Paeds - Symptoms and Signs Flashcards
Symptoms and signs required for the diagnosis of bronchiolitis
o Child has a coryzal prodrome lasting 1-3 days followed by
o Persistent dry cough and
o Tachypnoea and/or chest recession and
o Wheeze and/or fine end inspiratory crackles on auscultation
• Other
o Nasal flaring, grunting
o Tachycardia
o Cyanosis or pallor
o Hyperinflation of the chest
Prominent sternum
Liver displaced downwards
o Fever – 30%, <39
o Poor feeding– after 3-5 days
Indicates increasing dyspnoea
Indicator for admission
Bronchiolitis symptoms - when do they resolve?
- Self-limiting illness
- Peak between 3-5 days
- Lasts 3-7 days
- Cough resolves in 90% of infants within 3 weeks
Bronchiolitis - signs of impending respiratory failure
• Impending respiratory failure
o Signs of exhaustion – listlessness, decreased respiratory effort
o Recurrent apnoea
o Failure to maintain adequate O2 sats. despite O2 supplementation
Croup signs and symptoms
• Preceding 12-48h hx of non-specific cough, rhinorrhoea, fever
- Sudden onset of a seal-like barking cough
- Stridor (predominantly inspiratory)
- Hoarse voice
- Respiratory distress (due to upper-airway obstruction)
- Maybe fever (rarely >39 degrees)
Symptoms worse at night
Croup
Mild
Moderate
Severe
signs
Mild
• Seal-like barking cough
• Pink
Moderate • Seal-like barking cough • Stridor • Sternal recession at rest • Pink
Severe • Seal-like barking cough but may be quiet • Stridor • Sternal/intercostal recession at rest • Agitation or lethargy • May be cyanosed
Croup
Signs of impending respiratory failure
- Increasing upper airway obstruction
- Severe respiratory distress -RR >70
- Tachycardia
- Sternal/intercostal recession
- Asynchronous chest wall + abdominal movement (subcostal recession)
- Fatigue
- Pallor
- Cyanosis without oxygen
- Decreased LOC
- As the child tires – onset of respiratory failure, chest wall recession may diminish (this may appear to the as if the child is improving but is in fact deteriorating)
Describe the 3 phases of symptoms for whooping cough
o Catarrhal phase
1-2 weeks
Sx of URTIs – nasal discharge, conjunctivitis, malaise, sore throat, low-grade fever, dry, unproductive cough
Pertussis is rarely diagnosed during this stage unless there has been contact with a person who is known to be infected
o Paroxysmal phase After catarrhal phase, 1-6 weeks Coughing fits – • Cough, cough, cough without drawing breath until the lungs are virtually emptied • Child is left exhausted
Whooping
• Short expiratory burst followed by an inspiratory gasp causing the whoop sound
• Whoop is less common in older children, adults, children <3months (may present with apnoea alone)
Post-tussive vomiting
If severe
• Children cyanosis
• Adults sweating attacks, facial flushing, cough syncope
Person may be relatively well between paroxysms
More common at night
May be triggered by external stimuli (cold/noise)
There may be more than 30 paroxysms in 24 hours
Thick mucous plugs or watery secretions
No chest signs
o Convalescent phase
After paroxysmal phase, up to 3 months
Gradual improvement in the frequency and severity of symptoms
Paroxysms can recur with subsequent respiratory infections many months after the initial infection
Describe atypical symptoms in young infants or older children/adults with whooping cough
• Young infants
o Whoop may be absent
o Coughing spasms may be followed by periods of apnoea/cyanosis
o Rarely, very young children may die suddenly with no obvious symptoms of pertussis
• Whoop is less common in children <3months (may present with apnoea alone)older children, adults
Pneumonia in children symptoms
• Most often LRTI is accompanied by fever + may be preceded by a typical viral URTI
- Fever
- raised HR
- raised RR
- cough
- sputum (yellow/green/rusty in Strep. Pneumoniae),
- vomiting post-coughing
- Diarrrhoea
- Grunting
- Poor feeding
- Irritability + lethargy
- Cyanosis (severe infection)
- Cough
- Preceding of URTI (very common)
- Recessions
Toddlers/preschool children
• Post-tussive vomiting
• Pain (chest and abdominal)
• Lower lobe pneumonias may cause abdominal pain
Pneumonia in children examination findings
• Pulse oximetry
o In pneumonia may be <95%
• Fever >38.5
• Observation o RR – tachypnoea 0-5m - >60 6-12m - >50 >12m - >40 o Feeding - ?decompensation during feeding o Chest movements o Respiratory distress Cyanosis Grunting Nasal flaring raised RR Recessions – intercostal/suprasternal/subcostal recession Abdominal seesaw breathing • Complete (or almost) complete airway obstruction • As the patient attempts to breathe, the diaphragm descends, causing the abdomen to lift and the chest to sink. The reverse happens as the diaphragm relaxes. Tripod positioning O2 sats <95%
