Paediatrics Flashcards
Mnemonic for gluten foods?
BROWS: barley rye oats wheat and spelt (type of wheat).
HEADSS mnemonic
Home and environment Education and employment Activities Drugs Sexuality Suicide/ depression
Podophyllotoxin
Podophyllotoxin, also known as podofilox, is a medical cream that is used to treat genital warts and molluscum contagiosum. It is not recommended in HPV infections without external warts. It can be applied either by a healthcare provider or the person themselves.
aflatoxin
Bladder cancer
New differentials for paeds headache
Stress
Eye Strain
Dental Carries
Tumours: Medulloblastoma and infratentorial medulloblastomas.
How do paeds headaches present?
Irritability and changes in feeding, toileting/ nappies, behaviour, etc.
Paracetamol dosing in children? What is it in adults?
15mg/kg 4 hourly with a maximum of 100mg/kg/day OR 1g in a day according to Jess.
1g 4-6 hourly is max normal dose paracetamol for adults
How do we manage a simple headache in kids? What about migraine? What about meningitis if it’s under 2 months of age.
If it’s simple, give them paracetamol dude.
If they are a kid under 12, give them ibuprofen. If they are a kid over twelve, aspirin and sumitriptan can be added (INTRANASAL)
Cefotaxime and benzylpenicilin.
Questions to ask on a puberty history?
Age at takeoff (i.e. onset of growth acceleration)
- Age at peak height velocity + peak height velocity
- Duration of puberty
- Contribution of the pubertal growth spurt to final adult
height
HISTORY:
- Presence of absence of acne, body odour, oiliness of skin,
erections and nocturnal emissions in boys, PV discharge or
bleeding in girls
- Increase or decrease in growth rate
- Family history unexplained early death in male sibling (may
suggest CAH), PP in male relatives (suggests familial limited PP)
- Family history of pubertal onset
- Activities (e.g. ballet dancers and gymnasts tend to have delayed
puberty)
- Diet
Investigations for a precocious puberty?
Investigations: - Bloods: o FSH, LH, testosterone, estrogen o GnRH stimulation test o DHEA, DHEAS, hCG o TFTs o Tumour markes (alpha-fetoprotein, Bhcg)
- Imaging: o XR wrist + hand (bone age) o USS abdo (if adrenal tumour suspected + in girls) o Testicular USS o CT head o MRI brain + pituitary
What is Ramsay hunt?
Post herpes zoster infection, we get a facial nerve palsy and hearing loss in that ear.
DDX for precocious puberty?
It’s iether GnRH dpeendent or independent, and we test this by looking at the LH and FSH which will be elevated.
Idiopathic, hypothal hamartoma (also look for seizures, adipsia, diabetes inspidius, obesity or cachexia) and literally ANY intracranial pathology. Prolonged hypothyroid is also in this category.
Peirpheral (GnRH independent) includes CAH, Adrenal/ testicular neoplasm, exposure to exogenous testosterone.
Investigations for a delayed puberty?
Investigations: - FSH, LH, testosterone, oestrogen, serum prolactin, other pituitary hormones - FBC, ESR - Urea, creatinine, serum proteins - TFTs - Karyotype - Bone age - ?urine MCS (metabolic abnormalities assoc w/ assoc conditions) - ?MRI
DDX for dleayed puberty?
If there are normal or low serum gonadotrophins, the problem is central:
Constitutional delay. Usually familial.
Chronic illness/ poor nutrition.
Kallman’s/ hyperprolactin.
Elevated serum gonadotrophins:
- Primary gonadal failure (tunrner’s klinefelter’s Noonan’s)
ANorchia
Gonadal destruction secondary to trauma etc.
Child has a learning disability: how do you work this up?
History:
- Standard history and physical exam – include history from
parents/ caregivers regarding onset and source of symptoms and
family history of similar patterns
o Demographic data
o Birth, developmental and medical history
o Family and social history
- Hearing and vision assessment
- School history
- Consider contributing causes, e.g. anxiety, family dysfunction,
auditory processing problems
- Consider co-morbidities, e.g. ADHD, other behavioural disorders,
language disorders, developmental disorders, intellectual
disability
- Copies of any previous assessments (mental health, language,
cognitive, audiology)
DDX for a learning disability? Thus, ask around this.
Causes for learning difficulties: - Genetic syndromes: o Sotos o Tuberous sclerosis o Neurofibromatosis - Metabolic conditions: o Hypothyroidism o Diabetes - Common: o Dyslexia o ADHD o Down’s syndrome o Fragile X syndrome o qTuberous sclerosis o ASD o FAS o Absence epilepsy
Hx and exmaination for behavioural problesm?
History:
- full paediatric history
- ABC:
o Antecedent = what were the events preceding the
behavior?
o Behaviour = what is the behavior exactly?
o Consequence = what did the parents do to resolve the
situation?
- Clarify where the behaviours occurs behavior occurring acorss
two or more settings (home, educational and/or social setting)
are more likely to be indicative of an underlying mental health
problem
o Behavior occurring in one setting only may reflect an
issue specific to that setting
- Nutrition
- Sleep patterns
- Family functioning
- Ask about parent mental health, parenting practices
- Family risk factors – unemployment, drug and alcohol misuse,
financial stress
- Social support
- Family history of developmental/behavioural problems
Examination:
- Observe the child’s behavior
o But be aware that some kids behave well when they
know they are being observed
o Also observe parent-child interaction
- Dysmorphic features
- Full physical examination
- Consider brief developmental assessment
General management of behavioural problems?
- Establish clear goals: what do they want to improve? What is your capacity to do this?
- Set a positive example, and incentivise the kid with some rewards
- Set up consistency, between parents, at school and at other houses
- Set clear boundaries and expectations.
What are the specific behavioural problems for kids throughout different age groups and how are they managed?
Specific behavioural problems:
TANTRUMS + OPPOSITIONAL BEHAVIOUR IN TODDLER (1-3 yo):
- Can occur at any time, but commonly during meals and sleep time
- Management of tantrums:
o Stay calm, walk away and ignore behavior until
tantrum stops
o Praise child when appropriate behavior begins again
o Behavior will initially escalate, but quickly decline
- Management of aggressive behavior:
o Remain calm and don’t raise voice, ask child to stop and
redirect them to another activity
o If they do stop, praise them
o If they don’t stop ‘quiet time’ in same room
o If still don’t stop or leave quiet time go to time out in
another room
ANGER AND AGGRESSION IN PRESCHOOLERS (3-5yo):
Low priority behavior (e.g. whinging) can be dealt with by:
- ignoring the behavior
- distracting the child
- logical consequences for the child’s action, e.g. if draw on wall
with pen, take pen away from them for a few minutes but make
sure to give pen back so child can practice using it properly on
paper
High priority behaviour, such as behavior with associated safety
concerns (e.g. kicking, punching, absconding):
- time out
HYPERACTIVITIY OR INATTENTION IN SCHOOL AGED CHILDREN (5-
11yo):
Management needs to be implemented both at home and school.
