intussusception - Malrotation - Volvulus - Adhesions Raised ICP Coeliac disease Renal failure Testicular torsion Metabolism errors
Causes of vomiting in school age+ adolescents
Gastroenteritis Infection (sepsis, meningitis, pyelonephritis) Peptic ulcers H. pylori infection Appendicitis Migraine Raised ICP DKA Coeliac Alcohol/drugs Cyclical vomiting syndrome Bulimia, anorexia Pregnancy Testicular torsion
Red flags for vomiting
Bile stained Haematemesis Projectile vomiting in first few weeks Abdominal tenderness Abdominal distension hepatosplenomegaly Blood in stool Severe dehydration Bulging fontanelle FTT
What does bile stained vomit indicate?
Intestinal obstruction
Surgical emergency until proven otherwise
What does bulging fontanelle indicate?
Raised ICP
Define posseting
Small amounts of milk which accompany the return of swallowed air
GORD
Involuntary passage of gastric contents into oesophagus
Extremely common in infancy
Due to inappropriate relaxtion of LOS due to functional immaturity
Usually resolves by 1 year
More common in
- CP
- Pre-term infnats
- Post-op oesophageal atresia
Investigations for GORD
Usually just a clinical diagnosis
- 24 hour oesophageal pH monitoring to quantify degree of reflux
- 24 hour impedance monitoring
- Endoscopy and biopsy
Management of GORD
Parental reassurance Adding inert thickening agents to feed Position in 30 degrees prone after feeds Ranitidine/Omeprazole Consider cow's milk allergy Surgery only if unresponsive (Nissen fundoplication)
Pyloric stenosis
- Define
- Presentation
- Epidemiology
Hypertrophy of pyloric muscle causing gastric outlet obstruction.
Presents at 2-7 weeks
Increase in boys (4:1), first borns, maternal FHx
Vomiting increases in frequency and forcefulness, becomes projectile
Weight loss if delayed presentation
Hypochloraemic metabolic alkalosis
Diagnosis of pyloric stenosis
Give feed to calm the baby and then examine
- Gastric peristalsis may be seen as wave from L to R
- Palpable pyloric mass in RUQ
- US useful if diagnosis in doubt
Management of pyloric stenosis
Correct fluids and electrolytes
Pyloromyotomy - division of hypertrophied muscle
Can feed within 6 hours of Op
Discharged after 2 days
Infant colic
Paroxysmal, inconsolable crying or screaming
Drawing up of knees and passage of excessive flatus
40% of all babies in first few weeks, resolves by 4 months
Benign but frustrating
Give support and reassurance
May be due to milk protein allergy or GORD
Appendicitis
Most common cause of abdo pain requiring surgery
Uncommon in under 3s
Symptoms: anorexia, vomiting, central colicky abdominal pain
Signs: flushed face, low grade fever, abdo pain, increased on movement, tenderness at McBurneys point
Perforation is rapid as omentum less well developed
Appendectomy or IV ABx
Non-specific abdo pain and mesenteric adenitis
Abdo pain resolves in 24-48 hours
Pain less severe than appendicitis
Often accompanied by URTI and cervical lymphadenopathy
Can only be diagnosed if large mesenteric nodes notes on laparatomy
Intussusception
Invagination of proximal bowel into a distal segment
Most commonly ileum into caecum
Most common cause of obstruction after the neonatal period
Peaks at 3 months-2 years
Presentation of intussusception
Paroxysmal severe colicky pain and pallor
Draws up legs
Initially recovers between painful episodes then lethargic
May refuse feeds
May vomit, becomes bile stained
Sausage shaped mass in abdomen
Redcurrant jelly stool (blood stained mucus)
Abdominal` distension or shock
Investigations and management of intussusception
X-ray: distended small bowel, absence of gas pattern in distal colon
US can confirm diagnosis
Management
- Rectal air insufflation unless peritonitis present
- Surgery if that fails or peritonitis
Meckel diverticulum
Ileal remnant of vitello-intestinal duct which contains ectopic gastric mucosa or pancreatic tissue
Present in 2%
Asymptomatic in most
Severe rectal bleeding, neither fresh or melena
Can present as intussusception, volvulus or appendicitis.
Treat with surgical resection
Malrotation
During rotation of the small bowel in foetal life the mesentery is not fixed at the duodenojejunal flexure or ileocecal region.
Predisposed to volvulus
Ladd bands may cross the duodenum, contributing to bowel obstruction
Presents
- Obstruction with bilious vomiting
- obstruction with compromised blood supply
Surgery untwists the volvulus. Does not correct the Malrotation.
Remove appendix to avoid later confusion.
Define recurrent abdominal pain
Pain sufficient to interrupt normal activities
Lasts >3 months
10% of school age children
Causes of recurrent abdominal pain
Cause only found in 10%
- IBS. Constipation. Dyspepsia. Abdominal migraine. Gastritis. Peptic ulcer. IBD. Malrotation
- Dysmenorrhoea. Ovvairan cysts. PID
- Hepatitis, gallstones, pancreatitis
- UTI
- Bullying, abuse, stress
Abdominal migraine
Associated with abdominal pain and headaches.
