Paeds 2 - GU/Neuro/Endocrine/Haem etc Flashcards
what are 5 clinical features a urinary tract anomaly might present with?
UTI recurrent abdo pain palpable mass haematuria failure to thrive
how are urinary tract anomalies usually diagnosed?
antenatal USS - good as allows early treatment to avoid progressive renal damage
list some of the key urinary tract anomalies
- renal agenesis
- kidney dysplasia (MCDK)
- PKD (polycystic kidney disease - both autosomal recessive and dominant)
- tuberous sclerosis
- pelvic/horseshoe kidney
- duplex kidney
- bladder extrophy
- absent musculature syndrome
- obstructions - e.g. congenital hydronephrosis
what is renal agenesis and what does it result in?
absence of both kidneys –> Potter syndrome, in which oligohydramnios (due to lack of foetal urine) is associated with lung hypoplasia and postural deformities)
what is MCDK?
multicystic dysplastic kidney - failure of the union of the ureteric bud with the nephrogenic mesenchyme - kidney is non-functioning, with large fluid filled cysts, no renal tissue and no connection to bladder.
Potters syndrome if bilateral.
if unilateral - they’re fine, got a spare!
what are the main cystic kidney anomalies and how do they affect a patient?
autosomal recessive and autosomal dominant polycystic kidney disease
tuberous sclerosis
some/normal kidney function maintained (but always affects both kidneys).
hypertension and haematuria in kids, renal failure in adults.
what is pelvic/horseshoe kidney?
abnormal caudal migration, so lower poles of each kidney are fused in midline.
abnormal position means increased risk of infection/obstruction.
what is a duplex system (urinary tract anomaly)?
premature division of ureteric bud - varies in the extent, might have a bifid renal pelvis, might have complete division with two separate ureters (from one kidney).
lower pole ureter often refluxes, upper pole ureter often ectopic (draining into urethra or vagina).
where are the main sites for obstructive lesions of the urinary tract (in babies)?
pelviureteric (PU) junction
vesicoureteric (VU) junction
bladder
urethra
if an obstructive lesion of the urinary tract isn’t picked up antenatally, how might it present?
UTI
abdo/loin pain
haematuria
palpable bladder or kidney
what causes congenital hydronephrosis?
a pelviureteric obstruction - by a narrow lumen or compression by fibrous band or blood vessel, can vary from partial –> almost complete obstruction
mild obstruction can resolve spontaneously but if severe need surgery with conservation of renal tissue where possible
what causes vesicoureteric obstruction?
stenosis, kinking or dilatation of lower part of ureter.
may be unilateral or bilateral.
there’s a combo of hydroureter and hydronephrosis.
what is primary vesicoureteric reflux and what causes it?
reflux of urine from bladder into ureter (or if severe, all the way back to kidneys).
due to developmental anomaly of vesicoureteric junction where ureters enter directly into bladder instead of at an angle, and the bit of ureter in bladder is abnormally short.
during voiding, urine goes back up the ureter - risk of infection, hits kidneys with bacteria and high pressure.
what are the clinical features of vesicoureteric reflux?
associated w/ other GU anomalies, may be secondary to bladder pathology.
- get lots of UTIs
- when they get UTI, it’s severe ± pyelonephritis
- reflux nephropathy = destruction of renal tissue because of infection and back pressure - can get hypertension and renal failure
how is vesicoureteric reflux diagnosed?
MCUG - micturating cystourethrogram
how is vesicoureteric reflux managed?
if mild - resolves spontaneously, but prophylactic trimethoprim until child is infection-free, normal bladder control and >5 years.
if severe or prophylaxis fails = surgery.
investigate siblings!
what is phimosis and how is it treated?
adhesion of foreskin to glans penis after age 3 years.
mild = daily stretching routine (retraction)
some say topical corticosteroids may help.
circumcision if not.
what is a hypospadia and how is it treated?
abnormal position of external urethral meatus on the ventral penis - causes difficulty urinating while standing / cosmetic.
surgery, use foreskin for repair preschool.
what pathogens typically cause UTIs in children?
mostly E. coli (from bowel flora).
also - Proteus, Klebsiella, Pseudomona and Enterococcus
what is the most common predisposing factor to UTI in children?
urinary stasis (lack of flow) due to:
- vesicoureteric reflux
- obstructive uropathy (ureterocele, urethral valves)
- neuropathic bladder (spina bifida)
- habitual infrequent voiding
up to 50% of kids with UTI will have underlying structural anomaly!
how does UTI present in neonates/very young infants?
might see jaundice.
septicaemia develops quickly - leading to shock and hypotension.
how does UTI present in infants?
non-specific symptoms
fever (but can have without), diarrhoea, vomiting, lethargy/irritability, failure to thrive/poor feeding, jaundice, sepsis etc
may see febrile convulsions if over 6 months old.
how does UTI present in a young child (1-5yrs)?
dysuria and frequency, nocturnal enuresis, fever, malaise, abdo pain. may see febrile convulsions.