o Associated symptoms (e.g. rashes, pharyngitis)
• Auscultation o Coarse Crackles + fever pneumonia o Consolidation Decreased breath sounds Increased tactile/vocal fremitus o Bronchial breathing
• Percussion
o Dullness Consolidation
Later + less common finding than crackles
• Consider bacterial pneumonia if
o Persistent or repetitive fever >38.5 + chest recession + increased RR
Very uncommon:
o Wheeze is not seen very often in LRTI – common with more diffuse infections e.g. M. pneumoniae and bronchiolitis
o Stridor or croup suggests URTI, epiglottitis or foreign body aspiration
Mesenteric adenitis symptoms and signs
- Hx of URTI (most commonly viral)
- Symptoms often start following a sore throat or symptoms of cold
- Diffuse abdominal pain/tenderness
- Fever, feeling unewell
- N, D
- Hyperaemic pharynx or oropharynx (pharyngitis)
- Extramesenteric lymphadenopathy (usually cervical)
Biliary atresia signs and symptoms
• Jaundice • Pale stools – white to a tan or light yellow • Dark urine • Bruising o Coagulopathy developing secondary to vitamin K deficiency related to chronic cholestasis • Uncommon presentations o Hepatomegaly o Ascites
Intestinal atresia symptoms + signs
• Persistent vomiting
o Bilious
o Within hours of birth
o Sometimes may take a couple of days to develop – lower lesions take longer to develop symptoms
Cerebral palsy symptoms and signs in neonates
All signs in children with corrected age
• Neonates
o Early postnatal period – hypotonia
o Unsusual fidgety movements or other abnormalities of movements incl. asymmetry or paucity to movement
o Abnormalities of tone
Hypotonia, spasticity, dystonia (fluctuating tone)
o Abnormal motor development
Late head control, rolling, crawling
o Feeding difficulties
Poor weight gain, coughing and choking while eating, long mealtimes
May emerge before or be more apparent than motor symptoms in the early years
o Becomes progressively hypertonic at ages 16-18m
• <5 months
o Normally
Small, controlled, fidgety, spontaneous general movements of the neck, trunk, limbs in all directions
Continual movements except during focused attention or if the child is unsettled and crying
Best seen in the reclined or supine position
o CP
Absent or abnormal fidgety movements (exaggerated amplitude, speed or jerkiness)
• Delay in motor development
o Key diagnostic factor
o Should use corrected age for children born preterm
o Sit – 6m, crawl – 9m, walk – 12-18m, climb stairs – 3y
Most common delayed motor milestones – not sitting by 8m, not walking by 18m
o Early asymmetry of hand function (hand preference) before 1y
o The majority of movement delays will be evident by the time a child reaches 30m
Cerebral palsy symptoms + signs
• Spasticity
o Generally presents after 2 years of age
o Manifests when the child attempts activities
- All patients have motor impairment + muscle weakness
- Joint instability/dislocation – more common as severity of spasticity increases
- Persistent toe walking
- Pain – tight muscles, abnormal posture, stiff joints
- Sleep disorders
- Eating difficulties
• Delay in speech development
o Should use corrected age for children born preterm
o Talk in short sentences by 2y
• Delay in cognitive/intellectual development
o Observed in 40%
• Retention of primitive reflexes
o Reflexes + reactions that are poor prognostic factors for development of independent walking – asymmetric + symmetric tonic reflexes, retention of Moro (startle) reflex, retention of neck righting reflex, presence of lower-extremity extensor thrust response
• Lack of age-appropriate reflexes
o Poor prognostic factors for development of independent walking
o Lack of parachute reaction
o Lack of foot placement reaction
• Spasticity/clonus
o Typically develops after the 2nd year of life
o Manifests when the child attempts activities
o Confirmed by velocity dependent resistance to passive motion, abnormally deep tendon reflexes, clonus
Spasticity is an increase in resistance to sudden passive movement and is velocity dependent The faster the passive movement the stronger the resistance
o May be accompanied by a “clasp-knife” phenomenon – resistance to passive motion abruptly decreases
• Contractures
Spastic cerebral palsy symptoms and signs
• Spastic CP
o Selective voluntary motor control impairment
Inability to perform isolated motion of joints without obligatory movement of non-agonist joints – assess using SCALE (selective control assessment of the lower extremity)
o Gait
Toe walking/ knee hyperextension
- Excessive plantar flexion in patients with spastic hemiplegia
- Toe-walking in young child