In some abdominal symptoms predominate
Midline pain with vomiting
IBS
Altered GI motility and abnormal sensation of intra-abdominal events
Symptoms can occur post GI infection
Abdominal pain, often worse before or relieved by defaecation
Loose stools/constipation
Bloating
Tenesmus
Causes of gastroenteritis
Most commonly ROTAVIRUS (60% of <2s) Increased in early spring and winter - Adenovirus - Norovirus - Calcivirus - Coronavirus - Campylobacter - E.coli
Degrees of dehydration
No clinically detectable dehydration (<5% body weight)
Clinical dehydration (5-10%)
Shock (>10%)
Signs and symptoms of dehydration
Appears unwell or deteriorating Altered responsiveness, irritable, lethargic Decreased consciousness (shock) Pale or mottled skin (shock) Cold peripheries Sunken eyes Dry mucus membranes Tachycardia Tachypnoea Weak pulse Increased cap refill (shock) Decreased skin turgor Hypotension (shock)
Management of dehydration
CLINICAL DEHYDRATION Oral Rehydration Solution Often and small volumes Consider NG - If deteriorating step 2
SHOCK
- IV therapy
- Rapid 0.9% NaCl
- Consider ICU
- Then step 2
- IV therapy for rehydration. Replace deficit + maintenance
Monitor U&Es, creatinine, glucose
After: full strength milk. Reintroduce solid food. Diligent hand washing. No school for 48 hours.
Post-gastroenteritis syndrome
Introduction of normal diet can cause watery diarrhoea
Normally ORS for further 24 hours then reintroduce solids again.
Presentation of malabsorption
Abnormal stools
Failure to thrive
Specific nutrient deficiencies
Coeliac disease
Gliadin provokes immunological response in proximal small bowel.
1 in 3000
Presents as profound malabsorption aged 8 months - 2 years after introduction of gluten.
FTT and abdominal distension
Buttock wasting
Abnormal stools
Positive IgA tissue transglutaminase
Diagnosis on small bowel biopsy
Causes of nutrient malabsorption
Cholestatic liver disease or biliary atresia
Lymphatic leakage or obstruction
Short bowel syndrome
Loss of terminal ileum function (Crohn’s, resection)
Exocrine pancreatic dysfunction
- CF. Absent lipase, protease, amylase
Small intestine mucosal disease (Coeliac, lactase deficiency)
Acrodermatitis enteropathica
Due to zinc malabsorption
Erythematous rash and mouth and anus.
Red flags of constipation
Failure to pass meconium in first 24 hours (HIRSCHSPRUNG’S)
FTT/growth failure
Gross abdominal distension (Hirschprung’s)
Abnormal lower limb neurology
Spina bifida signs
Abnormal anorectal anatomy
Perianal bruising, fissures = sexual abuse
Long standing constipation
Rectum becomes over distended
Loss of sensation to poo
Involuntary soiling
Requiring long term laxative use
Hirschsprung’s disease
Absence of ganglion cells from myenteric and submucosal plexus of large bowel results in narrow contracted segment.
Abnormal bowel extends from rectum ending in normally innervated dilated colon
75% only affects rectum/sigmoid
10% whole colon
failure to pass meconium in first 24 hours
Later abdominal distension and bile stained vomiting
On DRE narrow segment and gush of fluid/stool/flatus on removal
Diagnosed by absence of ganglion cells and presence of ACHE + nerve trunks on suction rectal biopsy
Management: colostomy with later anastomoses.
Management of constipation
If faeces not palpable - encouragement and close supervision
If palpable
- Macrogol e.g. Movicol for 2 weeks
- If stools passed done
- If not then add stimulant laxative e.g. senna with or without lactulose
- If no success then consider enema or manual evacuation under GA
After - balanced diet, sufficient fluids, maintenance laxatives
Epidemiology of UTI
3-7% of girls <6
1-2 % of boys <6
12-30% have recurrence within 1 year
Up to 50% have structural abnormality
Presentation of UTI in infant
Fever Vomiting Lethargy FTT/ poor feeding Jaundice Septicaemia Offensive urine Febrile convulsion
Presentation of UTI in children
Dysuria Frequency Abdo/loin pain Fever/rigors Lethargy Anorexia D&V Haematuria Offensive cloudy urine Febrile convulsions Recurrence of enuresis
Collecting urine in children
Clean catch - waiting clean pot when nappy removed *recommended* Adhesive plastic bag on cleaned perineum Urethral catheter if urgent Suprapubic aspiration - rarely done In older children MSU
In UTI - dipstick findings and when to treat
Positive leukocytes and nitrites = regard as UTI and treat
Negative leukocytes, positive nitrites = start Abx, diagnosis depends on urine culture
Positive leukocyte, negative nitrites = only Abx if clinical UTI
If both negative - UTI unlikely.
Aetiology of UTI
- E.coli
- Klebsiella
- Proteus (increased in boys)
- Pseudomonas
- Strep faecalis
Factors contributing to UTI
Incomplete bladder emptying
- Infrequent voiding
- Vulvitis
- Obstruction from constipation
- Neuropathic bladder
- Vesicoureteral reflex
Vesicoureteric reflux
Developmental abnormality of vesicoureteric junctions.