DDx - balanitis / vulvovaginitis
how does UTI present in a child (>5yrs)?
classic cystitis features - frequency, dysuria, fever, enuresis
or pyelonephritis features - fever and loin pain. if <6y may see febrile convulsions.
NB - asymptomatic bacteruria common in school-age girls, don’t bother treating.
how should urine samples be collected from kids?
need a CLEAN CATCH - can use catheter/suprapubic aspiration if seriously ill.
bag sometimes used - not useful really as usually contaminated.
MSU can be used for older kids.
for young kids/infants basically parents have to sit around with nappy off and try and catch in a cup!
how should you investigate a child with suspected UTI?
send off urine sample for MC+S
controversial to follow up investigate for cause of UTI - moving towards only kids with recurrent/atypical UTI - for them do:
renal and urinary tract USS
±
MCUG (micturating cystourethrogram) - for vesicoureteric reflux
DMSA (static radioisotope scan) - looks for renal scarring
how would you manage a child under three months with a UTI?
needs hospital admission and IV abx e.g. ampicillin plus gentomycin/cefuroxime
how would you manage a child systemically unwell with a UTI, with signs of pyelonephritis and high fever (38+)?
IV abx e.g. ampicillin plus gentomycin/cefuroxime for 7-10 days
(might be able to give orally/switch to oral)
how would you manage a child with a UTI, no signs of pyelonephritis, not seriously unwell?
oral abx for 3 days - trimethoprim can be used
what advice might you give to prevent recurrence of UTI in a child?
lots of fluids, regular voiding, ensure complete emptying (double micturition), treat constipation, good perineal hygiene, probiotics
what is enuresis, how is it classified into different types?
defined as involuntary discharge of urine at an age when continence has been reached by most children (5y for girls, 6y for boys).
split into primary and secondary - primary when child has never been continent for a period of 3+ months.
nocturnal vs diurnal - nocturnal only at night, diurnal during day.
what might cause daytime enuresis?
lack of attention to bladder sensation (developmental or psychogenic) detrusor instability bladder neck weakness neuropathic bladder UTI constipation ectopic ureter (constant dribble)
how would you investigate and manage a child brought into general paeds clinic due to daytime enuresis?
examine and take sample for MC+S, consider USS.
use of star charts, bladder training, pelvic floor exercises.
might use moisture activated alarm with a pad, placed in pants - activated by urine, useful if there’s a lack of attention to bladder sensation.
last resort - oxybutynin (anticholinergic)
list some organic causes of nocturnal enuresis
UTI polyuria due to DM/chronic renal failure neuropathic bladder genital abnormalities faecal retention causing bladder neck dysfunction
what must you be aware of if a child presents with secondary nocturnal enuresis?
it can be due to emotional/stress causes - beware of neglect/abuse
what must be included in an examination and investigation of a child presenting with enuresis?
review growth, measure BP to identify renal failure.
careful abdo palpation to exclude enlarged bladder
inspect genitalia.
inspect spine and overlying skin for deformity, hairy patch, sinus - examine lower limb neurology thoroughly.
urine sample - urinalysis (proteinuria and glycosuria), MC+S.
describe some general measures that can be used to help manage a child presenting with nocturnal enuresis
reassure, explain how bladder works. discourage parental intolerance. identify ‘functional payoffs’ e.g. gets to sleep in parents bed after bed-wetting - stop doing this.
diary of wetting for at least 4 weeks.
star charts and praise etc.
use of pad alarm if not improving and over 7y - requires a lot of compliance and motivation but can be quite effective.
how would nocturnal enuresis be pharmacologically managed?
last resort!!
desmopressin - synthetic analogie of anti-diuretic hormone - effective short-term relief, but most don’t stay dry once it’s stopped.
oxybutynin used to same effect as well.
what is the most common cause of acute paediatric renal failure and what organism is it associated with?
