Paediatric History Taking and Management Flashcards
How can you structure a paediatric history?
Confirm full name and DOB
Presenting Complaint
How long have they been in hospital for? What brought them in? How have they been progressing? What treatment are they receiving – is it helping?
PDF BINDS
Past medical and surgical hx
Drug hx
Family hx
Birth history – how was the pregnancy? How many weeks were they born at? Mode of delivery? Birth weight? Complications after birth? SCBU stay?
Immunisations
Nutrition- how much do they eat and drink? Wet/dirty nappies?
Development
Social and sexual hx – including any previous social services input
How could you explore a presenting complaint of a child with a seizure?
Is there anything the parent thinks might have triggered it?
How were they leading up to the seizure? Any temperature? Complaining of a headache? Stiff neck? Any new rashes? N+V? Change in waterworks/bowel habit?
How did they look when they were seizing? One part of their body shaking or all of it? Was the child aware of what was happening? Tongue biting? Incontinence?
Eye rolling during the seizure?
How long did it last? How did it stop? How were they afterwards?
How would you investigate a child with a seizure?
measure their glucose and oxygen sats immediately
bloods for reversible causes e.g. electrolyte derangement
suspecting meningitis / encephalitis: inflammatory markers, viral PCR/ nasopharyngeal aspirates, blood cultures, LP, neuroimaging
ECG for arrythmia
EEG
DDx for a child with a seizure?
Febrile convulsions
Roseola infantum (can cause febrile convulsions)
Hypoglycaemia / hypoxia
Epilepsy
Meningitis
Encephalitis (e.g. herpes simplex)
SOL
How would you explain febrile convulsions and their management to a parent?
Explain that when some children run a temperature that their brain isn’t used to it and it may cause a seizure, occurs commonly in children from 6 months - 5 years
If they have had one febrile convulsion they are more likely to have another, but most children grow out of it by 5/6 years
Can give paracetomol to bring down the temperature but this doesn’t reduce the risk of them occuring
Safety netting advice: if seizing, clear obstacles, put cushion under head, call ambulance if lasting more than 5 mins
Explain that they don’t increase risk of epilepsy unless they are complicated / prolonged
How can non-blanching rashes be described?
Petechiae : < 5mm diameter
Purpura: 5-10mm diameter
Ecchymoses: >1cm diameter
What can cause non- blanching rashes in kids?
Meningococcal sepsis
Henoch-Schönlein purpura
Haemolytic uraemic syndrome
Idiopathic thrombocytopaenic purpura
Leukaemia
Forceful coughing/vomiting
Non-accidental injury
What features would you expect in the history and examination for a child with menigococcal sepsis?
Fever
Neck stiffness
Headache
Photophobia
Confusion and/or seizures
OE:
Kernig’s sign (pain and resistance on passive knee extension with hips fully flexed)
Brudzinski’s sign (knees and hips flex on bending the head forward)
Non-blanching rash
How could you investigate meningococcal sepsis?
MUST NOT DELAY TX
Baseline bloods (FBC, WCC CRP, U&E, clotting): inflammatory markers may be raised
Blood cultures
Pharyngeal swab: to screen for Neisseria meningitides in the pharynx
do not do lumbar puncture if signs of sepsis or rapidly evolving rash
How would you manage meningococcal sepsis?
GP: IM Benzylpenicillin
Hospital:
Intravenous cefotaxime and amoxicillin in patients under 3 months.
Intravenous ceftriaxone (and consider steroids) in patients over 3 months old.
What are the 5 key components of meningitis management in children?
Antibiotics
Steroids
Fluids
treat any shock, e.g. with colloid
Cerebral monitoring
mechanical ventilation if respiratory impairment
Public health notification and antibiotic prophylaxis of contacts - ciprofloxacin
Complications of untreated meningococcal sepsis?
Seizures
Raised intracranial pressure and hydrocephalus
Disseminated intravascular coagulation
What is Henoch-Schönlein purpura (HSP)?