• Knee hyperextension in the older child or adult
Scissoring
• Due to hip adductor or medial hamstring spasticity
Crouched gait
• Excessive dorsiflexion
Dyskinetic cerebral palsy symptoms and signs
o Dystonia – involuntary, sustained contractions resulting in twisting + abnormal postures
o Athetosis – slower, constantly changing, writhing or contorting movements
o Chorea – rapid, involuntary, jerky, fragmented motions, decreased tone but fluctuating
Ataxic cerebral palsy symptoms and signs
o Loss of muscular coordination with abnormal force + rhythm
o Impairment of accuracy – gait + truncal ataxia, poor balance, past pointing, terminal intention tremor, scanning speech, nystagmus
o Abnormal eye movements
o Hypotonia
Signs that a child with cerebral palsy has problems with eating/drinking/swallowing
o Problems with eating, drinking, swallowing – To a specialist for treating dysphagia if
Coughing, choking, gagging, altered breathing pattern, change in colour while eating or drinking
Recurrent chest infection
Mealtimes are stressful/distressing
Prolonged meal duration
Signs and symptoms of atopic eczema flares
o increased dryness o Itching o Redness o Swelling o General irritability
Signs and symptoms of atopic eczema with bacterial infection
o Weeping o Pustules o Crusts (golden coloured) o Atopic eczema failing to respond to therapy o Rapidly worsening atopic eczema o Fever o Malaise
Signs and symptoms of eczema herpeticum
o Areas of rapidly worsening painful eczema
o Clustered blisters consistent with early-stage cold sores
o Punched out erosions (circular, depressed, ulcerated lesions) usually 1-3mm that are uniform in appearance (may coalesce to form larger areas of erosion with crusting)
o Possible fever, lethargy, distress
DMD + BMD symptoms + signs
- Progressive proximal muscular dystrophy with characteristic pseudohypertrophy of calves
- All patients have symptoms by 3 years of age
• Imbalance of lower limb strength
o Hip + knee flexors + ankle plantar flexors stronger than hip + knee extensors + ankle dorsiflexors
o Patient tends to walk with increased LORDOSIS + on the toes to keep the centre of gravity behind the hips and in front of the knees to avoid jack-knifing
• Lower extremity musculotendinous contractures
o Increased lumbar lordosis
o Heel cord contractures
• Delayed motor milestones
o Mean age of beginning ambulation – 18 months
o Unaffected children already begin to ambulate by 18 months
• Ambulatory difficulty and falls
o Untreated patients rarely able to run or jump
o Waddling gait
o Initial complain of children – ambulation difficulty + falls
• Calf hypertrophy
o Due to ongoing regeneration of muscle fibres
o Characteristic of all muscle dystrophies
- Diminished muscle tone + deep tendon reflexes in all muscle groups
- Normal sensation
• Gower’s sign
o Patient needs to “climb up his body” to come to a stand from a seated position
o Using the hands when rising from the floor
o Because of the relatively weaker hip + knee extensors + ankle dorsiflexors
o Characteristic of children with DMD from ages 4-7
• Toe walking
o DMD – hypotonic, symmetrically affected
o However, the great majority of children who walk on their toes have static encephalopathies (not muscular dystrophies) and at least mild spasticity – asymmetrically affected
- Hypotonia
- Hyperactivity
- Urinary + bowel incontinence
• Mild to severe intellectual disability
o DMD – Speech delay or global developmental delay
o BMD – Learning difficulties, behavioural problems, ASD
• Failure to thrive, fatigue
• Respiratory problems
o Weakness of IC muscles nocturnal hypoxia daytime headaches, irritability, loss of appetite
o Loss of effective cough – infections, atelectasis
• Carriers
o risk of cardiomyopathy
o Most asymptomatic
o 2-5% may have skeletal muscle symptoms – mild muscle weakness, aches or calf muscle enlargement or a disease as severe as in boys (due to X-inactivation)
DMD vs BMD
DMD
• All patients have symptoms by 3 years of age
• DMD patients become wheelchair dependent between 7-12 years of age
• Lose the ability to walk by 12 years of age
• Require ventilatory support by 25 years of age
BDM
• Similar to those in DMD
• Patients usually able to walk throughout their teens and into early adulthood
• Muscle weakness may begin in teenage years or 20s, causing difficulty climbing stairs, fast walking + lifting objects
• Loss of independent ambulation in late 20s
• CHF, cardiac arrhythmias before complaining of muscle weakness (may be the first presenting feature if muscle weakness is mild) – fatigue, poor sleep, weight loss, vomiting
West syndrome/infantile spasm syndrome signs + symptoms