HUS - haemolytic uraemic syndrome
E. coli (specific strain) - produces a verocytotoxin (Shiga toxin)
briefly explain the pathology of HUS
diarrhoea - infected with E coli that produces Shiga toxin - this floats around body, causing damage to endothelial layers, mostly in renal, GI and central nervous systems.
thrombin and fibrin are deposited in vasculature early on.
RBCs get damaged trying to squeeze through narrow vessels - haemolysis.
how is HUS managed?
supportive - 90% of kids will recover full renal function.
abx contraindicated.
what is the triad associated with HUS?
- microangiopathic haemolytic anaemia (Coombes’ test negative)
- thrombocytopaenia
- AKI
NB - notifiable disease
how does HUS classically present?
hx of profuse diarrhoea that turned bloody after a few (1-3) days.
then abdo pain, fever and vomiting.
have proteinuria and haematuria
what investigations would you do if you suspected HUS?
urinalysis - proteinuria or haematuria
FBC and film - haemolyisis, anaemia and thrombocytopaenia
Renal function and electrolytes - failing kidneys with haemolysis and thrombocytopaenia = early onset of HUS
Lactate dehydrogenase = high LDH is an early sign of HUS
Stool culture
LFTs/CRP/clotting screen
what might indicate a child is going into AKI?
rapid rise of creatinine or oligouria/anuria
list some common causes of AKI in children in the developed vs developing world
developed - secondary to cardiac surgery, bone marrow transplant, drug toxicity (NSAIDs, aminoglycosides, vancomycin), sepsis
developing - diarrhoea/dehydration, glomerulonephritis, HUS
what investigations would you do if you think a child has gone into AKI?
blood chemistry (raised K+, creatinine, phosphate, lowered calcium, sodium, chlorine). MSU - check for red casts (glomerulonephritis) abdominal USS - any structural/surgical causes
how do you manage a child in AKI?
get paeds nephro team in ASAP!
treat shock and dehydration - oliguria will hopefully resolve with rehydration, try a diuretic as well if note (furosemide).
monitor BP (might be hypertensive)
monitor ECG (potassium levels, DON’T GIVE POTASSIUM)
haemofiltration (usually preferred over dialysis)
give some causes of chronic renal failure in kids
congenital dysplastic kidneys pyelonephritis glomerulonephritis recurrent infection reflux nephropathy AKI leading to cortical necrosis
what are the clinical features of chronic renal failure in a child?
weak, tired, vomiting, haedache, restless, twitching, hypertensive retinopathy, anaemia, failure to thrive, seizures, coma
how is chronic renal failure managed in children?
dialysis/haemofiltration
be aware of - nutrition (get dietician’s help), acidosis, renal osteodystrophy (disease involving poor mineralization due to renal failure, bit like rickets - pain, deformity etc), anaemia
what are the characteristic features of nephritic syndrome?
- fluid retention (oedema, puffy face)
- hypertension
- haematuria
- proteinuria
what causes most cases of nephritic syndrome? give some less common causes too
most cases are post-infectious - follow strep throat or skin infection with Group A beta-haemolytic strep.
others - HSP, IgA nephropathy, SLE, mesangiocapillary glomerulonephritis, Alport syndrome
how does nephritic syndrome present?
cloudy/smoky urine due to proteinuria + haematuria. may have progressed to oligouria.
oedema and raised BP on examination
how is nephritic syndrome diagnosed?
urinalysis = blood and protein
microscopy of urine = red cells and casts.
other Ix’s - assess renal function via bloods. might do abdo XR or US to exclude causes of haematuria.
throat swab, anti-DNAse B, complement C3 levels and biopsy - all to assess cause.
what features in a question would make you think of nephritic syndrome?
about 7 years old, haematuria and oliguria, raised BP, periorbital oedema, post streptococcal infection
how do you manage a kid with nephritic syndrome?
- control fluid and electrolyte balance by monitoring intake and output
- use of diuretics and antihypertensives as needed
- generally good prognosis (esp. if post strep)
rarely you will get a rapidly progressing glomerulonephritis with renal failure.
how does HSP present?
palpable purpura - small red/purple spots on extensor surfaces of legs/arms/buttocks - rash develops over several days
GI disturbance (in 50% patients) - colicky abdo pain, melena
arthritis (75% of patients)
glomerulonephritis (50% of patients) - haematuria, proteinuria, red cell casts
describe the pathology of HSP
IgA complexes deposited in small vessels –> complement activation
often follows respiratory infection
how is HSP usually diagnosed and treated?
typically a clinical diagnosis
can biopsy and see IgA deposits on small vessels - if renal disease, consider kidney biopsy.