School:
- In school, first priority is to exclude co-morbid learning
difficulties
o Test hearing + vision
o If required, special education and cognitive assessment
can be organized through school
- Classroom strategies:
o Sitting the child up front, next to quiet student
o Having frequent breaks
o Rewarding for staying on tasks
- Parents should liase with teacher for a management plan
- Fidget toys
Home:
- Withdrawal of privileges (e.g. no TV for 1 hour)
Social Hx for a fever? Remember I’m just going to write a huge list of differentials from the systems i covered last year and go through a review. Just remember otitis media, HIV, UTI and neoplasma, also osteomyelitis.
Travel history and sick contacts
Causes of chronic fever in kids?
Occult abscess Atypical pneumonia Hepatitis UTI Osteomyelitis HIV Infectious mononucleosis Tuberculosis Infective endocarditis Collagen vascular disease Neoplastic disease Factitious fever
What is the traffic light screening system for fever?
Looks at the risk of the deterioration by doing a full systems review etc. Looks at colour, activity, respiratory, hydration, and other.
How do we manage septic shock in a bebe?
Fluclox and gent if normal csf
If unknown csf do fluclox and cefotaxime
change once sensitivites come back. If culture negative treat for 48 hours or stop if clinically improving
UTI antibiotic in a kid?
Trimethoprim and not sulfa
Tonsilitis management?
Pencillin V if risk factors for ARF, but consider no antibiotics
Cellulitis management?
Cephalexin, and fluclox if severe
Discharge requirements for fever management?
Discharge requirements:
o Infants less than 1 month of age with fever should be admitted.
o Infants 1 to 3 months of age:
The child is well
All investigations are normal
The child has been reviewed by a senior registrar/consultant
Follow up in 12 hours has been arranged
o Children older than 3 months:
The child is well
Follow up has been arranged
Go back over fever investigations and management in notes. Not sure how to tackle this. Maybe just know the severe criteria.
KK
Go over the 6 week check notes from Shamwow
kk
When do we not use charcoal?
If they have swallowing difficulties, ALOC, or if they have ingested a drug that typically develops ALOC.
What are some ways we can decontaminate?
We can do activated charcoal, we can do gastric lavage, whole bowel irrigation. These are done with specialist consultations.
List some high risk paediatric ingestions in low doses? If you don’t know them before, what are some features?
Amphetamines, Calcium channel blockers, chloroquine, opioids, propranolol, sulfonylureas, theophylline, TCA’s, paraquat?
Calcium channel blockers: bradycardia, hypotension, refractory shock, delayed toxicity is possible due to the slow release formulations of nifedipine etc. that are possible.
Beta blcokers: hypoglycaemia, ventricular dysrhythmias, coma, seizures
theophylline: SVT and seizures
TCA’s: ventricular tachy, hypotension, seizures, coma
Paraquat: oropharyngeal burns, multi organ failure, pulmonary fibrosis.
Need to admit if they’ve ingested any of these substances.
Any child that has come in with a potential overdose how do we investigate and manage?
ECG and paracetamol levels in ALL cases
Monitor blood gases, anion gap and osmolality.
Consider doing specific drug levels and get specialist help with these:
Ethanol
Phenobarbitone, carbimazepine, valproic acid, salicylates if they have an unexplained metabolic acidosis
Urine drug screen can be used but shouldn’t change management.
Most are managed with supportive care.
Airway protection? Do we need to hyperventilate them?
Specific management points of delerium in kids?
Management
Follow general management principles as they apply to ABC stabilisation, blood glucose,
electrolytes, infection, trauma
Hyperpyrexia is a high risk situation and urgent advice should be sought
Specific management guidelines are:
o Calm environment with frequent reassurance, explanation and orientation.
o Physical restraint until pharmacological sedation can be achieved to ensure
safety for patient and staff if required
o IV diazepam titrated to effect is first line agent for sedation. An oral dose can be
tried in mild cases.
o Antipsychotic agents are effective second line agents to calm patients resistant to
control with diazepam alone.
o Haloperidol should be used with caution in cases of poisoning with agents
having anticholinergic effects.
o Olanzapine has a better side effect profile and can frequently be given orally to
augment diazepam in calming an agitated patient.
How do we manage drug induced seizures?
Usually we temrinate with some IV benzodiazepines as per local protocol. Probably use midazolam. Phenobarb is second line. I think for a drug induced seizure, you wouldn’t wait for that five minute mark before intervening because they are unlikely to stop.
Digoxin and calcium channel blockers can often cause arrhtyhmias in kids. How do we treat both?
Digibind (fab) and calcium lol.
Classic findings in an aspirin poisoning? WHat investigatiosn?
Met acid, resp alk, tinnitus, vomiting, hyperventilation, seizures.
Blood gas UEC ECG (hyperkal) BSL Salicylate concetation (remember they can be enteric, so you often have to repeat these levels).
Who gets treatment in an aspirin poisoning? How?
If they have more than 150mg/kg, if they have unknown amounts or if they are symptomatic.
Fluid resus, particularly correcting the hyperkalaemia (calcium gluconoate?)
May need intubation (note that you may need to load them with bicarb as they can worsen the acidosis). Maintaining an alkalosis can also prevent it from going into the CNS.
Activated charcoal can often be indicated because they have an enteric coating on the tablets.
Enhancing elimination is done by:
- COrrecting the acidosis (remember this limits the uptake to the CNS)
Alkalinse the urine with bicarb infusions and using a catheter to monitor (only done if we have high or normal K+)
Consider for haemodialysis if refractory or severe or can’t overload with fluid.
If asymptomatic after 6 hours, can go home.
Who needs paracetamol management? How?
What happens in allergies?
If they are having an acute ingestion of 200mg (aspirin was more than 150) or more, if unknown substance, or chronic ingestion of subtherapeutic amount (can get a chronic failure).
1) Paracetamol levels 4 hrs post and chart on nomogram
2) This data needs to be available within 8 hours
3) If they present beyond this or have symptoms like vomiting, tenderness etc. then put them on NAC.
4) Give them NAC based on the specialist advice.