Ureters are displaced laterally and enter the bladder directly rather than at an angle
Investigations for UTI
Some debate over benefit of investigating
Investigate atypical or recurrent UTI
Atypical:
- Seriously ill/ sepsis
- Poor urine flow
- Abdominal or bladder mass
- Raised CK
- Failure to respond to Abx in 48 hours
US to detect structural abnormalities
Further investigations depends on US findings
Management of UTI
If under 3 months - refer to hospital for IV Abx
If over 3 months - oral Abx for 7-10 days
If only LUTS then 3 days oral
High fluid intake Regular voiding Ensure complete emptying Prevent or treat constipation Good perineal hygiene Consider circumcision
Define enuresis
Lack of bladder control
Primary - lack of control to be continent
Secondary - loss of previously achieved enuresis
Aetiology of primary daytime enuresis
Lack of attention to bladder sensation - developmental or psychogenic Too preoccupied to respond Detrusor instability Bladder neck weakness Neuropathic bladder UTI Constipation Ectopic ureter
Examination/investigation in enuresis
Test perineal sensation - S4/5 Urine sample - dip, microscopy and culture US may show bladder pathology Urodynamic studies may be required Spine X-ray or MRI for defects
Management of enuresis
Once neurological cause excluded - star charts, bladder training, pelvic floor exercises
Treat constipation
Last resort - anticholinergic drugs (oxybutynin)
Causes of secondary enuresis
Emotional upset most common
UTI
Polyuria from osmotic diuresis (diabetes, CKD)
Test osmolality of urine
Management of nocturnal enuresis
Straightforward but pain staking
Treatment is rare in under 6s
Explain to parent and child than problem is beyond conscious control
Stop punishment
Star chart for each dry night
Enuresis alarm - ideally child should get up when alarm indicates wet pants
Desmopressin - short term relief (sleepovers, holidays) - synthetic analogue of ADH
Epidemiology of nocturnal enuresis
6% of 5 years olds 3% of 10year olds
Increased in boys (2:1)
Most are psychologically normal - child needs to be free from stress
Define encopresis
Voluntary or involuntary passage of faeces, usually into clothing, after the age at which bowel control is usually achieved (any defaecation not in toilet)
No known cause
Bowel control normally achived by age of 3
Soiling at 4 or older is abnormal
Epidemiology of encopresis
1% of 5 year olds
Increased in boys
Causes of encopresis
Bowel control never established - disorganised family, understaffed institution, mental retardation
Emotion causes -
- Regressive soiling due to upsetting event
- Aggressive soiling - poor relationships between sibling. Rebellious act.
Physical causes
- Faecal impaction
- Hirschsprung’s disease
management of encopresis
Assess possible cause
Treat faecal retention
Give adequate toilet training
Emotional support
Regressive usually settles with emotional problems. Aggressive more troublesome.
Causes of proteinuria
Orthostatic proteinuria (only proteinuria when child upright) Glomerular abnormalities - Minimal change disease - Glomerulonephritis - Abnormal GBM Raised glomerular filtration pressure Decreased renal mass Hypertension Tubular proteinuria
Nephrotic syndrome
Heavy proteinuria
Hypoalbuminaemia
Oedema
Investigations in nephrotic syndrome
Urine protein on dipstick FBC and ESR U&Es and creatinine Complement leves C3 and C4 Antistreptolysin O or anti-DNAase B titres Urine microscopy and culture Urine sodium concentration Hep B and C screen
Steroid sensitive nephrotic syndrome
85-90% of nephrotic syndrome Do not progress to renal failure Increased in boys Increased in Asians Often precipitated by respiratory infections
No macroscopic haematuria, normal BP, complement levels and renal function,
Most commonly minimal change disease
Management of nephrotic syndrome
Oral corticosteroids 60mg/m2
After 4 weeks decrease dose to 40mg/m2 on alternate days for 4 weeks
If not responding - renal biopsy
Biopsy of minimal change disease
Normal light microscopy
Fusion of podocytes on electron microscopy
Complications of nephrotic syndrome
Hypovolaemia - treat with IV albumin
Thrombosis - hypercoagulable state
Infection
1/3 resolve. 1/3 frequent relapses (steroid dependent). 1/3 infrequent relapses
Steroids resistant nephrotic syndrome
CAUSES
Refer to paeds nephrologist
- Focal segmental glomerulosclerosis
- Membranoproliferative GN (mesangiocapillary GN)
- Membranous nephropathy
Focal segmental glomerulosclerosis
Most common steroid resisntat nephrotic syndrome
Familial or idiopathic
30% cause end stage renal failure in 5 years
20% respond to cyclophosphamide/ciclolsporin/tacrolimus
Recurrence post transplant is common
Membranoproliferative glomerulonephritis
Also called mesangiocapillary GN
Increased in older children
Haematuria and low complement present
Decreasing renal function over many years
Membranous nephropathy
Associated with Hep B
May precede SLE
Most remit spontaneously in 5 years
Congenital nephrotic syndrome
Presents in first 3 months Rare Autosomal recessive Increased in Finnish High mortality Albuminuria is so severe that unilateral nephrectomy may be required to control it.
Appearances of haematuria
Glomerular haematuria - brown urine, deformed red cells and casts +/- proteinuria
LUT haematuria = red urine, beginning or end of urinary stream. No proteinuria
Causes of Haematuria
Non glomerular
- Infection
- Trauma
- Stones
- Tumours
- Sickle cell disease
- Bleeding disorders
- Renal vein thrombosis
- Hypercalciuria
Glomerular
- Acute glomeruloneprhtisi (usually with proteinuria)
- Chronic glomerulonephritis (usually with proteinuria)
- IgA nephropathy
- Familial nephritis (Alport’s)
- Thin basement membrane
Investigations in haematuria
Urine microscopy and culture
Protein and calcium excretion
Kidney and urinary tract US
U&Es, creatinine, calcium, phosphate, albumin
FBC, platelets, clotting screen, sickle cell screen
If suggestive of glomerular haematuria
- ESR. Complement levels. Anti-DNA antibodies
- Throat swab.