Rx is supportive/symptomatic - steroids relieve joint pain and swelling (NO affect on course of disease though)
what is Alport syndrome?
group of inherited, progressive haematuric nephropathies that can also affect cochlea (sensorineural deafness) and eye (lenticonus, dot-and-fleck retinopathy)
can cause nephritic syndrome.
Rx - none really, will need kidney transplant in the end.
what is nephrotic syndrome, what’s its triad?
glomerular disorder, presents with classic triad:
- heavy proteinuria
- oedema
- low plasma albumin
how does nephrotic syndrome present?
insidious onset of oedema - puffy eyes, swelling of feet and legs, the more generalised.
frothy urine.
how do you investigate a kid with suspected nephrotic syndrome?
urinalysis - frothy, albuminous, possibly red cell casts.
bloods - low albumin
renal biopsy - do in older kids with haematuria, hypertension, raised urea, treatment ‘failure’
how is nephrotic syndrome classified?
steroid sensitive
steroid dependant
steroid resistant
how is nephrotic syndrome diagnosed?
documentation of PROTEINURIA and HYPOALBUMINAEMIA (<25g/L)
how do you manage a child with nephrotic syndrome?
oral prednisolone, 60mg/m2/day
remission occurs within 10 days, dose is then tapered.
steroid resistance defined as no remission after 4 weeks.
monitor fluid balance.
prophylactic penicillin V (aka penicilliamine) during acute phase to prevent secondary infection
what are the possible complications of nephrotic syndrome?
- hypovolaemia
- thrombosis
- secondary infection
- hyperlipidaemia (not really a problem in kids)
what is the most common cause of nephrotic syndrome? give other causes
minimal change disease
congenital nephrotic syndrome, focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis
what atypical features would make you consider referral and renal biopsy in a child with nephrotic syndrome?
Age < 1 year or > 12 years Hypertension Impaired renal function Frank haematuria Steroid resistant nephrotic syndrome
what is developmental dysplasia of the hip (DDH)?
perinatal hip instability resulting in progressive malformation of the hip joint.
spectrum of disorders - dislocated hips, hips with varying degrees of acetabular dysplasia (femoral head in place but acetabulum is shallow)
how is DDH usually picked up / how does it present?
NIPE - Barlow and Ortolani manouevres.
repeated at 6 week check.
after that - presents with painless limp, sometimes presents as delayed walking.
give some clinical features of DDH, apart from limp?
asymmetrical skin folds around the hip, limited abduction of hip, shortening of affected leg (short femur = Allis sign)
give some risk factors of DDH
- congenital muscular torticollis
- congenital foot abnormalities
- breech or caesarean delivery
- family history
- neuromuscular disorders
- female sex
how is DDH diagnosed?
USS of the hip - often done in high risk babies anyway as clinical screening not especially effective
(UK used to do any risk factor, now mostly does it for breech babies/those with FHx)
how should you manage a baby with suspected DDH?
discuss with orthopaedics, request USS hip.
if under 8 months - use of splint/harness to keep hip flexed and abducted.
will need op if presented late - will probably also need hip replacement as adult.
what is scoliosis and how is it classified?
lateral curvature of the spine associated with a rotational deformity.
classified (by cause) into:
vertebral abnormalities (hemivertebra, osteogenesis imperfecta)
neuromuscular (polio, cerebral palsy)
miscellaneous (idiopathic, dysmorphic syndromes)
how does idiopathic (most common type) scoliosis present?
in adolescence, more common in girls.
painless curvature of spine, thoracic rotation causing a “rib hump” when bending forward.
how is idiopathic scoliosis managed?
mild = should resolve itself moderate = back brace severe = surgery, fuses spine
what is torticollis? what is the most common cause in infancy?
“wry neck” - neck is fixed to one side.
in infants - sternomastoid tumour, palpable as mobile non-tender nodule within sternomastoid muscle, in first few weeks of life.
in young kids can be self-limiting to do with URTI.
how is torticollis managed?
usually resolves by 1 year.
passive stretching of neck can help.
what is osteomyelitis?
infection of the metaphysis of long bones, usually the distal femur/proximal tibia
what causes osteomyelitis?
haematogenous spread of pathogen from elsewhere in body e.g. infected wound.
stasis of blood in metaphysis so infection starts there.
what are the common pathogens in osteomyelitis?