• Typically presents in infancy
- characteristic ‘salaam’ attacks: flexion of the head, trunk and arms followed by extension of the arms
- this lasts only 1-2 seconds but may be repeated up to 50 times
• progressive mental handicap
• Spasms
o Initial contraction phase
o Followed by a more sustained tonic phase
o Usually symmetrical, bilateral, brief contractions of the axial (neck, trunks, limbs) muscle groups
o Can be asymmetrical + only manifest as head nodding/drops or abnormal eye movements
Abnormal eye movements may be the only presenting symptom
o Sudden flexion, extension or mixed flexion-extension of proximal and truncal muscles
o Lasts 1-2 seconds
Longer than a myoclonic jerk (which lasts milliseconds)
Not as long as a tonic seizure (which lasts >2s)
o Typically occur in clusters of 20-100 spasms at a time with visible distress
o Isolated spasms can occur
o Often seen on waking or falling asleep, occasionally associated with feeding
• There may be an associated brief loss of consciousness
• Neurodevelopmental delay or regression
o Background of developmental delay – but occasionally development may be unaffected at presentation
o Plateauing or regression of subsequent development
o Important diagnostic feature – loss of previously acquired skills, notably affecting visual skills
Other signs
• Ash leaf macules
o Visualised using Wood’s lamp examination – lesions fluoresce under UV light
o Hypopigmented skin lesions – associated with tuberous sclerosis
• Microcephaly
o Can indicate an underlying cause e.g. brain malformations, perinatal injuries, neurometabolic disorders, intrauterine infections
Gastroenteritis symptoms + signs
• Bowel habits
o Sudden onset diarrhoea
Bloody diarhoea – Campylobacter, E.coli, Salmonellosis, Shigella, Yersinia, amaoeba
Watery – rotavirus, norovirus, salmonella, yersinia, cryptosporidiosis
o Sudden change in stool consistency to loose or watery stools, usually at least 3 times in 24h
o Blood or mucus in the stool
o Faecal urgency
o Hyperactive bowel sounds
- N or sudden onset of vomiting
- Fever or general malaise
- Abdominal pain or cramps
- Associated headache, myalgia, bloating, flatulence, weight loss, malabsorption
Clinical dehydration
Appears unwell or deteriorating
Altered responsiveness (e.g. irritable, lethargic)
Sunken eyes
Tachycardia
Reduced skin turgor
• Hypernatraemic dehydration signs and symptoms
• Hypernatraemic dehydration o Jittery movements o Hypertonia o Hyperreflexia o Convulsions drowsiness or coma
Severe dehydration signs and symptoms
- Apathetic or lethargic state
- Markedly decreased or absent UO
- Greatly increased thirst
- Very dry mucous membranes
- Greatly elevated heart rate
- Prolonged or minimal CRT
- Decreased skin turgor
- Very sunken eyes
- Very sunken anterior fontanelle
- Cold extremities
- Hypotension
- Coma
DDH symptoms + signs in <3m
o Asymmetry
Asymmetrical gluteal or thigh skin folds
Limb length discrepancy (Galeazzi sign)
Limitation + asymmetry of hip abduction when the hip is flexed to 90 – most important sign of a dislocated or dysplastic hip
DDH symptoms + signs in 3-6m
o >8w – unilateral limitation + asymmetry of hip abduction – most reliable sign of DDH
o If the hip is dislocated it is in a fixed position
o Galeazzi sign
Supine child, hips + knees flexed to 90, height of each knee is compared
Positive sign – one leg appears shorter than the other – usually due to dislocation of the hip
Unilateral femoral shortening hip dislocation or rarer abnormalities of the femur
o Other signs – asymmetry of gluteal thigh or labral skin folds, discrepancy in leg length, widened perineum on affected side, buttock flattening, standing or walking with external rotation of the affected leg
DDH symptoms + signs in older children
o Limited abduction when fully flexed
o Tip toe walk on the affected side
o Painless limb
• Abnormal positioning of the leg or delayed crawling/walking
DDh barlow + ortalani test
• Barlow + Ortolani tests
o Can detect an unstable hip
o Do not detect an irreducible dislocated hip or a stable hip with abnormal anatomy (e.g. acetabular dysplasia)
o Useful in neonates, become difficult by 2-3 months of age due to increased musculature
o Benign hip clicks (due to soft tissues snapping over bony prominences during hip movement) should be distinguished from the clunks produced during the Ortolani manoeuvre as the dislocated femoral head is reduced and from the subluxation felt during the Barlow test
• Positive Barlow test
o The hip is flexed to 90° and adducted, the examiner’s hand is placed on the knee
o Posterior pressure is placed through the hip in an attempt to identify dislocatable hips.