- Abtistreptolysin O / anti-DNAase B titres
- Hep B and C screen
- Renal biopsy if indicated
Acute nephritis
Hypertension
Haematuria
Oedema
Decreased urine output and volume overload
Causes of nephritic syndrome
Post infections (streptococcal) Vasculitis - Henoch-Schonlein putpura - SLE - Wegner's granulomatosis - Polyarteritis nodosa IgA nephropathy Mesangiocapillary GN Goodpasture's syndrome
Post-streptococcal glomerulonephritis
Following strep sore throat or skin infection Raised anti-DNAase B titres Low C3 complement Long term prognosis good ASO positive
Features of Henoch-Schonlein purpura
Characteristic skin rash
- Symmetrical, over buttocks and extensor limb surfaces
- Trunk spared
- Urticarial, rapidly becoming maculopapular and purpuric
- palpable
Arthralgia
Periarticular oedema
Adnominal pain - colicky. Haematemesis or malena
Glomerulonephritis
Increased in boys aged 3-10 years
Often preceded by URTI
Alport’s disease
X linked recessive
Haematuria
Progresses to end stage renal failure by early adult life
Associated with deafness and ocular defects
Pathophysiology of meningitis
Infection of meninges usually follows bacteraemia
Much of the damage is caused by the host response
Release of inflammatory mediators and leukocytes causes endothelial damage
Causes cerebral oedema. Raised ICP, decreased cerebral blood flow
Inflammation causes vasculopathy and cerebral cortical infarction
Fibrin deposits can block resorption of CSF causing hydrocephalus
Organisms causing meningitis in newborns
Group B streptococcus
E. Coli and other coliforms
Listeria monocytogenes
Organisms causing meningitis in 1 months - 6 years
Neisseria meningitides
Streptococcus pneumonia
Haemophilus influenza (not common beyond 6 years)
Presentation of meningitis (symptoms)
Fever Headache Photophobia Neck stiffness Irritable Reduced consciousness Lethartgy Poor feeding Seizures Vomiting Hypotonia
Signs of meningitis
Fever Purpuric rash neck stiffness (not always in infants) Bulging fontanelle Opistghotonus - arching back \+ Brudzinski's and Kernig's sign Signs of shock Focal neurology Papilloedema (rare)
Investigations for meningitis
FBC (raised WCC and platelets)
U&Es
LFTs
Raised CRP
Blood cultures
LP for red cells, white cells, glucose, culture and microscopy
Blood/urine/CSF for rapid antigen testing and PCR
MRI
Brudzinski’s sign
Lay supine
Flexion of neck causes flexion of the legs
Kernig’s sign
Lay supine with hips and knees flexed
On straightening of legs - pain
CSF changes in bacterial meningitis
Purulent CSF
Raised protein
Low glucose
Raised WCC
CSF changes in viral meningitis
Clear CSF
Normal or raised protein
Normal or low glucose
Raised lymphocytes
CSF changes in TB meningitis
Turbid/Clear or viscous CSF
Mildly raised lymphocytes
Very raised protein
Very low glucose
CSF changes in encephalitis
Clear CSF
Normal or raised protein
Normal or low glucose
Raised lymphocytes
Management of meningitis
No delay in IV ABx and supportive therapy
ABx depend on pathogen found
Start with 3rd gen cephalosporin - cefotaxime or ceftriaxone
Dexamethasone to decrease complications
Complications of meningitis
Hearing loss
Local vasculitis - CN palsies or other focal lesions
Local cerebral infection - epilepsy
Subdural effusion - particularly in H. influenzae or pneumococcal. Most resolve spontaneously
Hydrocephalus
Cerebral abscess
Causes of viral meningitis
2/3 are viral Enteroviruses EBV Adenovirus Mumps
Less severe, makes full recovery
If fail to respond to treatment or supportive therapy consider atypical pathogens
- Mycoplasma or Borelia burgdorferi (lyme disease)
Encephalitis
Inflammation of brain substance
Meninges can also be affected
Can be caused by
- Direct invasion of cerebrum by neurotoxic virus e.g. herpes simplex
- Delayed brain swelling following disordered immunological response (post-infectious encephalopathy from chicken pox)
- Slow virus infection (HIV)
Causes of encephalitis
Enteroviruses Respiratory viruses Herpes viruses (HSV, varicella, HHV6) Mycoplasma Boreglia burgdorferi Rocky mountain spotted fver
Herpes simplex virus is rare but has devastating consequences
Presentation of encephalitis
As meningitis - manage as meningitis until proven otherwise
Fever Headache Photophobia Neck stiffness Irritable Reduced consciousness Lethartgy Poor feeding Seizures Vomiting Hypotonia
Management of encephalitis
High dose IV aciclovir
HSV encephalitis
Destructive infection
EEG and CT/MRI may show focal changes particularly in temporal lobes
3 weeks of acyclovir required
Untreated mortality rate = 70%
Survivors often have severe neurological problems
Define fever
Temperature over 37.5 degrees
How to measure fever
In under 4 weeks - electronic thermometer in axilla
Over 4 weeks as above or tympanic infrared thermometer
Fever & age of child
Under 3 months - often bacterial
Over 3 months - more likely to be viral
RFs for infection
Illness of other family members Prevalent illnesses in community Unimmunised recent travel abroad Contact with animals - brucellosis Immunodeficient
Red flags for child with fever
Maculopapular non blanching rash Irritable/reduced consciousness Over 38 degrees if <3m, over 39 if >3m Bulging fontanelle, neck stiffness, seizures, focal neurology Bile stained vomiting Significant respiratory distress Severe dehydration or shock
Septic screen
Blood cultures
FBC
CRP
Urine sample
Consider
- CXR
- LP
- Rapid antigen screen on blood/urine/CSF
- Meneningococcal and pneumococcal PCR on blood/CSF
Causes of fever & presentation
Meningitis Seizures - meningitis, encephalitis Otitis media Tonsillitis Epiglottitis, viral croup - stridor URTI Appendicitis, pyelonephritis, hepatitis - abdo pain Gastroenteritis - diarrhoea Septicaemia - shock Septic arthritis
Causes of prolonged fever
Bacterial infection - endocarditis Kawasaki disease Drug reaction Malignant disease Connective tissue disorder
Toxic shock syndrome
Caused by toxin producing Staph aureus and Group A strep Characterised by: - Fever > 39 - Hypotension - Diffuse erythematous macular rash
1-2 weeks later - desquamation of fingers and toes.