Anaphylactoid reactions to NAC may occur (wheeze, rash). In these cases, cease the
infusion for 30 minutes, give promethazine then recommence the infusion at half the
previous rate. Slowly increase the rate until the desired rate is again reached.
Worrying foreign bodies?
Multiple magnets and button batteries. Will need to do endoscopic removal if they are in the stomach (do an x-ray) but if they are beyond this then if they need close follow up and may need surgical intervention if it causes an obstruction.
Management protocol for a foreign body ingestion? I
If radio-opaque, do an x-ray. If it’s seen in stomach or beyond, observe at home. Watch for abdo pain, persistent vominting, haematemis, melena, fever. If in oesophagus, consult surgeons.
If radiolucent, watch for symptoms of drooling, chest pain, can’t tolerate diet. If so, call surgeons as in oesophagus. If not, observe at home.
IF IT IS A BUTTON BATTERY, OGD.
Management - Oesophageal Foreign Bodies
Button batteries lodged in the oesophagus need urgent removal.
http://www.poison.org/battery/guideline
An object causing total oesophageal obstruction requires removal under anaesthesia.
An object causing partial obstruction where the child is able to swallow saliva
successfully and the object has a good chance of passing, may be observed for a few
hours if it does not pass it will need to be removed.
Once the object is in the stomach it will almost certainly pass spontaneously.
If food is thought to have impacted in the lower oesophagus, small amounts of fizzy
cola drink may help move it.
Inform parents to return immediately if there is abdominal pain, vomiting,
haematemesis or melaena.
There is no place for arranging follow-up visits, repeat X-rays or parental faecal examination.
This does not apply to the ingestion of lead foreign bodies which can cause systemic lead
absorption if they are retained for more than a few days.
What are some symptoms aside from cardiac and respiratory symptoms in congenital heart defects? Note remember that they can get a cardiac wheeze
Failure to thrive Poor feeding Developmental delay Diaphoresis Easily fatigued Poor exercise tolerance
What are some substances associated with heart defects in utero?
FASD (ASD, VSD, ToF)
SSRI’s (mild VSD and bicuspid aortic valve)
Valproate coarctation and hypoplastic left heart
Maternal diabetes: hypertrophic cardiomyopathy, ToF.
Marfan’s, Turner’s and Down’s are associated with which cardiac defects?
Marfan’s: aortic regurg, aortic root dilatation and mitral valve prolapse
Turner syndrome: coarctation of the aorta, LVH
DOwn’s: ASD, VSD, tet of fallot. Also PDA.
Red flags of mumurs?
Multiple Pansystolic or diastolic Grade 3 or higher Harsh quality Abnormal S2 Heard loudest at the left sternal edge Systolic click Increased intensity on standing
List some examples of innocent murmurs? What are the 7 S’s?
Aortic systolic, peripheral pulmonary stenosis, pulmonary flow murmur, venous hum
Sensitive (changes with respiration or posture), short, single (no others or it’s got added sounds), small, soft, sweet, systolic
Come back to murmurs
kk
What examinatin features are important in scabies?
Need to look for superinfection and also BP and vitals because of PSGN
ddx for the Kawasaki?
Measles, EBV and amoxicillin, lepto, arbovirus, Steven’s Johnson, Scarlet fever, parvovirus, Still’s disease
Warm cream is the diagnosis of kawasaki (note that the rash is POLYMORPHOUS). What are some other features?
Cough and coryza Vomiting and diarrhoea Uveitis Gallbladder hydrops Arthritis Myocarditis Nappy rash
Helpful investigations despite it being a clinical diagnosis?
Rule out differentials basically. ASOT and Anti DNAse B
FBC (neutrophilia and can have an anaemia)
CRP ESR
UEC
LFT (low albumin)
Blood cultures
ECHO needs to be done both on the day of presentation and at 6 weeks.
You know the management of Kawasaki. Why do we delay the MMR vaccine by 3-6 months?
2% rate of recurrence is something I also need to remember.
We delay it because the immunoglobulins can reduce the effectiveness of the MMR vaccine.
What is Nokolsky sign? What other features are typical of SSSS
How do differentiate from TENS?
When you rub the skin it disintegrates.
They will be in a lot of pain, and they won’t like being in contact with Mum.
It starts as exudation and crusting, which progresses to wrinkling, bullae formation and the exfoliation.
TENS will have mucosal involvement (they have eye involvement). Also note SSSS does not scar because it’s only the epidermis.
Clinical features of varicella? What are some complications?
They get a viral prodrome of fever, lethargy and anorexia, before progressing to a rash over 3-5 days which is vesicular, extremely itching, and they crust over. Crusted by 10 days.
Complications are Reye’s (happens when given a virus in a period of being systemically unwell), pneumonias, shingles, encephalitis/ cerebellitis, hepatitis, arthritis, bacterial superinfection.
Manage varicella infection?
Vaccines…
Symptomatic treatment (calamine lotion, cool compresses, antihistamines can be used to improve the patients sleep), keep skin cool to reduce number of lesions
Avoid scratching - trim the nails
Aciclovir if they are immunocompromised and avoid aspirin at all costs
They are infectious even before the onset of the rash, and should be excluded from school until they have all crusted over. Also you need to avoid the hospital because of the rate of transmission.
Investigate and manage impetigo?
Investigations:
- Swab for Gram stain + MCS is discharge present
- FBC + BC if systemic symptoms present – low yield
- ESR, XR +/- bone scan if osteomyelitis suspected
- USS if fluctuance present
Management:
- Wash crusts off – topical mupirocin 2% ointment 8 hourly
- If extensive / multiple lesions / not responding to topical
treatment treat as for cellulitis
o Flucloxacillin 25mg/kg (max 500mg) PO Q6H for
7 days
- Highly contagious
o Exclude from school until treatment has started
and sores need to be completely covered with watertight dressing (school sores).
If get time go over bruising, but mostly just think about the NAI case on the OSCE.
k
Is there a way to diagnose meningococcal on blood cultures after antibiotics were started?
Yeah do a PCR.
Why do you have to be careful of giving too much fluid in meningitis?
How do you isolate the cases?
Chemoprophylaxis?
SIADH and overload (worsen the oedema).
Isolate on the ward until 12 hours of IV antibiotics.
Chemoprophylaxis is rifampicin to close contacts and should be given within 24 hours. Give them ceftriaxone.
COmmonest vasculitides in children?
HSP and Kawasaki. Kawasaki under 2 and HSP above 2 - 8.