IgA mediated vasculitis usually triggered by group A strep
peaks at 4-6 years
A prodromal URTI or GI infection
Generalised abdominal pain
N+V, sometimes bloody diarrhoea
Joint pain
IgA nephropathy - haematuria
Symmetrical rash on the back of the legs, buttocks and arms
What is an important differential for HSP?
intussusception : also presents as bloody diarrhoea and abdominal pain
Intussusception can also be a complication secondary to HSP
How can HSP be investigated?
Urinalysis: to test for the presence of haematuria or proteinuria
monitor blood pressure (renal involvement)
Baseline blood tests :FBC, clotting profile, (bc bleeding) U&Es, LFTs (bc diarrohea) CRP
Skin biopsy: can be considered if there is doubt surrounding the origin of the rash
Can do USS if worried about intussuception
How can HSP be managed?
Complications?
supportive care, analgesia, excellent prognosis (usually gone in a few weeks)
Complications:
recurs in 1/3 of patients
Nephrotic or nephritic syndrome
Renal failure
Intussusception
What is ITP? How does it present?
development of a purpuric rash in those with low circulating platelets with the absence of any clear cause
viral illness
followed by epistaxis / new rash
How could you investigate ITP?
Baseline blood tests (FBC) and blood film: thrombocytopenia
Bloodborne virus screen (HIV, hepatitis C): to exclude secondary cause of ITP
Bone marrow biopsy: only required if there are atypical features e.g.
lymph node enlargement/splenomegaly, high/low white cells, failure to resolve/respond to treatment
How can ITP be managed?
self limiting, ITP resolves in around 80% of children with 6 months
medical management:
avoid contact sports
if very low platelets or significant bleeding can consider steroids and platelet transfusion
What is Haemolytic Uraemic Syndrome?
follows infection with the Shiga toxin, commonly associated with E.coli 0157
peaks at 6 months to 5 years
Triad of:
Microangiopathic haemolytic uraemia
Acute kidney injury
Thrombocytopaenia
How will HUS present in the history?
Diarrhoea, which typically turns bloody around day three
Abdominal pain
Fever
Vomiting
make sure you ask about recent exposure to farm animals
What examination findings might there be for HUS?
Abdominal tenderness
Hypertension secondary to acute kidney injury
Small petechiae on the skin can occur due to low platelet count
How may you investigate HUS?
FBC, U&E, CRP, clotting: may show thrombocytopenia, raised WCC, anaemia and acute kidney injury
Urinalysis: to screen for haematuria and proteinuria
Stool cultures: to screen for the presence of E.Coli O157
How can HUS be managed?
supportive care, consider fluids
notifiable disease
How can you differentiate clinically between HSP and HUS?
both present with fever, abdo pain, bloody diarrhoea and a non blanching rash
purpuric rash over extensor surfaces and buttocks in HSP V widespread small petechial rash in HUS
joint pain and haematuria in HSP V not present in HUS
How could you explore a non-blanching rash in a history?
Rash - when did it come on, has it changed over time, is it itchy or sore?
triggers? have they been poorly recently?
high temperature, headache, photophobia, neck stiffness?
abdominal pain, N+V, diarrhoea (bloody? from onset or did it turn bloody?), joint pain? blood in urine?
nose bleeds? (ITP)
any recent exposure to farm animals? (HUS)
B symptoms - ALL!!!
Biliary atresia presents in the first few weeks of life with what symptoms and signs ?
Jaundice extending beyond the physiological two weeks
Dark urine and pale stools
Appetite and growth disturbance, (however, may be normal in some cases)
Hepatomegaly with splenomegaly
Cardiac murmurs if associated cardiac abnormalities present
How should biliary atresia be investigated?
Serum bilirubin : Total bilirubin may be normal, whereas conjugated bilirubin is abnormally high
LFTs including serum bile acids and aminotransferases : usually raised but cannot differentiate causes of neonatal cholestasis
Serum alpha 1-antitrypsin: Deficiency may be a cause of neonatal cholestasis
Sweat chloride test: check for CF
Ultrasound of the biliary tree and liver: May show distension and tract abnormalities
How can biliary atresia be managed? Complications?