Toxin causes organ dysfunction: mucositis, D&V, renal and liver impairment, altered consciousness
need to surgical debride areas of infection + 3rd cephalosporin + clindamycin
Necrotising fascitis
Severe subcut infection involving skin, fascia and muscle
Enlarges rapidly, leaving poorly perfused areas of necrotic tissue
Severe pain and systemic illness requiring ITU
Surgical debridement necessary + IV abx`
Caused by Staph Aureus or group A strep
Impetigo
High contagious skin infection with staph or strep
No school until resolved
Weepy red honey coloured crush
Increased if pre-existing skin disease
Start as erythematous macules then vesicular/pustular then secretes the honey coloured exudate.
Lesions common on hands, face and neck
Topical antibiotics
Cuases of maculopapular rash + fever
Human herpes virus 6&7 Enteroviral rash Parovirus (slapped cheek) measles rubella scarlet fever (group A strep) erythema marginatum (rheumatic fever) Salmonella typhi (rose coloured spots_ Lyme disease Kawasaki disease Juvenile idiopathic arthritis
Causes of vescicular/pustular rash + fever
Varicella zoster Herpes simplex Coxsackie (hand foot and mouth) Impetigo Boils Toxic epidermal necrolysis Erythema multiforme Steven-Johnson's syndrome
Causes of petechial purpuric rash + fever
Meningitis Infective endocarditis Enterovirus Henoch-Schonlein purpura Vasculitis Malaria Thrombocytopaenia
Herpes viruses
HSV 1 HSV 2 - Herpes simplex 1 and 2. Responsible for cold sores and genital Varicella Zoster CMV EBV Human herpes virus 6, 7 and 8 HHV8 is associated with Kaposi's sarcoma
Hallmark
1. Primary infection
2, Latency and long term persistence
3. Reactivation
Herpes simplex 1 & 2
Wide variety of presentations
Treat with acyclovir
Can by asymptomatic
Can cause:
- Gingivostomatitis - most common in children, 10mont-3years. vesicular lesions on lips, gums, tongue and soft palate. Painful ulceration
- Eczema herpeticum - herpes infection + eczema
- Herpetic whitlow
Chicken pox
Primary infection with varicella zoster
200-500 lesions on head and trunk then progresses to limbs
Appears as crops of papules, vesicles with surrounding erythema and pustules for up to 1 week
lesions may occur on palate.
Can causes permanent depigmentation from scratching
If new lesions after 10 days = defective immunity
Complications:
- Staph/strep infection
- Encephalitis
- Purpura fulminans - large areas of skin necrosis
Supportive treatment unless immunocompromised then IV acyclovir
EBV infection
Causes infectious mononucleosis, Burkitt's lymphoma or associated with nasopharyngeal carcinoma - Fever - Malaise - Tonsillopharyngitis - Lymphadenopathy - Splenomegaly (50%) hepatomegaly (10%) - Maculopapular rash Symptoms persist for 1-3 months ` Diagnosed with atypical lymphocytes, Positive monospot and IgM and IgG to EBV
CMV infection
Transmitted in saliva, genital secretions or breast milk Can cause infectious mononucleosis symptoms can cause - retinitis - pneumonitis - bone marrow failure - encephalitis - hepatitis - colitis - oesophagitis
Human Herepes virus 6 and 7
Most children are infected by age of 2 from family members
Can cause exanthem subitum - roseola infantum
High fever and malaise for few days followed by macular rash as fever wains
Parvovirus B19
Slapped cheek
Causes erythema infectiosum or 5th disease
- most common
- fever, malaise, headache, myalgia
- followed by slapped cheek rash on face
- then maculopapular rash “lace like rash” on trunk and limbs
outbreaks in spring
Infects erythroblastoid red cell precursors in bone marrow
Can cause aplastic crisis - in children with chronic haemolytic anaemias
Maternal transmission can cause foetal hydrops
Enteroviruses
Includes coxsackie, echovirus, poliovirus
Transmission if faecal oral
90% are asymptomatic
Hand, foot and mouth disease - painful vesicular lesions on hands, feet or mouth. Self resolving
Herpangia - vesicular and ulcerated lesions on soft palate and uvula.
Meningitis/encephalitis
Bornholme disease/ Pleurodynia = fever, pleuritic chest pain and muscle tenderness
Measles
Rash
- Spreads downwards from behind ears to whole body
- From discrete maculopapular to confluent and blotchy
- May desquamate in 2nd week
Cough
Conjunctivitis and cold symptoms
Koplik’s pots - white spots on buccal mucosa
Complications
- Encephalitis (mortality 15%0
- Subacute sclerosing panencephalitis - 7 years post infection
Treatment symptomatic
Mumps
Spread via droplet infection.