o Used in infants <6m
• Positive Ortolani test
o In Ortolani, the back of your hand should go flat against the bed as you abduct the thighs
o The hip is flexed to 90° and abducted, with the examiner’s fingers are placed laterally over the greater trochanter or hip joint
o In Ortolani, the back of your hand should go flat against the bed as you abduct the thighs
o The examiner then uses anterior pressure over the trochanter in an attempt to identify a dislocated hip that is relocatable
o Used in infants <6m
o If frank instability is appreciated during the Barlow/Ortolani test – refer to a paediatric orthopaedist
Perthes disease symptoms and signs
• Presentation
o Onset over weeks
o No hx of trauma
o Limitation of hip rotation + subacute limp
o Referred pain to the groin, thigh, knee
o Child is systemically well with no other joint involvement and no evidence of joint inflammation
• Typically unilateral
o Bilateral in 10% (sequential, not simultaneous)
• Patients commonly have a characteristic phenotype
o Short stature
Children shorter than their peers
They attain puberty and a normal final height by mid teen
o Delayed bone age
o Hyperactivity
• Gait
o Painless limp
o Antalgic gait (due to pain) during acutely painful episodes
o Trendelenburg gait is seen in the late phase
• Limited range of motion at the hip joint
o Flexion deformity in the acute setting
o Impingement lesions lead to limited adduction in flexion, internal rotation and abduction in extension
o O/E all movements of the hip are limited
o Early phase
Limited abduction of the hip
Limited internal rotation in both flexion + extension
• Hip pain
o Frequently radiating to the thigh, knees, groin, buttocks
o Gets worse with activities
• Muscle wasting of the gluteal muscles + quadriceps
o Trendelenburg’s sign might be positive
• Later stage of the disease
o Global reduction in all ranges of motion with associated pan indicative of joint arthritis
• Roll test
o Patient lying in supine position
o Examiner rolls the hip of the affected extremity into external and internal rotation
o Test should invoke guarding or spasm, especially with internal rotation
Hand foot and mouth disease signs + sx
• Prodromal period – may last 12-3 hours
o Fever (38-39)
o Malaise
o Loss of appetite
o Cough
o Abdominal pain
o Myalgia
o Sore mouth/throat
o Vomiting if enterovirus 71
• Vesicular eruptions in the mouth (enanthem)
o Scattered ulcerative lesions
o Occur within 1-2 days
o Begin as 2-8mm erythematous macules + papules
o Appear most commonly on the hard palate, tongue, buccal mucosa, lips, pharynx
• Papulovesicular lesions of the distal limbs (exanthem)
o Macules + papules of the hands + feet usually soon follow oral lesions
o Progression – flat pink patches small elongated greyish blisters with an erythematous halo peel off + leave no scars within week/10days
o 2-5mm sparse erythematous macules + pappules
o Central greyish vesicle
o Sides of fingers, dorsum of hands, margins of heels > palms, soles
o Elliptical lesions, long axis running parallel to the skin lines
o Buttocks + groin area may also be affected
o Lesions may be asymptomatic or painful or puritic
• Coxsackie virus A6
o More widespread rash
o Extends beyond the palms + soles
o May preferentially occur in areas prone to atopic dermatitis (antecubital + popliteal fossae)
o Petechiae + severe blistering
o Skin peeling and/or nail shedding
• Other sx
o Vesicle + ulcers in the mouth may make eating difficult – child eats little, frets, may complain of a sore throat or mouth sores
Chickenpox symptoms + signs
• Prodrome
o Fever
o Malaise
o Nausea
o Myalgia
o Anorexia, loss of appetite, feeding problems
o Headache
• O/E
o Vesicular rash
Small, erythematous macules appear on the scalp, face trunk, proximal limbs
Progress over 12-14 hours to papules, clear vesicles (which are intensely itchy), pustules
vesicles can also occur on the palms and soles
Mucous membranes can also be affected with painful + swallow oral or genital ulcers
Vesicles appear in crops – stages of development of the rash can therefore differ on different areas of the body
Crusting occurs usually within 5 days of the onset of the rash + crusts fall off after 1-2 weeks
o Fever
Mumps symptoms and signs
• Parotid swelling
o Typically, 1 parotid gland is affected first, reaching a maximal size after 2-3 days with the other gland closely following it
During the period of enlargement the person may complain of earache and have difficulty with pronunciation of words or chewing
o About 25% of people have unilateral parotitis
Affected gland may be tender to touch
“ear pain”, “pain on eating”
• Earl lobe over affected gland may be deflected upward + outward
• Angle of the mandible may be obstructed (this does not occur with cervical lymphadenopathy)
• Non specific symptoms – might precede parotitis – typically occur 1 day before overt signs of parotitis + peak around the time the parotid glands are most swollen
o Low grade fever
o Headache
o Earache
o Malaise
o Muscle ache
o Loss of appetite
• 15-20% of people may be asymptomatic (more common in children)
Measles symptoms and signs
• Prodromal symptoms
o Occur 10-12 days after contracting the infection
o 2-4 days (incl. malaise, fever, cough, rhinorrhoea, conjunctivitis) before the characteristic skin rash develops