Surgical intervention is only definitive tx
Medical intervention includes antibiotic coverage and bile acid enhancers following surgery
Complications :
Unsuccessful anastomosis formation
Progressive liver disease
Cirrhosis with eventual hepatocellular carcinoma
What is Bronchiolitis? Offending pathogen? Presenting features?
acute bronchiolar inflammation
Usually RSV (respiratory syncytial virus)
other causes: mycoplasma, adenoviruses
may be secondary bacterial infection
coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles
feeding difficulties
In which patients is bronchiolitis more likely to be severe?
bronchopulmonary dysplasia (e.g. Premature), congenital heart disease or cystic fibrosis
How can bronchiolitis be investigated and managed?
immunofluorescence of nasopharyngeal secretions may show RSV
Management is largely supportive:
humidified oxygen is given via a head box
nasogastric feeding may be needed if children cannot take enough fluid/feed by mouth
suction is sometimes used for excessive upper airway secretions
Chickenpox is caused by primary infection with varicella zoster virus. How does it present?
fever initially
itchy rash starting on head/trunk before spreading - macular then papular then vesicular
systemic upset is usually mild
infectivity = 4 days before rash, until 5 days after the rash first appeared
How can chickenpox be managed?
keep cool, trim nails
calamine lotion
school exclusion: until lesions have crusted over (usually about 5 days after the onset of the rash)
immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG)
If chickenpox develops then IV aciclovir should be considered
Complications of chickenpox?
Secondary bacterial infection of the lesions - NSAIDs may increase risk, group A strep may cause necrotising fasciitis
pneumonia
encephalitis (cerebellar involvement may be seen)
disseminated haemorrhagic chickenpox
What are the causes of constipation in children?
Idiopathic - most common
dehydration
low-fibre diet
medications: e.g. Opiates
anal fissure
over-enthusiastic potty training
hypothyroidism
Hirschsprung’s disease
hypercalcaemia
learning disabilities
What red flags might suggest an underlying condition as opposed to idiopathic constipation?
Reported from birth or first few weeks of life
Passage of meconium > 48 hours
‘Ribbon’ stools
Abdominal distension
Faltering growth is an amber flag
Previously unknown or undiagnosed weakness in legs, locomotor delay
Signs of maltreatment
Prior to starting treatment for constipation, the child needs to be assessed for faecal impaction. Factors which suggest faecal impaction include:
symptoms of severe constipation
overflow soiling
faecal mass palpable in the abdomen (digital rectal examination should only be carried out by a specialist)
How can children with constipation be managed?
If faecal impaction is present
polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment
Can add a stimulant laxative after 2 weeks if needed
consider regular toileting and non-punitive behavioural interventions
consider asking the Health Visitor or Paediatric Continence Advisor to help support the parents
How can constipation in an infant be managed?
Infants not yet weaned (usually < 6 months)
bottle-fed infants: give extra water in between feeds. Try gentle abdominal massage and bicycling the infant’s legs
breast-fed infants: constipation is unusual and organic causes should be considered
Infants who have or are being weaned
offer extra water, diluted fruit juice and fruits
if not effective consider adding lactulose
Give some features of Cow’s milk protein intolerance/allergy (CMPI/CMPA)
regurgitation and vomiting
diarrhoea
urticaria, atopic eczema
‘colic’ symptoms: irritability, crying
wheeze, chronic cough
rarely angioedema and anaphylaxis
How can cows milk allergy be investigated and managed?
Diagnosis is often clinical (e.g. improvement with cow’s milk protein elimination)
Ix:
skin prick/patch testing
total IgE and specific IgE (RAST) for cow’s milk protein
Mx:
Management if formula-fed =
extensive hydrolysed formula (eHF) milk is the first-line replacement formula
Management if breastfed =
continue breastfeeding
eliminate cow’s milk protein from maternal diet. Consider prescribing calcium supplements for breastfeeding mothers
What is Croup? What is the causative organism? What age group is most commonly affected?
also known as laryngotracheitis
URTI characterised by stridor which is caused by a combination of laryngeal oedema and secretions
Usually caused by parainfluenza virus
typically affects children aged 6 months to 2 years
Presenting features of croup?
stridor
barking cough (worse at night)
fever
coryzal symptoms
How can croup be managed?
single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity
high-flow oxygen
nebulised adrenaline
Coeliac disease is caused by sensitivity to gluten, with repeated exposure leading to villous atrophy which in turn causes malabsorption. Children normally present before the age of 3 years.