Discuss the clinical features of HSP
Palpable purpura with arthritis, arthralgia, abdo pain and / or renal involvement (haematuria, proteinuria, HTN)
Pulmonary + neuro involvement are both rare but may be life threatening if present.
PAAR
Remember the abdo pain is in intussuseption.
Investigations for HSP?
Urinalysis
Only need to do further investigations if there is severe abdo symptoms, or significant renal impairment (BP, gross haematuria).
FBE, UEC, LFT (albumin)
BC + Urine MCS
Abdominal imaging
ANA, ANCA, C3/C4 (this will tell if there is any unclear dx features).
USS for intususception if severe pain.
How would you manage the
Depends if there is mild or moderate/ severe pain.
Mild: subcut oedema managed by bed rest + elevation of the affected area. Paracetamol and NSAID’s.
Mod/ severe: glucocorticoids reduce the duration of joint pain and abdo pain. No impact on long term kidneys.
If there is significant renal, pulmonary, neurological or abdo comp, refer to paeds and consider admission.
Follow up is referral to the GP or paediatrician to identify subsequent renal involvement, monitoring for HTN, proteinuria or macroscopic haematuria.
What is global developmental delay?
MOre than two domains of development impaired. Cognitive is included in this.
Developmental history?
Start from before birth:
- Drugs? Infections? Alcohol or smoking? Any problems with the pregnancy? Folate supplements?
Birth: Method? Trauma? Complications?
Post-partum? APGAR, NICU, ventilation?
Full developmental history: ask how they started doing the different milestones. DID THEY REGRESS?
Vision or hearing concerns?
Behaviour? Sleep? Toileting? Growth? Diet?
Also do a full history.
Examination is vitals, anthropometry, and a general exam looking for dysmorphic features and neurocutaneous markers like NF1, 2 and Sturge Weber port wine spots.
Investigations for a developmental delay?
Screen using a developmental screening tool (we use Denver II) and work up based on hx.
Hearing and vision should be assessed in most patients. Consider that they might be having NDIS funding available.
DDX for infant or child with an abnormal gait or sore joints?
Toddler 1-4 DDH Toddlers fracture Transient synovitis of the hip Talipes equinovarus, talipes calcaneovalgus,
Child 4-10 Transient synotivitis of the hip DMD Perthes Growing pain
10 to ado SUFE Overuse syndromes (Osgood)
Also note that we can get at any age: infectious (osteomyelitis, septic arthritis), HSP, ARF, JIA, Trauma, Malignancy (bone tumours, ALL), NAI, APpendicitis/ IBD), Testicular torsion, functional limp, cerebral palsy, neural tube defects
How do we follow up our HSP patients?
Review urinalysis and check BP at these intervals – weekly for 1 month,
fortnightly from weeks 5-12, single reviews at 6 and 12 months
Rf’s for DDH and how do we diagnose and manage?
Risks include a family history, being a breech, being a first born, and being a twin.
Before 6 months do an ultrasound, after 6 months do an x-ray.
Management by either using a Pavlik Harness for several months or by doing an open or closed reduction.
What is a toddler’s fracture?
Spiral or oblique undisplaced fracture to the distal shaft of the tibia with intact periosteum and no fibula involvement. Usually occurs in a twisting injury. THey will not be weight bearing.
We manage with supportive care and a backslab! Most heal without complications in 8-12 weeks.
MOst common cause of limp in childre?
How do we manage it?
Transient synovitis of the hip joint. Often follows falls and viruses. Usually unilateral. Diagnosis of exclusion. Can get pain all along the leg, and they find it difficult to move. If severe limitation, suspect a septic arthritis.
Paracetamol and rest. Resolves around 2 weeks and gets better at 3 days.
Bishop score mnemonic?
C the PEDS!
Consistency position effacement dilation station
Talipes equinovarus vs positional talipes?
Positonal is that it can be moved, whereas talipes equinovarus is when it’s pixed. Calcaneovalgus is when it’s fixed dorsiflexion.
Toe walking is a sign of tight achilles or possibly DMD.
How do we manage talipes equinovarus, talipes calcaneovalgus, genu varum, genu valgum, or toe walking?
Talipes equinovarus is managed with ponsetti method which is a series of casts and manipulations
Talipes calcaneovalgus is managed by managed by a long leg cast, the genu’s are resolving over time and toe walking is managed with physical therapy.
History of Perthe’s disease?
It’s a painful hip joint that’s worst with movement and is stiff. Change in gait, and may have pain in the knee due to compesation. Assess for JIA by asking about systemic symptoms and morning stiffness, and transient hip synovitis by asking about recent viral infections.
Dx of Perthe’s disease?
INvestigations and diagnosis of this condition is with an x-ray of the hip and a bone scan (nuclear medicine technetium 99)
How do we manage Perthe’s?
Usually just conservative. Obsevartion is they are between 2 and 6, but we may do surgery or something more urgently if they are older than 8. Limit movements, and give them ibuprofen. Limit movements, especially runnning and jumping.
Surgery is also recommended when we have over 50% necrosis as well. Prognosis is usually good, but return to activity usually takes between 18 and 24 months.
Advice to the patient with growing pains?
They’re not actually growing pains. More linked with excessive physsicial activity, lower pain thresholds, and reduce d bone strength or hypermobility.
They are more common in preschoolars, and they don’t have pain that follows a pattern. Pain is often at night, but we don’t have a limp. Usually the pain is bwtween joints of the leg! They have no other features of pain, and they can carry on.
Manage with stretching, heat packs and paracetamol.
How do we manage and diagnose DMD?
Do a muscle biopsy which will show fatty infiltrations of the muscles.
Neurologist, paediatrician, physiotherapy and psychological supports are needed.
Which of the following is diagnostic of ARF by itself?
How do we manage
It’s just Sydenham’s lol
Salter Harris Fractures? How do we manage each?
Straight across Above Lower or below Two or through Erasure of growth plate
1,2 with closed reudction and casting
3,4 ORIF
5 usually are not actualy diagnosed on x-ray, and a more seen retrosepctively as a diagnosis for growth retardation.
Juvenile idiopathic arthritis
It is an autoimmune disease that causes a chronic synovitis. Eventually this causes a release of proteases and collagenases and this causes tissue destruction.
JIA can be oligoarticular or polyarticular, and it has those classic seronegative arthropathy findings!!!!!!! Destructive, eye signs, etc. as well as axial spondyloarthropathy.
SYstemic onset is also seen with rash, pleuritis and hepatosplenomegaly.
How do we diagnose Still’s disease? Manage?