Staph aureus
also - group B strep, E coli (in neonates)
how does osteomyelitis present?
painful, immobile limb in child with acute febrile illness -refusal to move affected limb.
directly over infected site = swelling, exquisite tenderness. erythematous and warm.
what investigations would you do for a child with osteomyelitis?
blood cultures (may also aspirate bone) white cell count and CRP (both raised) XR - initially will be normal, after 7-10 days will see subperiosteal bone rarefaction. bone scans can be more useful than XR as will show changes earlier.
how would you manage a child with osteomyelitis?
early Rx with IV abx - until clinical improvement and normalising of acute phase reactants.
then weeks of oral abx.
if don’t respond - surgical drainage.
rest limb in splint initially, then mobilise.
what is transient synovitis?
irritable hip - self-limiting condition occurring in children age 2-12 years following viral infection
how does transient synovitis present?
sudden onset hip pain, limp, refusal to bear weight on affected side.
no pain at rest, decreased range of movement (esp internal rotation).
afebrile, well child.
how do you treat transient synovitis?
bed rest - make sure to differentiate it from septic arthritis though!
what is Perthes’ disease?
avascular necrosis of capital femoral epiphysis of the femoral head
due to interruptions of blood supply - avascular necrosis causes flattening and fragmentation of femoral head.
followed by revascularisation and reossification over the next 18-36 months, normal growth resumes.
results in growth disturbance - may remain abnormal even after recovery.
affects mainly boys age 5-10.
what are the clinical features of Perthes’ disease?
insidious onset of limp between ages 3-12 years (mostly age 5-7).
pain (might be intermittent) can be felt in hip, thigh or knee. minority of cases are bilateral.
limited abduction and rotation.
what is slipped upper femoral epiphysis (SUFE) and when does it occur?
progressive posterior and medial translation of the femoral head on the femoral neck through the epiphysis
occurs during adolescent growth spurt - most common in boys age 10-15yrs
how does SUFE present and how is it managed?
limp and/or hip/referred knee pain.
diagnose by XR.
manage - surgery, pinning of femoral head or osteotomy
what is septic arthritis?
purulent infection of a joint space, can lead to joint destruction, usually from haematogenous spread (or can spread from osteomyelitis, puncture wounds or infected skin lesions), most commonly kids < 2 yrs.
what pathogens are usually responsible for septic arthritis?
staph aureus
occasionally H influenzae prior to vaccination.
how does septic arthritis present?
erythematous, warm, acutely tender joint (usually only 1, often hip in infants, knee in older child). reduced range of movement. acutely unwell febrile child.
child will be irritable, refuse to bear weight, infants hold limb rigid.
how would you investigate septic arthritis?
raised white cell count and CRP.
blood cultures.
aspirate joint and culture (ideally before abx!)
USS can identify effusions, XR often normal to begin with.
how would you manage a child with septic arthritis?
early and prolonged IV abx needed.
surgical drainage/washout if recurrent/affecting hip.
what is Osgood-Schlatter’s disease?
self-limiting condition of the knee in sporty adolescents.
occurs in growth spurt, basically quads contracting loads is stronger than tibial tuberosity (as it’s immature) - lots of tiny fractures of that results in enlarged tubercle (due to healing of the tiny fractures)
how does Osgood-Schlatter’s disease present and how is it managed?
gradual onset pain and swelling below the knee, improved with rest and worse on exercise.
O/E - pain invoked by knee extension against resistance, or knee hyperflexion.
management - rest, ice, physio, analgesia - self-limiting (2-3 weeks)
what is osteogenesis imperfecta? how is it managed?
genetic disease causing brittle bones.
mutation in type I collagen genes.
fragile bones and frequent fractures.
Rx - genetic counselling of parents, orthopaedic treatment of fractures
what are the 4 forms of osteogenesis imperfecta?
I - most common, autosomal dominant. recurrent fractures, blue sclerae, conductive hearing loss.
II - severe and lethal, multiple fractures before birth. autosomal recessive.
III - severe bone fragility but no blue sclera, don’t normally live to adulthood, autosomal recessive.
IV - mild, only bone fragility, later onset
what is rickets?
vitamin D deficiency leading to inadequate mineralisation of bone matrix. results in bowing of legs, enlarged metaphyses, craniotabes (soft skull), plus developmental delay and growth failure.
how is rickets diagnosed and treated?