What features may the present with?
Features may coincide with the introduction of cereals (i.e. gluten)
failure to thrive
diarrhoea
abdominal distension
older children may present with anaemia
many cases are not diagnosed to adulthood
How is coeliac diagnosed?
jejunal biopsy showing subtotal villous atrophy and crypt hyperplasia
First line blood tests:
Total IgA levels (to exclude IgA deficiency)
Anti-tissue transglutaminase antibodies (anti-TTG)
(anti-endomysial and anti-gliadin antibodies are also useful)
What other conditions are associated with coealic disease?
Down’s syndrome
autoimmune thyroid disease
IDDM
Complications of coeliac disease?
Nutritional deficiencies
Anaemia
Osteoporosis
Hyposplenism
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL)
Non-Hodgkin lymphoma
Small bowel adenocarcinoma
Give some signs of respiratory distress in a child
Raised respiratory rate
Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles
Intercostal and subcostal recessions
Nasal flaring
Head bobbing
Tracheal tugging
Cyanosis (due to low oxygen saturation)
Abnormal airway noises
What is palivizumab?
a monoclonal antibody that targets the respiratory syncytial virus
A monthly injection is given as prevention against bronchiolitis caused by RSV to high risk babies, such as ex-premature and those with congenital heart disease
Most common cause of gastroenteritis in the UK?
rotavirus
What is the usual course of D&V in kids?
diarrhoea usually lasts for 5-7 days and stops within 2 weeks
vomiting usually lasts for 1-2 days and stops within 3 days
What are signs of clinical dehydration in children who have had prolonged D&V?
Appears to be unwell or deteriorating
Decreased urine output
Altered responsiveness (for example, irritable, lethargic)
Sunken eyes
Dry mucous membranes
Tachycardia
Tachypnoea
Reduced skin turgor
Normal peripheral pulses, cap refill and bp
What are signs of shock in children who have had prolonged D&V?
Decreased level of consciousness
Cold extremities
Pale or mottled skin
Tachycardia
Tachypnoea
Weak peripheral pulses
Prolonged capillary refill time
Hypotension
Features suggestive of hypernatraemic dehydration:
jittery movements
increased muscle tone
hyperreflexia
convulsions
drowsiness or coma
When should you do a stool culture in children with diarrhoea?
you suspect septicaemia or
there is blood and/or mucus in the stool or
the child is immunocompromised
consider when:
the child has recently been abroad or
the diarrhoea has not improved by day 7 or
you are uncertain about the diagnosis of gastroenteritis
How should you manage children with D&V who are becoming dehydrated?
give 50 ml/kg low osmolarity oral rehydration solution (ORS) solution over 4 hours, plus ORS solution for maintenance, often and in small amounts
continue breastfeeding
consider supplementing with usual fluids (including milk feeds or water, but not fruit juices or carbonated drinks)
Causes of chronic diarrhoea in infants?
most common cause in the developed world is cows’ milk intolerance
toddler diarrhoea: stools vary in consistency, often contain undigested food
coeliac disease
post-gastroenteritis lactose intolerance
How can you explain toddler’s diarrhoea to a parent? What management would you suggest?
It is thought that some children may have a fast gut transit time (the time it takes for the food to move through the bowel). As part of the role of the bowel is to absorb water, if things more through too quickly, a lot of the fluid
remains in the poo.
avoid sugary drinks and fruit squashes as they can irritate the gut
need enough fat in their diet - slows down movement in the gut, things like rice pudding and full fat milk
What is the commonest cause of vomiting in infancy?