• Cough + coryzal symptoms + conjunctivitis + fever of >39oC without antipyretics + maculopapular rash
• Rash
• Fever
o Increases during the prodromal phase to around 39 at about the time the rash appears, then gradually decreases
• Koplik’s spots
o Appear on the buccal mucosa at the end of the prodroma phase + around the same time a the rash, disappear over the next couple of days
o 2-3mm red spots with white or blue-white centres
o Pathognomonic for measles
• Rash
o Starts on the face and moves downwards
Appears on the face + behind the ears first (when other symptoms tend to be at their most severe) before descending down the body to the trunks and limbs + forming on the hands + feet last over the course of about 3-4 days
o Then fades after it has been present on an area for about 5 days
o Total duration of rash – 1 week
CF signs and symptoms
• Clubbing
- Failure to pass meconium
- Meconium ileus – bowel obstruction with meconium, can lead to bowel peroration + meconium peritonitis
- Bowel obstruction – hx of decreasing stool numbers over time +/- abdominal distension or vomiting
• Voracious appetite – infants never seem satiated
• Respiratory tract disease o Mucus retention infection inflammation o Wet sounding cough o Recurrent infection o Chronic sinusitis
• Pancreatic dysfunction
o Calorie malabsorption
o Malabsorptive stool with steatorrhoea (bulky, greasy stools)
• Failure to thrive
- Genital abnormalities in males – bilateral absence of vas deferens
- GORD
• Distal intestinal obstruction syndrome • Meconium ileus = in neonate • DIOS = after neonatal period o Acute onset peri-umbilical or RLQ abdominal pain + o Palpable mass in RLQ o Faecal loading in RLQ, small intestine air-fluid levels on plain AXR o Vomiting (esp. bilious), abdominal distension – i.e. clinical features of partial or complete intestinal obstruction
Faecal impaction signs and symptoms
overflow soiling +/or faecal mass palpable abdominally +/or rectally if indicated
can be seen on AXR
Red flag symptoms in a child presenting with constipation
Failure to pass meconium/delay (>48 hours after birth [in term baby])
Previously unknown or undiagnosed weakness in legs, locomotor delay (e.g. falling over in a child/young person >1y)
Marked abdominal distension with vomiting
Abnormal appearance/position/patency of anus: fistulae, bruising, multiple fissures, tight or patulous anus, anteriorly placed anus, absent anal wink
Gross abdominal distension
Abnormal: asymmetry or flattening of the gluteal muscles, evidence of sacral agenesis, discoloured skin, naevi or sinus, hairy patch, lipoma, central pit (dimple that you can’t see the bottom of), scoliosis
Deformity in lower limbs e.g. talipes
Abnormal neuromuscular signs unexplained by any existing condition e.g. cerebral palsy
Abnormal reflexes
Pyloric stenosis signs + symptoms
• Hx of feeding intolerance with multiple formula changes
• Progressive, recurrent, projectile, non-bilious vomiting
• Failure to thrive/weight loss may progress to increasing volume depletion
• Olive shaped mass may be palpable in the right upper abdomen
• Dehydration
• Other signs – tachycardia, wet nappies, dry mucous membranes, flat or depressed fontanelles, constipation, irritability
• Visible peristalsis can be visualised as the stomach tries to push its contents past the obstruction
• US
o Pyloric channel length >17mm
o Pyloric muscle thickness >4mm
GORD symptoms and signs in <1
• <1
o Effortless spitting up of 1 or 2 mouthfuls of stomach contents = normal, common, consistent with GOR
o Difficult to differentiate between gastro-oesophageal reflux (GOR) + gastro-oesophageal reflux disease (GORD) – no reliable diagnostic test
o GOR – more common after meals + when infant is in a recumbent position
• <1 o Excessive crying o Crying while feeding o Adopting unusual neck postures o Hoarseness and/or chronic cough o A single episode of pneumonia o Unexplained feeding difficulties e.g. refusion to feed, gagging, choking o Faltering growth
GORD red flags
o Frequent, forceful (projectile) vomiting – hypertrophic pyloric stenosis in <2m
o Bile-stained vomit – intestinal obstruction
o Abdominal distension, tenderness, palpable mass – intestinal obstruction or acute surgical condition
o Blood in vomit – potentially serious bleed from oesophagus, stomach or upper gut
o Bulging fontanelle or altered responsiveness - ICP, meningitis
o Rapidly HC (>1cm/week), persistent morning headache, vomiting worse in the morning - ICP (hydrocephalus, SOL)
o Blood in the stool – bacterial gastroenteritis, infant cow’s milk protein allergy
o Chronic diarrhoea – cow’s milk protein allergy
o With, or at high risk of atopy – cow’s milk protein allergy
o Dysuria – UTI
o Appearing unwell or fever – infection
o Onset of regurgitation and/or vomiting >6m or persisting after 1y – suggest other cause rather than reflux e.g. UTI
GORD symptoms and signs in >1
o Heartburn
o Retrosternal pain
o Epigastric pain
Non bullous impetigo signs and symptoms
• Non-bullous impetigo
o Usually asymptomatic
o May be mildly itchy
o Systemic features are uncommon
Regional lymphadenopathy + fever in severe cases
o Lesions begin as thin-walled vesicles or pustules (seldom seen on clinical examination as they rupture quickly) release exudate forming a characteristic golden/brown crust