NEED TO BE LESS THAN 16
Also, you need to have CRP ESR high, FBC excludes complications, ANA, ANti RF, Anti CCP to exclude RA, and aspirate if there is a monoarthritis. Also you do an x-ray to assess joint damage or defomirty.
Manage it by doing physio and NSAID’s, as well as steroids for severe cases. Sulfasalazine is SECOND LINE, and DMARD’s can also be used (methotrexate, influximab, etanercept).
How do we diagnose Still’s disease? Manage?
NEED TO BE LESS THAN 16
Also, you need to have CRP ESR high, FBC excludes complications, ANA, ANti RF, Anti CCP to exclude RA, and aspirate if there is a monoarthritis. Also you do an x-ray to assess joint damage or defomirty.
Manage it by doing physio and NSAID’s, as well as steroids for severe cases. Sulfasalazine is SECOND LINE, and DMARD’s can also be used (methotrexate, influximab, etanercept).
FASD is a risk factor for ADHD and intellectual impairment. What is the physical features of this disease?
Downs is a risk factor for congeital heart defects and for intellectual impairment. How do we investigate these babies? What are some physical features (goes beyond their face)?
Short palpebral fissures, flat midface, short nose, flat philtrum and thin upper lip, micrognathia, minor ear abnormalities, low nasal bridge, epicanthal folds
Chromosomal analysis, echo, TFT and FBC, auditory screening and specialist referral.
Mental retardation, growth failure, flat back of head, simian single palm crease, absence of one rib, umbilical hernia, diminished muscle tone, Broad flat face with slanting eyes, epicanthal folds and a short nose, small arched palate, enlarged colon.
DDx for primary nocturnal enerusis, secondary enuresis, or diurnal enerusis.
Primary nocturnal: genetics, emotional stress, reduced bladder awareness
Secondary; emotional stress, UTI, DM OR DI
Dieurnal: UTi, neurogenic bladder i.e. spina bifida, congenital abnormality, severe constipation, sexual abuse, extreme stress
Have a read over these history questions for this presentation?
Before Any stress? PMH? PSH? Medications? Ever been dry? What age did it change? Family history of thise? Pai, fevers? Bowels
During
Other symptoms? Constipation or faecal incontinence, how frequently do they do it and do they wake up? Is it uregency or is it dribbling,
Blood in the urine or is it cloudy?
After
Have the child or parents become stressed by it?
Has the child been punished?
What has been done so far? Fluid restriction or increased night time toileting?
What do we do to examine? v
Look for the differentials mate, but also:
- HTN?
Leg reflexes and perianal sensation? Same nerve roots as the bladder (S2-S4)
Evidence of spina bifida occulta?
ABdo pain, faeces, or masses?
Renal disease?
Just do MCS and a Renal US
Management of a nocturnal enruesis or a diurnal enuresis?
A nocturnal enuresis should first have the problems excluded. If they are less than six, then the parent should be reassured because there is likely going to be spontaneous resolution.
There are rarely serious causes to this, particularly in a baby who is otherwise well. AVOID PUNISHMENT
Advice: avoid caffeine and evening fluids.
QUality mattress protectors
Rewards charts, and get the child involved in washing the sheets with the parent
Bedwetting alarms are the most successful way.
Desmopressin can be used if going to hoidays and sleep overs, but at home this is usually not required because better to get the kid involved in managing themselves.
Diurnal enuresis is managed by encouraging the child to go to the toilet regulardly throughout the day, treating the underlying constipation or UTI, and considering an anticholingeric.
Aetiology of bronchiolitis?
RSV, Parainfluenxa, influenza, adeno, corona,
Risk factors for bronch?
Low birth weight or prem
Less than 6 weeks (early in the under one category)
Sick contacts
Cigarette smoking at home
Conditions that make the child constitutionally week.
What are some signs and symptoms of bronch?
Prodrome of runny nose, cough and fever that progresses to increased work of breathing. Also get apnoeic episodes, poor feeding and signs of dehydration.
List all the signs of increased work of breathing please
Nasal flaring Grunting Intercostal indrawing Subcostal recessions Reduced sats Cyanosis but this is uncommon in kids. Tacheal tug Gasping/ stridor/ wheezing/ crackles on auscultation Tachypnoea
When do you do superficial nasal suction, and when do you do PAP?
If sats lower then 90% give PAP and do nasal suction if they have a lot of secretions.
Indications for a PICU admission? When do we discharge?
Severe hypoxaemia, unable to feed, fatigue, prolonged apnoea, marked nasal flaring.
Discharge home when there is adequate oxygenation, and they have enough oral intake. This is the same for paediatric pneumonia as well.
Describe the aetiology of pneumonia in kids?
It’s more commonly viral than bacterial. It also has the same risk factors of RSV.
SMARTCOP Score?
Systolic blood pressure < 90mmHg Multilobar CXR Albumin Respiratory rate tachy Tachycardia
Confusion
Oxygen dats diminished
pH
If less than 2, low risk of itensive respiratory or vasopressor support
If 3-4 moderate
5-6 high
7+ very
SMARTCOP is done for adults. How do we assess the severity in kiddies?
Resp distress, hypoxamiea, marked tachycardia, altered mental state. We do not do CXR. If no wheeze, pneumonia. 2 criteria of these means it’s severe. OR IF THEY HAVE EMPYEMA.
Also, in these patients we need to do blood cultures and FBC if they are severe.
If admitting, do a CXR and UEC because looking for SIADH (don’t aggressively rehydrate them in these conditions).
Management of pneumonia?
Admit to hospital if:
Signs of moderate to severe WOB or oxygenation required
Fluid therapy required
o Supplemental O2 if sats ≤92%
<2 years = maximum of 2L per minute nasal prong O2
>2 years = maximum of 4L per minute nasal prong O2
o Fluids:
1/2 or 2/3rds normal maintenance to avoid fluid overload
If signs of an empyema or effusion, then you need to insert a chest drain. THis is absent breath sounds and a dullness to percussion.
How do we manage pneumonia in kiddies?
Amoxicillin if going home
If admitting, work out if it’s severe or not. If not, give oral amoxicillin. Benzylpenicillin if can’t do orals. If severe give them ceftriaxone and consider adding vanco or azithromycin.
If there is no clinical improvement in 48 hours, consider doing a CXR. Thus, consider oseltamivir. Consider changing to IV antibiotics or admitting to intensive care.
If improving, continue the current management. If a causative organism has been identified, you can switch the antibiotic but this is unliekly.
Risk factors for croup?
Pre-existing narrowing of the upper airway (subglottal stenosis, Down’s Syndrome) or previous admission for croup (Sam O’Dempsey lmao)
Investigations for Croup
NPA and CXR (bloods not routine). DON’T CXR.