Gastro-oesophageal reflux
Infant < 8 weeks, presents with milky vomits after feeds, often after being laid flat, excessive crying –>
?GORD
How should GORD be managed in infants?
advise regarding position during feeds - 30 degree head-up
ensure infant is not being overfed (as per their weight) and consider a trial of smaller and more frequent feeds
a trial of thickened formula
a trial of alginate therapy e.g. Gaviscon. Alginates should not be used at the same time as thickening agents
Complications of GORD in infants?
distress
failure to thrive
aspiration
frequent otitis media
in older children dental erosion may occur
What organism causes Hand Foot and Mouth Disease? Clinical features? Mx?
coxsackie A16 and enterovirus
mild systemic upset: sore throat, fever
oral ulcers
followed later by vesicles on the palms and soles of the feet
symptomatic mx
reassurance no link to disease in cattle
children do not need to be excluded from school
Most common cause of primary headache in children?
Migraine without aura
Mx of paediatric migraine?
ibuprofen
triptans may be used in children >= 12 years but follow-up is required
What is Intussusception? What features does it present with?
invagination of one portion of the bowel into the lumen of the adjacent bowel, most commonly around the ileo-caecal region
Features:
intermittent, crampy, progressive abdominal pain
inconsolable crying
during paroxysm the infant will characteristically draw their knees up and turn pale
vomiting
bloodstained stool - ‘red-currant jelly’ - is a late sign
sausage-shaped mass in the right upper quadrant
How should intussuception be investigated and managed?
Ix: USS: target like mass
Mx: reduction by air insufflation under radiological control , peritonitis = surgery
What should be done if there are still signs of neonatal jaundice after 14 days ?
a prolonged jaundice screen is performed:
urine for MC&S
FBC, U&Es and LFTs
TFTs
conjugated and unconjugated bilirubin: look for biliary atresia
Direct antiglobulin test (Coombs’ test)
Blood film
What can cause prolonged jaundice (over 14 days)?
prematurity ( immature liver function)
congenital infections e.g. CMV, toxoplasmosis
biliary atresia
breast milk jaundice (jaundice is more common in breastfed babies)
galactosaemia
hypothyroidism
UTI
How can neonatal jaundice be managed?
Phototherapy is usually adequate to correct neonatal jaundice. Extremely high levels may require an exchange transfusion.
Kawasaki disease is a type of vasculitis which is predominately seen in children.
How does it present?
Major complication?
high-grade fever which lasts for > 5 days
conjunctival injection
bright red, cracked lips
strawberry tongue
cervical lymphadenopathy
red palms of the hands and the soles of the feet which later peel
complication : coronary artery aneurysm
How can Kawasaki disease be investigated?
FBC: anaemia, leukocytosis and thrombocytosis
LFTs: hypoalbuminemia and elevated liver enzymes
Inflammatory markers (particularly ESR) are raised
Urinalysis can show raised WCC
Echocardiogram can demonstrate coronary artery pathology
How can Kawasaki disease be managed?
High dose aspirin to reduce the risk of thrombosis
IV immunoglobulins to reduce the risk of coronary artery aneurysms
What is Laryngomalacia?
seen in infants - the supraglottic larynx is structured in a way that allows it to cause partial airway obstruction. This leads to a chronic stridor on inhalation, when the larynx flops across the airway as the infant breathes in
may resolve on its own or rarely requires tracheostomy
How should nappy rash be managed?
disposable nappies are preferable to towel nappies
expose area to air when possible
apply barrier cream (e.g. Zinc and castor oil)
mild steroid cream (e.g. 1% hydrocortisone) in severe cases
management of suspected candidal nappy rash is with a topical imidazole. Cease the use of a barrier cream until the candida has settled
Necrotising enterocolitis is one of the leading causes of death in premature infants. Initial symptoms can include feeding intolerance, abdominal distension and bloody stools.
How can it be investigated?
abdo x-ray
dilated bowel loops (often asymmetrical in distribution)
bowel wall oedema
pneumatosis intestinalis (intramural gas)
portal venous gas
pneumoperitoneum resulting from perforation
air both inside and outside of the bowel wall (Rigler sign)
air outlining the falciform ligament (football sign)
How does neonatal sepsis present?
What causes it?
Grunting and other signs of respiratory distress are the most common presentation
Early-onset neonatal sepsis is most commonly caused by group B streptococcus
Late- onset can be caused by Staphylococcus epidermidis, Pseudomonas aeruginosa, Klebsiella and Enterobacter
How should neonatal sepsis be investigated and managed?