Infection from parotid gland before dissemination
Fever, malaise, parotitis (earache and pain on eating)
Fever settles in 3-4 days
Raised amylase
Mild and self-limiting
Hearing loss can occur (transient)
Rubella
German measles
- Causes damage to foetus
- Prodrome with mild low grade fever
- Maculopapular rash from face down
- Fades in 3-5 days
- Not itchy (in children)
- Prominent lymphadenopathy (particular post-auricular)
No treatment
Kawasaki disease
Systemic vasculitis
6 months - 4 years
Increased in Japanese and Blacks
High fever, difficult to control for > 5 days
Need 4 of 5 other features
- Conjunctival infection
- Mucus membrane changes
- cervical lymphadenopathy
- polymorphous rash
- peeling of skin on fingers and toes
Can cause coronary aneurysms
Mortality 1-2%
Pathogens causing respiratory infections
80-90% are VIRAL
- Respiratory syncytial virus
- Rhinovirus
- Parainfluenza
- Influenza
- Metapneumovirus
- Adenovirus
Bacterial
- Streptococcus pneumoniae
- H. influenzae
- morexella catarrhalis
- Bordetella pertussis
- mycoplasma pneumoniae
RF for respiratory infection
Parental smoking Low socioeconomic status Decreased nutrition Underlying lung disease Congenital heart disease Boys Immunodeficiency
Classification of respiraotyr infections
URTI laryngeal/tracheal infection Bronchitis Bronchiliolitis Pneumonia
URTI
Includes
- Common cold (coryza)
- Sore throat (pharyngitis, tonsillitis)
- Acute otitis media
- Sinusitis
presentation of URTI
Nasal discharge and blockage Fever Painful throat Earache Cough Difficulty feeding febrile convulsions Acute exacerbation of asthma
Causes of coryza
Most common infection
- rhinovirus
Coronavirus
Respiratory syncytial virus
Causes of pharyngitis
Sore throat Adenovirus Enterovirus Rhinovirus In older child Group A beta haemolytic strep
Causes of tonsillitis
Group A haemolytic strep
EBV
Symptoms and management of tonsillitis
Sore throat Headache Apathy Abdo pain Cervical lymphadenopathy White exudate
Treat with penicillin (erythromycin)
Avoid amoxicillin as maculopapular rash if EBV infection
Otitis media
Increased at 6-12 months
Tympanic membrane = red and bulging and loss of light reflection
Caused by RSV and rhinovirus
OR pneumococcus, H.influenzae or M. catharalis
Regualr analgesia
If ABx = amoxicillin
When is tonsillectomy indicated
Recurrent severe tonsillitis
Peritonsilar abscess
Obstructive sleep apnoea
Causes of upper airways obstruction / STRIDOR
* viral laryngotracheobronchitis * - "Croup" Epiglottiits Bacterial tracheitis Inhalation of smoke and hot air Trauma to throat Foreign body Hypocalcaemia Measles Infectious mononucleosis Diphtheria
Characteristic features of laryngeal and tracheal infections
Stridor
Hoarseness
Barking cough
Dyspnoea
Can rapidly be life threatening in young chgildren
Croup
Laryngotracheobronchitis
Mucosal infections & increased secretion
Can cause critical narrowing if subglottic
95% viral - parainfluenza, RSV, influenza
6 months - 6 years
Barking cough, hoarseness, stridor, fever
Symptoms worse at night
Low threshold for admission in < 1 year due to narrow airway
If severe mange with nebulised adrenaline and ITU
Acute epiglottitis
Life threatening emergency Caused by H. influenza B Intense swelling of epiglottis 1-6 years Acute onset Toxic looking child Saliva drooling Soft inspiratory stridoe Child sitting immobile, upright with mouth open Admit to ICU ASAP, RSI under GA IV abx
Whooping cough
Bordetella pertussis
Bronchitis
highly contagious
Catarrhal phase - week of coryza (cold symptoms)
Characteristic - INSPIRATORY WHOOP
Paroxysmal cough
Spasms of cough - worse a night
Can cause vomiting, conjunctival haemorrhages, epistaxis
3-6 weeks
Symptoms decrease slowly
Complications - pneumonia, bronchiectasis
Bronchiolitis
Rare after age of 1
90% aged 1-9 months
80% due to RSV (respiratory syncytial virus)
Others: metapneumovirus, parainfluenza, rhinovirus, adenovirus, influenza
Coryzal symptoms precede a dry cough and SOB
Feeding difficulty due to SOB
Signs and symptoms of bronchiolitis
Sharp dry cough Tachypnoea Subcoastal and intercostal recession Hyperinflation of chest - prominent sternum, downwards displaced liver high pitched wheeze exp>ins Tachycardia Fine end expiratory crackles Cyanosis Pallor
Features of croup
Onset over days Preceding coryza Cough severe and barking Able to drink No drooling of saliva Appears unwell Fever <38.5 Harsh rasping stridor Hoarse voice
Features of epiglottiits
Onset over hours No preceding coryza Absent or slight cough Not able to drink Drooling saliva Toxic looking child Fever > 38.5 Soft whispering stridor Reluctant to speak
Investigations in URTI
PCR of nasopharyngeal secretions
CXR unnecessary if straightforward
CXR - hyperinflation of lungs and focal atelectasis
Causes of pneumonia in childhood
Newborn - group B strep. gram negative enterococci
Infants - RSV, Step pneumoniae, H. influenza, Bordella pertussis, chlamydia trachomatis
Over 5s - mycoplasma pneumoniae, strep pneumoniae, chlamydia pneumoniae
Symptoms and signs of pneumonia
Fever SOB Usually preceded by URTI Cough Lethargy Unwell Tachypnoea Nasal flaring Chest in drawing End expiratory crackles
Management of pneumonia
Most managed at home Admit if sats < 93%, severe raised RR, SOB, grunting, apnoea, not feeding Oxygen for hypoxia Analgesia if required ABx IV fluids for dehydration
Malaris
From female anopheles mosquito - plasmodium falciparum
700,000 deaths per year
Fever, diarrhoea, vomiting, flu like symptoms, jaundice, anaemia, thrombocytopaenia
Typical onset 7-10 days after inoculation
