paeds ILA Flashcards
what is a septic screen?
- blood culture - septicaemia (other bloods to consider = FBC, U&E, CRP, blood gas, coagulation profile, acute phase reactants ESR and CRP)
- urine culture
- stool swab
- CSF - LP unless contraindicated
- chest XR if indicated
why is a septic screen performed?
To identify the cause of infection – because in children often the come in with a temperature with no focus
how would bacterial meningitis show in the CSF?/
- cloudy and turbid
- opening pressure would be elevated
- WBC elevated >100cell/uL
- low glucose level (<40% of serum glucose level)
- protein level will be elevated
what are the common causes of meningitis in newborns and in older children?
newborns: listeria monocytogenes, E.coli, Group B streptococci
Older children: Neisseria meningitides, haemophilia influenza type B
how would viral (aseptic meningitis present in the CSF?
- appearance - clear
- opening pressure - normal or elevated
- WCC - elevated (primarily lymphocytes)
glucose level - normal
protein level - elevated (>50mg/dl)
if there was predominantly polymorphonuclear leukocytes/neutrophils in the CSF what would it suggest?
bacterial meningitis
if it was predominantly lymphocytes in the CSF what would it suggest?
viral meningitis
if there was a HSV meningitis what would you see that was different to CSF in other viral meningitis?
the glucose may be low where as usually it is normal
what are the causes of viral meningitis?
herpes simplex virus enterovirus varicella zoster virus mumps HIV adenovirus
what would you see in CSF of someone with fungal meningitis?
appearance - cloudy or clear opening pressure elevates WBC elevated 10-500 cells/uL glucose low protein elevated
what are the causes of fungal meningitis?
cryptococcus neoformans
candida
hoe would TB meningitis show on CSF?
appearance - opaque, if left to settle it forms a fibrin web
opening pressure elevated
WBC - elevated - early PMNs and then mononuclears
glucose level - low
protein level - elevated
The microbiologist rings to confirm a CSF white cell count of 500 with no red cells. The cells are predominantly neutrophils. CSF glucose is low and CSF protein raised. Gram film shows gram negative diplococci.
Later, Jon becomes hypotensive with a delayed capillary refill time, and develops tachycardia and a purpuric rash.
diagnosis?
meningococcal septicaemia with meningitis
what is the immediate management of meningococcal septicaemia with meningitis?
ABCDE approach A - airway B - breathing C - circulation, IV access, bloods, fluid bolus, antibiotics D - disability - AVPU E - environment - temp and glucose
if a child presents with meningococcal septicaemia shock what fluids would you prescribe?
20mls/kg 0.9% sodium chloride fluid bolus over 10 mins
if no improvement then repeat but this can lead to pulmonary oedema
what fluid bolus would you give in trauma or DKA?
10ml/kg 0.9% sodium chloride over 10 minutes
what antibiotics should be given for meningococcal septicaemia?
third gen cephalosporin e.g. IV ceftriaxone
it is able to cross the blood brain barrier and it is a broad spectrum antibiotic with activity again gram positive and negatives to cover most likely organisms
if under 3 months give cefotaxime
what causes the purpuric rash in meningitis?
they are caused by bleeding underneath the skin
caused by DIC
consumptive coagulopathy
bacteraemia leads to widespread thrombosis in microvassaculature, platelets being used up and clotting factors not being produced by liver which leads to bleeding tendancy
what measures should be taken to stabilise and manage a patient with meningococcal septicaemia?
airway and breathing management - intubation and ventilation
circulation - fluid bolus/fluid management
vasoactive agents - vasosupressors and inotropic agents
how would meningitis be spread?
exchange of respiratory secretions
what is the first line treated that is recommended to reduce the risk of meningitis in those who have been in close contact with someone who has had it?
prophylactic treatment with rifampicin or ciprofloxacin to eradicate nasopharyngeal carriage - for meningococcal
flu vaccination for those with Hib infection
what is classified as close contact when conisdering prophylaxis for meningitis?
those who have prolonged close contact with the case in a household type setting during seven days before the onset of the illness
e.g. living/sleeping in same household, pupils in same dorm, boyfriend/girlfirend, uni students sharing kitchen in halls
when should rifampicin be avoided?
people with severe liver disease
should try to be avoided in those who are on medication for epilepsy
- it is fine in breast feeding
what are the side effects of meningococcal prophylaxis?