Ix:
- Urine MCS
- FBC, CRP
- Blood culture
- Blood gases: metabolic acidosis is particularly concerning for neonatal sepsis, particularly a base deficit of ≥10 mmol/L
- LP
Mx:
IV benzylpenicillin with gentamicin
How does pyloric stenosis present?
Ix? Mx?
M>F
5-10% Family history in parents
Projectile non bile stained vomiting at 4-6 weeks of life
Diagnosis is made by test feed or USS
Treatment: Ramstedt pyloromyotomy (open or laparoscopic)
How does intestinal malrotation present? Ix? Mx?
High caecum at the midline
bilious vomiting and obstruction (volvulus)
Ix: upper GI contrast study and USS
Mx: laparotomy, if volvulus is present (or at high risk of occurring) then a Ladd’s procedure is performed
How does Slipped upper femoral epiphysis present? Mx?
typically obese male adolescents
pain is often referred to the knee
limitation to internal rotation
Bed rest and non-weight bearing
internal fixation: typically a single cannulated screw placed in the centre of the epiphysis
What is Perthe’s disease? Presenting features?
degenerative condition affecting the hip joints of children (typically 4-8 years) , due to avascular necrosis of the femoral head
hip pain: develops progressively over a few weeks
limp
stiffness and reduced range of hip movement
x-ray: early changes include widening of joint space, later changes include decreased femoral head size/flattening
Complications of Perthe’s disease?
osteoarthritis
premature fusion of the growth plates
How should Perthe’s disease be managed ?
To keep the femoral head within the acetabulum: cast, braces
If less than 6 years: observation
Older: surgical management with moderate results
Operate on severe deformities
Spot diagnosis:
Softening of the cartilage of the patella
Common in teenage girls
Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
Usually responds to physiotherapy
Chondromalacia patellae
Spot diagnosis:
Pain, tenderness and swelling over the tibial tubercle
Seen in sporty teenagers
Osgood-Schlatter disease
(tibial apophysitis)
What can cause a napkin (nappy) rash?
Irritant dermatitis
most common cause, irritant effect of urinary ammonia and faeces, creases are characteristically spared
Candida dermatitis
erythematous rash which involve the flexures and has characteristic satellite lesions
Seborrhoeic dermatitis
erythematous rash with flakes, may be coexistent scalp rash
Psoriasis
erythematous scaly rash also present elsewhere on the skin
Atopic eczema
Other areas of the skin will also be affected
Complications of measles?
otitis media: the most common complication
pneumonia: the most common cause of death
encephalitis: typically occurs 1-2 weeks following the onset of the illness)
How can measles be investigated and managed?
Ix: IgM antibodies
Mx: mainly supportive
notifiable disease → inform public health
What features does measles present with?
prodromal phase:
irritable, conjunctivitis, fever
Koplik spots:
typically develop before the rash
white spots (‘grain of salt’) on the buccal mucosa
rash:
starts behind ears then to the whole body
discrete maculopapular rash becoming blotchy & confluent
desquamation that spares the palms and soles may occur after a week
What organism causes measles? What is the incubation period?
RNA paramyxovirus
infective from prodrome until 4 days after rash starts
incubation period = 10-14 days
How should a non-immunised child be managed if they come into contact with measles?
MMR within 72 hours
Contraindications to lumbar puncture in children with suspected meningitis?
Any signs of raised ICP:
focal neurological signs
papilloedema
significant bulging of the fontanelle
DIC
signs of cerebral herniation
meningococcal septicaemia:blood cultures and PCR for meningococcus instead
What are the potential complications of mumps?
orchitis - occurs four or five days after the start of parotitis
hearing loss - usually unilateral and transient
meningoencephalitis
pancreatitis
How can mumps be investigated and managed?
Ix:
PCR testing on a saliva swab. The blood or saliva can also be tested for antibodies to the mumps virus
Mx:
rest
paracetamol for high fever/discomfort
notifiable disease
What clinical features does mumps typically present with?
fever
malaise, muscular pain
parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%
Mumps is a caused by RNA paramyxovirus and tends to occur in winter and spring. What is the incubation period?
14-21 days