Children are susceptible to severe anaemia and cerebral malaria
Quinine required in most cases
Typhoid
Worsening fever, headaches, cough, abdominal pain, anorexia, malaise and myalgia
Salmonella typhi
GI symptoms may not appear until 2nd week
Rose colour spots on trunk
Complications: GI perforation, myocarditis, hepatitis, nephritis
Dengue fever
Viral infection transmitted by mosquitos
Fine erythematous rash, myalgia, arthralgia, high fever
2y rash with desquamation after
Dengue haemorrhagic fever when previously infected child reinfected with different strain: severe capillary leak, hypotension
most recover
Common allergies in children
Food allergy Eczema Allergic rhinitis and conjunctivitis Asthma Urticaria Insect sting hypersensitivity Anaphylaxis
Define hypersensitivity
Objectively reproducible symptoms or signs following exposure to defined stimulus at a dose which is tolerated in normal people
Define allergy
Hypersensitivity reaction initiated by specific immunological mechanism. Can be IgE mediated (peanut allergy) or non IgE mediated (Coeliac)
Define atopy
Personal or familial tendency to produce IgE antibodies to potential allergens, usually proteins. Strongly associated with asthma, allergic rhinitis and conjunctivitis, eczema and food allergy
Pathophysiology of atopy
Allergens bind to IgE sensitised mast cells and basophils
Histamine is released from intracellular granules
mast cells are concentrated in skin, lungs and GI
Histamine causes:
- Local vasodilation (erythema)
- Increased capillary permeability (wheal)
- Vasodilation of surrounding arterioles (flare)
- Stimulation of sensory nerves (itching)
- Smooth muscle contraction (bronchoconstriction and increased GI motility)
- Increased nasal, salivary and gland secretions
As histamine is a potent vasodilator, can cause peripheral blood pooling, hypotension and circulatory shock
Allergic march
Children develop allergic disorders at different ages
- Eczema and food allergy in infancy
- Allergic rhinitis and conjunctivitis in preschool/primary school
- hayfever often precedes asthma
Epidemiology of food allergies
5% of children
3% of adults
Increasing incidence ? processed diet ? hygiene hypothesis
2% of infants have cow’s milk protein allergy
Symptoms of IgE mediated food allergy
Pruritus Erythema Diarrhoea Abdominal pain Acute urticaria Acute angio-oedema (usually facial) Oral itching Nausea and vomiting Nasal itching, rhinorrhoea, sneeze Allergic conjunctivitis Cough, SOB, wheeze, asthma Feeling of impending doom CV collapse
Symptoms of non-IgE mediated food allergy
Pruritus Erythema Diarrhoea Abdominal pain Atopic eczema GORD Infantile colic Stools loose/frequent/blood/mucus Constipation Perianal redness Pallor and tiredness FTT Food aversion or avoidance
Investigations for food allergy
Food diary
Physician supervised oral food challenge, skin prick, food specific IgE tests
Describe skin prick testing
Drop of food placed on forearm
Needle pricks skin through food
Saline for comparison
Reaction read after 15-20 minutes
Common food allergen
Milk Eggs Fish and seafood peanuts Sesame Tree nuts Soybeans Wheat Kiwi
Investigations for non-IgE mediated food allergy
2-6 weeks trial elimination and reintroduce after to determine symptoms
Food protein induced enterocolitis
Presents with projectile vomiting, diarrhoea and FTT for first few months.
Usually due to Cow’s milk and soy protein formulas
non-IgE mediated
Eosinophilic oesophagitis and gastroenteritis
Nausea, abdominal pain, reflux, FTT
Does not respond to antacids.
Non-IgE mediated food allergy
Management of food allergies
Food avoidance - particularly if anaphylactic
Dietician referral - reading food labels, preventing deficiencies
Antihistamines - for mild symptoms e.g. urticaria, itching
Adrenaline - if resp symptoms or anaphylaxis
Medical emergency bracelets
Injection immunotherapy (desensitisation) only used for pollen and venom
Non-immunologically mediated food intolerance causes
Metabolic: lactase deficiency
Pharmacological: preservatives, artificial food colours, sweeteners, alcohol, caffeine
Toxic - contaminated foods
Psychological: food aversion
Avoid trigger foods
Non-immunologically mediated food intolerance symptoms
Headache Fatigue GI upset Urticaria Behavioural problems
Define anaphylaxis
Severe life threatening generalised or systemic hypersensitivity reaction
- Sudden onset and rapid progression of symptoms AND
- life threatening A/B/C problem
Aetiology of anaphylaxis
Occurs when allergen reacts with IgE antibodies on mast cells in type 1 hypersensitivity reaction
Rapid release of histamine
- Peanuts, pulses, tree nuts (brazil, almond, hazelnut), fish, shellfish, eggs, sesame, milk
- bee/wasp sting
- antibiotics, NSAIDs, contrast media, anaesthetic drugs
presentation of anaphylaxis
Initially skin symptoms: generalised itching, urticaria, erythema, rhinitis, conjunctivitis, angio-oedema Dyspnoea Stridor Wheeze Palpitations Tachycardia nausea and vomiting Abdominal pain LOC
Management of anaphylaxis
ABCDE
High flow O2 through non-rebreathe
Lie flat
Raise legs
Adrenaline IM 0.5ml of 1:1000 (500 micrograms)
Repeat after 5 minutes if no improvement
May benefit from IV adrenaline (anaesthetist only)
Establish airway (often intubation)
IV fluid challenge - 1L in 10 minutes if hypotensive
If further deterioration: salbutamol, ipratropium, aminophylline, mag sulphate)
After initial resus
- Chlorphenamine 10mg
- Hydrocortisone 200mg
Lower doses for children - age appropriate
Investigations for anaphylaxis
Serum mast cell tryptase can be measured for diagnosis if required.