Side effects of ciprofloxacin – common – diarrhoea, dizzieness, headache, nausea and vomiting.
Side effects of rifampicin – hepatitis, orange urine and tears, interaction the with contraceptive pill, flu like symptoms.
Laura, a two year old, presents to her general practitioner with a two month long history of malaise, pallor and reduced appetite. She has occasional febrile episodes, associated with a pink rash, and with a persistent complaint of soreness in her left thigh. Despite walking at the age of 13 months, she is now reluctant to weight bear. Her birth and development history show no concerns and all her immunisations are up to date.
what aspects of clinical examination are important?
full clinical examination - particularly CVS, euro, gastro, skin
fundoscopy - to check for uveitis
height and body weight
Laura, a two year old, presents to her general practitioner with a two month long history of malaise, pallor and reduced appetite. She has occasional febrile episodes, associated with a pink rash, and with a persistent complaint of soreness in her left thigh. Despite walking at the age of 13 months, she is now reluctant to weight bear. Her birth and development history show no concerns and all her immunisations are up to date.
low grade fever and generalised cervical lymphadenopathy, walks with a limp but no discomfort - rest of examination pretty much unremarkable.
DD??
what further tests would you want to perform?
transient synovitis - very common
infection (osteomyelitis, septic arthritis)
malignancy (leukaemia, lymphoma, neuroblastoma)
connective tissue disorder (SLE, RA)
juvenile idiopathic arthritis
Bloods
Xray/USS of limb
echo
what is juvenile idiopathic arthritis?
Systemic onset – rash, temp
Oligoarthritis (less than 4 joints) JIA more common – more common in girls
When you are thinking about if a child has JIA then test for their ANA +ve because in increases their risk of chronic anterior uveitis.
there will be raised ESR
JIA - rash that comes on with temp and inflammation of the synovium
in children with JIA who is common to develop uveitis?
girls
under 7 years, especially if under 4 years
oligoarticular subtype
antinuclear antibody (ANA) positive on blood tests
how is JIA managed?
it a chronic childhood disease so needs an MDT
NSAIDs for early therapy - pain relief, anti-inflammatory and anti pyretic
Longterm - DMARD (disease modifying anti-rheumatic drug - methotrexate
2nd line - TNF alpha inhibitors e.g. infliximab
alternatives - intra-articular corticosteroid injections - if only a few joints affected, systemic corticosteroids, cytokine modulators
teams involved - paediatric rheumatologist, nurses, physics, OTs, social workers, paediatric opthalmologist, dietician, school lesion workers, GP, child psychology
Jirou, a three year old boy presents with a seven day history of high fevers. He has now developed red eyes, a rash and is complaining of a sore mouth and throat.
On examination he appears miserable and unwell with a diffuse maculopapular rash mainly on his torso. He has bilateral injected conjunctiva, red cracked lips and a strawberry tongue. He has a unilateral 3cm x 2cm cervical swelling, and swollen reddened palms.
DD?
Scarlet fever – group A beta haemolytic strep
Measles
Toxic shock syndrome caused by staphylococcal toxins
Staphylococcal scolded skin syndrome – fluid filled blisters
Kawasaki disease
what is Kawasaki disease and what criteria are used to diagnose it?
Kawasaki disease- a systemic vasculitis, common in children of a Japanese origin
Criteria
the presence of a fever for five days plus four of the five criteria constitutes Kawasaki disease
MY HEART
M- mucosal involvement - dry lips and strawberry tongue
H - hands and feat with oedema and desquamation
E - eyes - non-perulent conjunctivitis
A - adenopathy - unilateral, cervical
R - rash usually truncal and pleomorphic
T temp non remitting for at least 5 days
what is the management of Kawasaki disease? and complications of the treatments?