o Once crusts have dried they separate mild erythema which then fades
o Healing occurs spontaneously without scarring within 2-3 weeks
Course may be more prolonged in people with pre-existing skin conditions (e.g. eczema, scabies) or in hot/humid climates
o Lesions can develop anywhere in the body – most common on exposed skin on the face (peri-oral + peri-nasal areas), limbs, flexures (e.g. axillae)
o Satellite lesions (smaller lesions near the edges of the principal lesion) may develop following autoinoculation
Bullous impetigo sgns and symptoms
impetigo
o Systemic features if large areas of skin are affected – fever, lymphadenopathy, diarrhoea, weakness
o Lesions appear as flaccid fluid filled vesicles + blisters (diameter 1-2cm) – can persist for 2-3 days
o Blisters rupture thin flat yellow/brown crust
o Healing usually occurs without scarring within 2-3 weeks
o Lesions can develop anywhere in the body – most common on flexures, face, trunk, limbs
o May be particularly widespread in infants
Kawasaki disease symptoms and signs
• Fever
o >39
o Abrupt onset
o At least 5 days duration
o Unresponsive to abx
• Extreme irritability
o Much greater that would be expected for the magnitude of fever
o Poor intake, abdominal pain, nausea, diarrhoea
• Polymorphic rash – maculopapular erythematous rash
o Comes on within 3-5 days
o Begins with nonspecific erythema of the soles, palms, perineum
o Spreads to involve the trunk and the rest of the extremities
o Itchy
o Never vesiculo-bullous
• Conjunctivitis/ conjunctival injection – non-purulent, non-exudative
• Mucosal erythema
o Hx or physical findings of dry, erythematous, fissured lips that bleed easily
o Erythema of the oral + pharyngeal mucosa
o Strawberry tongue with prominent papillae + erythema
o No oral exudates, ulcerations, Koplik spots
• Strawberry tongue
• Skin changes in the peripheral extremities
o Tender Induration (sclerosis) of hands and feet
o Refusing to ambulate
o Acute changes – swelling + erythema of the hands + feet
o Subacute changes – desquamation
May affect the perineal area, moving to fingers and then toes
o Nails
Periungual desquamation of fingers + toes about 2 weeks after onset
Beau lines – 1-2 months after onset
• Unilateral non-purulent cervical lymphadenopathy
• Coronary artery aneurisms
o Not a key feature in the classic presentation of Kawasaki disease
o Key feature in incomplete/atypical presentation
• Other sx
o Lethargy, urethritis, D+V, abdominal pain, myalgia, arthralgia, arthritis
o Neck stiffness – aseptic meningitis
o Hepatomegaly, jaundice
o CV – pancarditis, aortic or mitral incompetence
o GI – hydrops of gallbladder, jaundice, D
o Blood – mild anaemia
o Renal – sterile pyuria, mild proteinuria
o CNS – aseptic meningitis
o MSK – arthritis, arthralgia
o Others – anterior uveitis, BCG- site inflammation
Acute phase Kawasaki disease
Time from fever onset
predominant features
1-2 weeks
Highly febrile Very irritable. Toxic-appearing. Oral changes rapidly following. Oedema and erythema of feet. Rash especially common in the perineal area.
Subacute phase Kawasaki disease
Time from fever onset
predominant features
2-8 weeks
Gradual improvement. The fever settles. Desquamation of the perineum, palms, soles. Arthritis, arthralgia. Thrombocytosis. Coronary artery aneurysms. Myocardial infarction.
Convalescent phase Kawasaki disease
Time from fever onset
predominant features
Months to years
Resolution of remaining symptoms. Laboratory values return to normal. Aneurysms may resolve or persist. Beau's lines. Cardiac dysfunction and myocardial infarction may still occur.
Precocious puberty symptoms and signs
• Pubic/axillary hair
o Pubic + axillary hair, acne, body odour androgens
o Onset of axillary hair typically occurs in mid-puberty
o Pubic/axillary hair in the absence of breast development in girls/ testicular enlargement in boys premature adrenarche CAH, adrenal gland tumours, Cushing’s syndrome
• Menarche
o Occurs in stage 4 puberty, within 2-3 years after the onset of breast development
• Increased growth velocity
o Oestrogen is the factor that mediates the increased growth hormone response during puberty
o Tall structure in childhood due to an accelerated rate of linear growth
o Normal or short stature as an adult due to early fusion of the epiphyseal growth plates
• Tall stature
• Girls – breast development
• Boys – testes >4ml or >2.5cm longest axis (prader orchidometer)
CAH symptoms + signs
• Salt-wasting CAH
o Can occur as early as 1-4 weeks of age
o In utero getting hormones/steroids from mother(mother’s cortisol stays in baby for 1 day). After 1 day Addisonian crisis
o Poor feeding
o Weight loss
o Failure to thrive
o Vomiting
o Hypotension
o Hyponatraemia, hyperkalaemia
• Signs of hyperandrogenism
o Children– precocious puberty, early onset of facial, axillary, pubic hair, adult body odour, rapid somatic growth
o Adolescents + adults – temporal balding, severe acne, irregular menses (primary/secondary amenorrhoea, delayed menarche), hirsutism, infertility
o Females – virilised at birth or may become virilised post-natally, Oligomenorrhoea, amenorrhoea, delayed menarche, PCOS, acne, hirsutism, alopecia, impaired fertility, temporal baldness
o Males – no signs at birth except subtle hyperpigmentation, early beard growth, enlarged phallus, small testes, short stature, oligozoospermia