XR imaging and blood biochemistry
XR wrist shows cupping and fraying of metaphysis and widened metaphyseal plate.
vitamin D3 supplements.
what is juvenile idiopathic arthritis (JIA)?
persistent joint swelling (>6 weeks) presenting before 16 years of age, in the absence of infection or any other defined cause
explain the subtypes of JIA
7 (some books say 8) subtypes, according to no. joints involved in first 6 months, also divided by presence of rheumatoid factor and HLA B27 type.
3 key subtypes = oliogoarticular (1-4 joints), polyarticular (>4 joints), systemic (variable no. joints, presence of fever and rash).
what features of a joint issue history would make you consider JIA?
gelling - stiffness after periods of rest
morning joint stiffness
pain
if young child - may have intermittent limp, or deterioration of mood/avoidance of previously enjoyed activities
what causes the joint swelling seen in JIA? if left untreated what complications may occur?
swelling is due to fluid, inflammation and (chronically) proliferation of synovium.
if untreated - bone expansion leads to leg lengthening or valgus deformity (knock knees), discrepancy in digit length etc
describe the general management of JIA
education, physio, ophthamology visits (anterior uveitis), NSAIDs, joint injections, methotrexate, steroid, biologics
what are the features of a tension headache?
symmetrical headache of gradual onset - tightness, band etc
what are the features of a migraine?
with or without aura lasts 1-72h often bilaterally pulsatile over temporal or frontal area often w/nausea, vomiting, abdo pain, photophobia
give some causes of headaches in children
primary: tension, migraine
secondary:
- raised ICP/SOL
- head/neck trauma
- vascular malformation, intracranial haemorrhage
- substance use/withdrawal
- visual acuity issues
- infection - meningitis/encephalitis
- hypercapnia, hypertension
- acute sinusitis
- psychiatric
what features of a headache would make you worry about raised ICP/SOL?
- worse when lying down (first thing in AM)
- morning vomiting
- night-time waking
- accompanying change in mood/personality etc
also:
visual field defects, CN abnormalities (new squint etc), abnormal gait, torticollis, growth failure, papilloedema
what are febrile seizures? what age group do you see them in?
seizure accompanied by a fever, in absence of intracranial infection (e.g. bacterial meningitis, viral encephalitis)
age 6 months –> 6 years
usually occur early in a viral infection when the temp is rising rapidly
usually generalised tonic-clonic seizures
how would you manage a child who’s had a febrile seizure?
investigate infection, usually viral so just supportive treatment (e.g. paracetamol to control fever)
can give buccal midazolam or rectal diazepam if fitting is prolonged (>5 mins)
what are “breath-holding attacks”?
occur when a child is crying, holds their breath and goes blue - might lose consciousness but will recover quickly.
not really a problem tbh
what are reflex anoxic seziures?
triggered by pain/discomfort (esp from minor head trauma), cold food, fright or fever.
after trigger, child goes very pale and falls to floor.
hypoxia may then induce a generalised tonic-clonic seizure
list some causes of faints/fits/funny turns that AREN’T epilepsy
breath holding attacks reflex anoxic seizures febrile convulsions syncope migraine benign paroxysmal vertigo cardiac arrhythmia non-epileptic attack disorder
what is the difference between epilepsy and an epileptic seizure?
epilepsy is a chronic disorder featuring abnormal neuronal activity + neurological signs/symptoms
an epileptic seizure is a transient episode of abnormal and excessive neuronal activity in the brain.
briefly explain how epilepsy is classified
divided into generalised vs partial/focal
generalised = arises from both hemispheres
partial/focal = only one/part of one hemisphere
partial then split into simple (consciousness retained) and complex (consciousness is impaired/lost)
generalised is then split into: absence seizures myoclonic clonic tonic tonic-clonic atonic
how would you investigate and diagnose a child with two or more previous seizures?
take a thorough history, ideally with a video (ask parents to record future eps!)
EEG - helps rule out other causes
if neuro signs between seizures or if very focal seizures - consider MRI/CT brain or functional scans
only diagnose epilepsy after at least two seizures that you’re confident were actually seizures (not faints etc), and if you’re fairly sure there’s not an underlying cause
what causes epilepsy?
most generalised epilepsy is idiopathic (and likely that’s due to some genetic cause)
for focal epilepsy there’s more chance of finding a specific cause