Management for croup?
Remember to make a clinical diagnosis based on the stridor, barking cough, and the respiratory distress. Additionally, they come in during the middle of the night. Croup peaks day 2-3 on RCH.
Management of mild: stridor when upset.
Prenisolone is given. Two doses for this. Orals.
moderate: stridor when at rest. Same as above.
Severe: they have an oxygen requirement.
Nebulised adrenaline and IM/IV dexamethasone.
Discharge based on half an hour after their PO steroid or 4 hours post neb adrenaline and stridor free at rest.
If they have no response to therapy, they need to be put in PICU.
Which age do we get concerned about for whooping cough? When is it infectious?
Less than 6 month old. It is infectious just prior to and up to 21 days after the onset of symptoms.
When do we we give anti-D?
First trim: After chorionic villous sampling MIscarriage Termination Ectopic
2nd and third: Haemorrhage Amniocentesis ECV Abdo trauma
Don’t give if less than 12 weeks gestation or is a threatened miscarriage.
Kleihauer Betcke test is only done if it’s an APH or a placental abruption. Remember this is for foetal haemoglobin.
Fibronectin predicts in the next 7 days the liklihood of going into labour in the next 7 days.
Describe the clinical features of pertussis
Risk factors is exposure to infected people and not being.
Catarrhal phase: cough and coryza for 1 week.
Paraoxysmal phase: more pronounced cough in paraoxysms that can cause them to vomit.
Often there are no clinical signs, or could present as a non specific chronic cough.
Apnoea and cyanosis may occur with coughing. Usually most of the family has a cough, and a fever is uncommon.
Investigations and diagnosis of pertussis:
NPA is PCR but usually negative after 21 days
Pertussis IgA serology can be used.
Management of pertussis:
COnsider ab’s if it’s in the catarrhal phase, cough is less than 14 days to reduce spread, if they’re admitted to hosp or they have complications like pneumonia or apnoea.
Give azithromycin. or yucky clarithro fluid if they don’t want tablets.
They cannot go back to school unless they have absence of symptoms for 21 days. Continue vaccination schedule as planned. Also give them the antibiotics during the infectious.
How do people who have inhaled a foreign body present? How does the maangement differ?
If the impaction is above a main bronchus, hen we can get sudden coughing, choking and collapse.
If it’s below the main bronchus, we ccan get couhging, choking or wheezing when icnreased resp demand. May have normal exam. Could have obstructive signs.
Do a CXR to look for radio opaque foreign bodies or for collapsed lungs.
For complete obstructiion, we use a laryngoscope to extract with foreceps. Can also lie them down prone with five back blows the the interscapular region, and repeat as necessary. Positive pressure ventilation can push it down a bronchus.
Surgical airway can be made if it’s in the larynx or cannot be removed.
If they have a subtotal occlusion, do a surgery referral.
Theca cells do what?
Aromatase.
Management of upper airway obstruction including anaphylaxis:
Adrenaline and repeat in five minutes if necessary.
Ceftriazone and involve PICU if epiglottitis.
Quinsy is benzylpenicillin and metronidazole.
What is an apparent life threatening event? Discuss some fewatures
An episode of apnoea, colour change, change in muscle tone, or gagging. It’s not a diagnosis, but a feature of many diagnoses.
Most are not associated with SIDS, most are not pathological, and it’s got the highest frequency in the first 3 months of life.
What are some causes of ALTF?
We usually investigate based on the history. How do we manage?
Child abuse
o Infection: pertussis, pneumonia, meningitis, septicaemia
o Airway obstruction
o Abdo: intussusception, testicular torsion
o Metabolic: hypoglycaemia, hypocalcaemia, hypokalaemia
o Cardiac: congenital, arrhythmias
o Toxic/drug
o Neuro: head injury, seizure
- Risk factors associated with more severe underlying cause: o Age <28 days o Significant prematurity o Significant medical problems present o Clinically unwell in appearance o Recurrent presentations
Management:
o May require admission for observation
o Term babies with minor presentations who are well on examination and whose
parents can be appropriately educated, discharge with GP/paediatric follow-up
What is the Duke’s criteria for endocarditis?
2 major or 1 major or 3 minor or 5 minor
Major: Typical microorganism for IE on two seperate cultures (Strep viridans, HACEK), Staph aureus). OR three or more positive cultures of an atypical organism 1 hr.
AND
Positive echocardiographic findings of vegetations or a new regurgitant murmur.
Minor: - Presdisposing valve or cardiac problem - Intravenous drug misuse - Fever Embolic phenomenon Vasculitic phenomenon BLood cultures grown but not achieving major criteria Suggestive echographic changes
Waiters tip posture?
Think of Erb’s palsy (C5, C6)
Common asthma triggers?
Respiratory infections, allergens, air pollutants, cigarette smoke, non complicance with the medication
How do we assess for asthma severity, aside from panicking at their hx of previous hospital and ICU admissions?
Confusion, WOB, heart rate, talking. Note that heart rate could be from too much salbutamol.
Mild, moderate, severe, critical.
Mild is normal mental state, subtle or no increased work of breathing, no changes in heart rate and able to talk normally.
Moderate is normal mental state, some increased WOB, tachycardia, some limited talking
Severe is that they are agitated/ distressed, moderated - marked WOB, tachycardia, marked limitations in ability to talk.
Critical: confused/ drowsy. Maximal WOB, marked tachycardia, unable to talk, silent chest.
Clincal diagnosis son.
Mild, moderate, severe and critical asthma. How do we manage each?
ABC’s and IV access for each. A salbutamol burst is 100mcg/ puff. 6 puffs are given if less than 6 and 12 are given if over 6. It’s 4 ipratropium if under 6 and 8 if over 6.
Mild specific: Salbutamol is given by a MDI in one burst and reviewed in 20 mins.
If good response, discharge on the beta 2 agonist on a stretch.
Poor response, treat them as moderate. Can also give oral pred and continue for several days. Provide written advice on when to return, and GP letter.
Moderate: Give the burst therapy for an hour. Give same frequency of oral pred (1-2 days)
Severe: involve senior staff, and give O2 if sats under 92 (same as above). If they need more than 3 bursts, treat as critical.
Ipratropium burst is also provided. Aminophylline if deteriorating or the child appears ill. Mag sulf also given over 20 minutes. Oral pred or IV methyl pred. Needs admission.
Critical:
- Involve seniors and PICU for CPAP or intubation
- O2 as above
Continuous nebulise salbutamol (2x5mg ) MOnitor for hypokal.