• Atypical genitalia
o Males – smaller testes in comparison to the phallus, hyperpigmentation of the scrotum (might be the only presenting sign)
o Females – clitoromegaly, fused labia, common urogenital sinus in place of a separate urethra + vagina
o Degree of virilisation in females can be graded based on the Prader score
• Premature adrenarche
• Precocious puberty
• Infertility
• Short stature
o adrenal androgens through conversion to oestrogen early fusion of epiphyseal growth plates
o Children with CAH have advanced bone age + accelerated linear growth velocity
o Patients are often tall initially but shorter than mid-parental target height
• Males with salt losing form – present at 7-14 days of life with salt losing crisis
• Males with non-salt losing form – present with early virilisation at 2-4y
Delayed puberty symptoms + signs
• Boys – tests <3ml (Prader orchidometer)
• Girls – absent breast development – the first demonstrable sig of puberty in girls
• Absent pubic/axillary hair
• Absence of menarche
o Menarche occurs in Tanner stage 4 breast development in the majority of girls
• Absent growth spurt
o Oestrogen either from the ovary or aromatised from testicular testosterone, is the factor that mediated the increased GH response during puberty
o Growth spurt occurs in mid- to late puberty in boys + in stage 3 breast development in girls
o It contributes 25cm of height in females + 30cm in males, on average
• Anosmia
o Kallman’s syndrome = hypogonadotropic hypogonadism + hypoplastic olfactory nerves
• Short stature
JIA symptoms + signs
• Joint pain – esp. during motion + on palpation
• Joint swelling
o Commonly at the knees in oligoarticular JIA
o May be the only presenting symptoms
o Examination of affected joints may reveal oedema
o Synovial effusions + thickening
• Morning stiffness
o Stiffness upon waking or after periods of inactivity
o Stiff gaits in the morning which improve after a few hours when lower extremity joints are involved
o If wearing nappies – reluctance of the child to have a nappy change first thing in the morning
• Limp – more pronounced in the mornings
• Limited movement
o Active disease – limitation secondary to pain
o Long-standing disease – limitation secondary to joint contractures due to ligament/tendon tightening
• Fever
o High spiking fevers in systemic-onset JIA + not unusual in other subtypes
o Dx of systemic JIA
• 1-2 spikes of fever a day interspersed by normal temperature
• Occurring daily for 2 weeks
• Rash
o Systemic onset JIA (key factor if SoJIA is suspected)
• Evanescent, non-pruritic, non-fixed, erythematous rashes
• Salmon coloured, seen on trunk + proximal extremities
• Not typically seen on palms, soles or face
• Co-occur with fevers – tends to disappear when fever is down
• Koebner’s phenomenon – Rash can be elicited by scratching the skin
• Enthesitis
• Uveitis
o Most common extra-articular manifestation
o Can lead to visual impairment if disease is poorly controlled
Syndromes that can cause intellectual disability/ developmental delay - characteristics
DS
fragile X syndrome
Prader-Willi syndrome
William’s syndrome
Turner’s syndrome
DiGeorge syndrome
craniosynostosis
Rett’s syndrome
DS
Oblique palpebral fissures, median epicanthic fold, low nasal bridge, low-set ears, central iris Brushfield spots, short curved fifth finger, and a single palmar crease
fragile X syndrome
Macrocephaly, long face, high arched palate, prominent jaw, epicanthic folds, macro-orchidism, and large ears are characteristic of fragile X syndrome. Strabismus may also be present.
Prader-Willi syndrome
Short stature, hypotonia, small hands and feet, and incomplete sexual development, often with cryptorchidism
Children with mild cognitive impairment who have eaten poorly and been of low weight in early life, but who subsequently eat excessively and gain large amounts of weight at the age of 4 to 5 years
William’s syndrome
Widely spaced teeth, long philtrum, wide mouth, and full lips
Turner’s syndrome
Short stature, low-set ears, webbed neck, low hairline, and cubitus valgus
DiGeorge syndrome
Cleft palate, micrognathia, low-set ears, and facial dysmorphism
craniosynostosis
Skull deformity
Rett’s syndrome
Girls with an initial normal development followed by regression of skills at age 1 to 2 years and epilepsy
Symptoms and signs of SOL in pt w • If acute onset or regression of previously acquired skills consider acquired disability due to intracranial pathology
o Other specific LD or cognitive impairment may have been present for some time but only recently noted (e.g. starting school)
• SOL o Severe headaches that are worse in the morning o Vomiting o Visual disturbance o Newly developed squint o Focal neurological deficit
Tic disorder signs and symptoms
• Start caudally (usually with blinking + coughing)
• Premonitory sensation
o Feeling of mounting inner tension or urge (premonitory urge) which is transiently relieved by tic expression
• Ability to suppress tics
o Involuntary but are usually temporarily suppressible
• Increase by stress, fatigue, anxiety, excitement
• Decrease with distraction
• Otherwise normal neurological examination
tics can include
• Can include any muscle group or vocalization but certain tic symptoms are more common – eye blinking, throat clearing