IV Immunglobulin in the first 10 days and aspirin (to reduce risk of thrombosis)
IVIG- anaphylaxis, renal failure, headache, myalgia, N&V
Aspirin - reyes, bleeding/bruising, GI upset
children with giant coronary aneurysms may require long term warfarin
what further investigations would you perform for Kawasaki disease?
echo - to look for coronary artery aneurysm
magnetic resonance angiography
cardiac catheterisation and angiography
what is the long term prognosis of Kawasaki disease?
- usually an acute, self limiting illness,
- overall mortality is less than 0.05%
- if left untreated it can be associated with significant morbidity and mortality
- IVIG immediately improves outcome
what is the emergency management of an unwell child with 5% dehydration?
A - intubation if needed
B- 100% oxygen
C - perfusion, blood sample, HR, BP, fluids
Blood investigations
what would be suggestive of DKA and so not to give normal fluid bolus?
if the child had been drinking a lot and peeing a lot
child is 5% dehydrated with DKA - what fluids do you give them?
only give fluid bolus if necessary - 10mls/kg 0.9% sodium chloride
deficit: assume 5% deficit if pH >7.1, assume 10% deficit if pH below 7.1 - give deficit fluids over 48 hours
10% deficit - 100mls/kg
5% deficit 50mls/kg
DKA reduced maintenance volume rues
<10kg - 2ml/kg/hour
10-40kg - 1mls/kg/hour
>40 kg - 40mls/hour
*ensure all fluids contain potassium chloride apart from bolus
in someone with DKA when should you start insulin
1-2 hours after fluid administration
0.05-1 unit/kg/hour
monitor - cap blood glucose, vital signs, fluid balance, level of consciousness
some one with DKA, their blood glucose is now <14, how do you manage?
if ketones <3: 0.9% NS, glucose 5%, KCL 20mmmol in 500ml and maintain or reduce insulin 0.05 unit/kg/hour
ketones >3: glucose 10%, KCL 20 mol in 500ml and maintain insulin at 0.05-0.1 unit/kg/hour
what are the complications of DKA management?
hypoglycaemia, hypokalaemia, hpoxaemia, pulmonary oedema
cerebral oedema is a rare but potentially fatal complication - avoid rapid fluid and electrolyte replacement
what are the symptoms of DKA?
increased thirst, polyuria, recent unexplained weight loss or excessive tiredness along side any of the following symptoms
- nausea and vomiting
- abdominal pain
- hyperventilations
- dehydration
- decreased level of consciousness
10 day old neonate with TSH very high? what is the likely diagnosis?
congenital hypothyroidism
what are the most likely causes of congenital hypothyroidism?
world wider - iodine deficiency
in the uk - dysgenesis thyroid gland defects - a missing or ectopic or poorly developed thyroid gland
consanguineous (cousins) (dyshormonogeneis) - a problem with the hormone production line
how can you distinguish between dygenesis and dyshormonogenesis causes of congenital hypothyroid?
radioisotope and USS examination
what is the screening for congenital hypothyroid and what has this helped prevent?
Guthrie test
prevents cretinism - stunted mental and physical growth
what does the Guthrie test screen for?
congenital hypothyroidism
sickle cell disease
CF
inherited metabolic diseases
how is congenital hypothyroidism managed?
thyroxine - levothyroxine
what are the differentials for an unwell neonate (collapsed and shocked)?
sepsis/infection congenital heart defects surgical emergencies inborn errors of metabolism congenital adrenal hyperplasia
what would you see on investigations for CAH?
hyponatremia hyperkalemia hypoglycaemia acidosis elevated hydroxyprogesterone rapid ACTH stimulation test plasma renin-aldosterone
how would a baby girl with CAH present?
ambiguous genitalia
could CAH be managed antenatally?
hoe is CAH managed subsequently?
dexamethasone
glucocorticoid (hyrdrocortisone) and mineralocorticoid (fludrocortison) with sodium chloride supplementation
how do males with CAH present?
they usually present with a neonatal salt losing crisis - usually within the 1st 4 weeks of life
long term complication of meningitis (always comes up in exams)
SENSORINEURAL DEAFNESS