Nebulised iptratropium 20 minutely with salbutamol.
Methylpred.
Mag sulf.
IV salbutamol possible.
Aminophylline consider.
How to assess the placenta for completion?
Check the umbilicus, I’m not sure if there’s anything else.
Acute or chronic constipation cause?
Acute is just fluid depletion or bowel obstructions
Chronic is functional (painful shit or spina bifida), behavioural (toddlrs and small kids), secondary (cow milk allergy, coeliac, cf, hypothyroid, Hirschprung’s, Meconium ileus, anal malformations.
On history, ask about all of the above.
How to investigate constipation?
Often not indicated
- Abdo X-ray may show faeces but most likely won’t change management
- Hirschsprung’s requires colon biopsy
- If suspecting hypothyroidism, TFT
- If suspecting Coeliac: ensure patient is eating gluten then do total IgA and anti-tTG +/- DGP
+/- EMA
How do we manage constipation in kids?
Also just remember to do an abdo and a neuro examination.
Aside from treating specific causes, the following are useful treatment modalities:
Behavioural modification:
o Position: footstool to keep knees high, lean forward with elbows on knees
o Toilet sits: 5 minutes 3 times per day, preferably after meals
o Chart or diary: positive rewards to frequent bowel motions
o Delay toilet training until child painlessly passing stool
- Diet:
o Increase fibre and fluids
o Decrease cow’s milk as this can exacerbate problem in some kids
- Disimpaction (only for kids >2yo with severe constipation before starting maintenance):
o Use Movicol sachets with the following regime
Maintenace therapy is coloxyl drops if under 12 or movicol if older. Keep up the changes mentioned above.
APGAR?
Activity Pulse (over 100 = 2) Grimace (prompt response to stimulation) Appearance (pink) Resp (vigorous cry)
DDX for acute diarrhoea in kids outside of acute infectious causes?
Chronic diarrhoea?
You can ask questions around this.
Pneumonia or sepsis (meningococcal) C diff, food poisoning
IBD,
DKA, uraemia, thyrotoxicosis, toxins, heavy metals
LI: IBD, colitis, chronic, IBS,
SI: IBD, NSAID’s, infections
Malabsorption: coeliac disease, CF, lactose intolerance, cow’s milk or soy protein intolerance, toddler’s diarrhoea, or short gut.
Red flags on a diarrhoea history?
Persistent, young age, significant pain, bile stained vomit, vomiting without diarrhoea, blood in the stool, presenceof ileostomy or past surgery, hx poor growth, repeated presented.
Infant or child with jaundice
<24 hours of life
Haemoyltic disease of the newborn (Rh or ABO), infections (GBS sepsis), RBC defect (G6PD)
24-72 hours
Physiological: immaturity of bilirubin metabolism at any strep (UDP gluconryl)
Infection (sepsis)
Polycythaemia (delayed clamping)
Concealed haemorrhage secondary to instrumental delivery
Increased enterohepatic circulation (secondary to hirschprung’s) GI ilerus or obstruction.
> 72 hours of life
Congenital (Dubin Johnson, Criggler Najjar etc.)
Sepsis
hypothyroid
Extra hepatic biliary atresia
Neonatal hepatitis (viruses and a1 deficiency)
RBC defect
Breast milk jaundice
Describe hydrops foetalis
It’s an accumulation of oedema in at least two copartments.
Prophylaxis for pertussis?
Done with azithromycin or yucky clarithromycin if they can’t take tablets. If they’ve had a close contact with the patient while they’ve been infectious (21 days and just before the onset of symptoms) or any at risk person (kid < 6 months, not vaccinated, healthcare workers, or people with young kids). Also give them dtpa.
Also remember you would admit any kid less than 6 months of age or with complications
BRUE is the new term. Brief Resolved Unexplained Event. It has a wide differential including basically anything that causes foetal distress. A lower risk BRUE is when there are no concerning features on examination, and it fit the specified criteria. A BRUE in a <60 day old or premmie is pathological. What is the diagnostic criteria, and what is the management?
Diagnostic crtieria are that it’s in a kid less than 12 months old, it’s occurring for less than a minute, they return to baseline, not explained by a medical condition (although it has a wide differential, and is basically any severe acute illness you can think of).
Needs one of the following CCAM features Choking Colour change Aponoea Muscle tone (increase or decrease)
We manage by assessing the baby for potential causes of these features, and identify if they are low risk. Reassure the parent, or admit under the paediatric team if they are having concerning features.
When does crying peak? Define colic? How much sleep do bebes usually need?
Crying peaks around 6 weeks, just before they smile. They can cry up to 2-3 hours per day. Colic is defined as more than 3 hours of crying for 3 or more days during the week for more than 3 weeks.
Before 6 weeks, they need 16 hours of sleep, and get tired after 1.5 hours.
2-3 months, they need 15 hours, and get tired after being awake for 2 hours. It’s a gradual process.
DDx for excessive crying in babies?
Usually it’s physiological, and due to fatigue, hunger, temperature, wet/ soiled nappy, wind, environmental stress or teething (must be painful, remember Fletcher).
Chronic pathological causes of such colic include cow milk/ soy protein allergy, gastro-oesophageal reflux, lactose overload or malabsorption syndromes.
Acute can be UTi, otitis media, intus, incarcerated inguinal herniae, raised ICP, corneal abraision, hair torniquet of the fingers, toes or penis!!!!
Approach to the patient with colic?
Sudden onset should never be diagnosed as colic, and should be investigated. Take a full hx, exploring the differentials. Look for signs of low SES.
Remember vomiting may be a sign it’s reflux (more than more per day. Vomiting can be normal in kids). DIarrhoeal causes could be cow’s milk protein intolernace or lactose intolerance depending on the symptoms.
Figuring out the sequence of events of the crying (antedecent, behaviour, consequence) is always good.
Also, always remember to check with the parents.
Usually very rarely need to do an investigation.
MOst important question to ask in an OSCE station for paeds?
ASK HOW THE PARENTS ARE COPING! Remember, if the parents are not coping, then the baby is going to have a poor outcome because it’s so dependent.
Outline your basic management for a baby with colic please?
Reassure it’s very common, and that it settles around 6-16 weeks.
Educate them on the amount that the baby should be sleeping, and what the signs of fatigue are (i.e. frowning, clenching their little fists, jerking arms and legs, crying), and refer them to the appropriate support groups!
If suspected, cow milk/ soy protein allergy can be done by eliminating the products from the mother’s diet (remember they get it even if breast fed) or change to a formula and reassess after 2 weeks.