Peak at 1 hour, Do at emergency and then 1-2 hours later
Follow up management of anaphylaxis
Observe for 6-12 hours If under 16 admit to paediatric ward - Organise allergen testing - Organise epi pen and training - Written management plan - Encourage emergency medical bracelet
Types of allergic rhinitis
Seasonal allergic rhinitis (hayfever): occurs at certain times of year. Tress grass or pollen
Perennial rhinitis - persistent, occurs year round. dust mites, domestic pets
Occupational: flour, wood dust, latex gloves
Pathogenesis of allergic rhinitis
IgE mediated inflammation of nasal mucosa due to histamine release
- Acute phase (mins) - sneezing, increased nasal secretion
- Late phase (6-12hours) - nasal obstruction
Epidemiology of allergic rhinitis
20% of UK population
Children and adolescents tend to have seasonal, adults = perennial
Peak onset is in children, 80% diagnosed under 20
10% of 6 year olds, 15% adolescents
Often persists into adult hood
RFs
- History or FH of atopy
- Exposure to common allergens
- Air pollution
- Decreased exposure to infection
- Exposure to cigarette smoke
Conditions associated with allergic rhinitis
Asthma
Eczema
Conjunctivitis
Presentation of allergic rhinitis
If seasonal. Spring = tree pollen, summer = grass pollen
If house or dust mites = worse on waking and worse in winter
Sneezing Rhinorrhoea and nasal congestion - usually bilateral - Normal = clear - Infection: yellow/green - If blood and unilateral: tumour, foreign body, nose picking - Blood and bilateral: nose picking, bleeding points, granulomatous disorder Itchy nose and/or palate Eyes: watering, itchy, red, swollen
Controlled by antihistamines or topical steroids
Nasal mucosa appears swollen and greyish
Investigations for allergic rhinitis
usually a clinical diagnosis
RAST testing
Skin prick testing
Management of allergic rhinitis
Education, allergy avoidance, antihistamines, topical steroids
- Avoid open grassy spaces, keep windows closed, no animals in the house
- Topical nasal antihistamines AS REQUIRED
- Oral antihistamines REGULAR THERAPY (cetirizine)
- Topical nasal steroids - in obstruction. Slower onset than antihistamines
Other
- nasal saline washouts
- sodium cromoglicate (less effective)
- intranasal ipratropium
Surgery - reduction of inferior turbinates or to correct a deviated septum
Define wheeze
High pitched whistling sounds that occurs when smaller airways are narrowed Occurs in - bronchospasm - swelling of mucosal lining - excessive secretions - foreign body
Causes of wheeze in the child
Asthma Bronchiolitis URTI Transient wheezing in infancy Croup Pneumonia Cardiac failure Recurrent feed aspiration GORD Foreign body inhalation CF Congenital abnormality of lung, airway or heart Idiopathic
Key features of bronchiolitis
Aged 1-9 months
Poor feeding, apnoea, dry cough
Laboured breathing
Apnoea, cyanosis, resp failure
Transient wheezing in infancy
Often after viral infection (RSV)
Disappears by 3 years
Increased in pre term babies or maternal smokers
How long do maternal antibodies circulate in the neonate
First 3 months
Causes of prolonged fever
Atypical infections Connective tissue disease Kawasaki's disease Systemic JIA (juvenile idiopathic arthritis) SLE Malignancy (lymphoma or leukaemia)
Kawaski’s disease
Fever > 5 days Rash Conjunctivitis Cervical lymphadenopathy Peeling of hands and feet Strawberry tongue
Untreated causes coronary aneurysms
Treat with aspirin and steroids (serial echoes)
Systemic juvenile idiopathic arthritis
Extraarticular manifestations apart from arthritis
Splenomegaly
Fever (high grade)
Anaemia
Salmon pink rash - seen on trunk or pressure areas
Fever and rash can come and go - often at the same time every day or twice a day
Anaemia of chronic disease
Neutrophilia
Thrombocytosis
Raised ESR and CRP
Investigations for fever in under 1 month old
FBC CRP Blood culture Urine culture LP ALWAYS Treat ABx empirically
Measles
Caused by measles virus
Fever > 40 Cough Runny nose Coryza Inflamed eyes Kolpik's spots (white spots in the mouth) / Enanthem Red flat rash starts on face and spreads - Cephalocaudal progression
No treatment!
Complications of measles
Occur in 30%
Diarrhoea
Blindness
Inflammation of the brain
Pneumonia
Subactue sclerosing panencephalitis
Subacute sclerosing panencephalitis
Inflammation of the entire brain
Can occur 7-10 years after measles virus
Symptoms initially subtle - Mood changes Then severe - Seizures - Coma - Death
Mumps
Also known as epidemic parotitis
Caused by the mumps virus
Fever Muscle pain Headache Fatigue Trismus - spasm of muscles of mastication
Followed by painful swelling of one or both parotid salivary glands
Can be associated with ear ache
No treatment
Complications of mumps
Meningitis Encephalitis Orchiditis (usually unilateral) Epididymitis (usually unilateral) Rarely causes infertility
Glomerulonephritis
Arthritis of large joints
Myocarditis
Pancreatitis
No increased risk of congenital malformation in pregnant women
Rubella
Also known as German measles or 3 day measles
Caused by rubella virus
Rash starts 2 weeks after exposure and lasts 3 days - pink or light red
Starts on face and spreads
Rash is not as bright as measles
Lymphadenopathy Flu like symptoms Exanthem (rash on face) Joint pains Headache Conjunctivitis
Which of the MMR can cause congenital malformations?
Rubella