If reflux, sit them upright after a feed for 20 minutes, don’t bounce them around, and burp them regularly.
Switch to lactose free products.
SIgns of cow milk allergies or GORD are vomiting, diarrhoea, eczema, failure to thrive, feeding difficulties
How do we differentiate GOR and GORD, and define failure to thrive?
GOR is just the passage of gastric contents up the oesophagus in children. GORD is when it causes vomiting with
pronounced irritability with arching refusal to feed weight loss or crossing percentiles haematemesis chronic cough, wheeze apnoeas
GORD is just GOR with complications. Other complications include oesophagitis, failure to thrive and aspiration events.
Failure to thrive is an older term to describe inadequate weight gain in infants and children. We prefer to use poor growth now because it’s less stressful to parents.
DDx of not passing meconium?
Hirshcprung’s, meconium plug, meconium ileus, imperforate anus,
Ddx of a neonate coming in with abdo pain?
HIrschprung’s incarcerated hernia, incarcerated, intussuseption, Meckel’s diverticulum, UTI, Volvulus, NEC
When does NEC present? How do what are some risk factors?
Bowel obstruction with dyesntery and bilious vomiting. Diminished bowel sounds. Presents 2-3 weeks.
Prematurity, asphyxia and shcok, hyperosmolar feeds, enteral formula feeds (breast feeds protective) and sepsis.
Intestinal inflammation with ulceration. Colon and terminal ileum. Due to bowel ischaemia. Enteral feeding leads to bacterial overgrowth.
Investigations:
Babygram. Look for pneumonitis intestinalis.
FBC and VBG (avidosis)
Blood cultures
UEC
Laparotomy.
Treat NBM for 7-10 IV resus Decompresion with NGT TPN Antibiotics: gent, amoxicillin, metro. Add metro only if there is risk of perf.
Serial AXR is good because you need to watch for perf.
Peritoneal drain if there is perf.
Lap for necrotic bowel.
+/- stoma +/- primary anastomosis.
Neonate, Infant, toddler, Pre school aged child
Neonate is first 28 days Infant up to 12 months Toddler is 1-3 Pre school is 3-5 School aged child is beyond
Note that in an intus we get diarrhoea and the pallor, drawing up associated with a refular obstruction signs. WHat are some advanced signs of the disease?
Billious vomiting
Less pressure and less pain as the intestine continues to dilate
Obstruction of venous outflow causing oedema, and that currant jelly and third space losses
Lethargy
Sausage shaped mass in the epi\gastrium or RUQ
Investigations for an intuss
BSL FBC UEC if unwell
G&H before theatre
Plain abdo x-ray excludes perforation or other obstructive causes, but does not exclude it. Target sign is the diagnostic pattern on the x-ray and crescent sign as well.
An abdo ultrasound is the diagnostic method of choice!
A pneumatic or contrast enema under fluoroscopy can be used. It’s indicated if USS is positive or if good visualisation is not achieved. It’s useful for diagnosis and treatment. Small risk of bowel perforation and bacteramia, but risk is outweighed by the avoidance of getting an operation.
Pneumatic reduction has slightly higher success rate, does not prevent
subsequent radiological studies and no risk of barium peritonitis if
perforation occurs
Success rate approaches 90% if symptoms present <24 hours
Should NOT be attempted if patient unstable or has signs of
peritonism
How do we treat intus?
As I would have said, but note that you can actually give them morphine, and you should consider the IV antibiotics before you do the air enema.
Admit to hospital overnight if there is a spontaneous or an pneumatic/ hydrostatic reduction, because it is associated with a recurrence.
Surgical management is with gentle manual reduction on a laparotomy, with resection of the impacted bowel because of severe oedema, perforation, necrosis, or pathologic lead points such as a polyp, meckel’s diverticulu`m.
Appendicitis is the most common surgical emergency in childhood and peaks at age 10-12. How do we diagnose it?
Diagnose it clinically. Urinalysis can help exclude a UTI, an upright CXR will help use look for perforation and we can look for riggler’s sign etc. on abdo x-ray to look for signs of a perforation. Clacified faecaliths will also be seen.
Please also note that an USS or a CT will be indicated if the patient is having inconclusive findings.
Constipation in kids has a number of differentials. When does it commonly present.
It’s commonly when we introduce solids, during toilet training, school entry, dehydration, intercurrent illness, or if they are stressed out/ acting out. Most do 2-3 daily stools. Breastfed babies can be as infrequently as once weekly, but they can also get diarrhoea remember.
What are some red flags for constipation?
If it’s less than 6 weeks, or associated with other symptoms. It’s likely organic.
Painful defaecation can lead to apprehension, retention, passage of hard stools. young children may ignore the urge to defaecate, causing a build up of large, hard bowel actions.
Less common causes are medical: cow milk allergy, coeliac disease, hypercalcaemia, hypothyroid
Surgical: hirschsprung, mec ileus, imperforate anus, spina bifida.
What are some questions to ask about the constipated child?
History
Timing of meconium passage – most infants pass
meconium in the first 24hrs of life
Painful/ frightening precipitant
Straining
Toilet refusal, hiding while defaecating, crossing
legs or other withholding behaviour
Faecal or urinary incontinence, day or night
Weight loss, vomiting or PR blood loss – suggests
possible organic disease
Stool description
Examination
Height and weight failure to thrive
Abdomen – palpable faeces
Spine – deep sacral cleft or tuft of hair
Neurological – assessment of lower limbs
Anal area – visually examine for fissures (internal examination not required)
Conservative management steps of constipation in children?
Treatment
Behaviour Modifications
Position – footstool to ensure knees are higher than hips. Lean forward and put elbows
on knees. A toilet ring should be placed over the toilet seat if needed.
Toilet sits – 5 minutes three times a day, preferably after meals. A timer in the bathroom
can help. Encourage child to bulge out their abdomen. Praise child for sitting on toilet,
keep toileting a positive experience.
Chart or diary – to reinforce positive behaviour and record frequency of bowel actions.
Delay toilet training attempts until child is painlessly passing soft stool.
Diet
Increasing dietary fibre is not adequate for treatment of constipation, but can help
prevent future episodes
Ensure adequate fluid intake
Excessive cow milk intake may exacerbate
Medications
Osmotic and lubricant laxatives can be used safely on a long-term basis
Titrate medication aiming for one soft, easy to pass bowel action per day
First line options:
o Children: Stool softener (paraffin oil) or iso-osmotic laxative (Movicol or
Osmolax)
o Infants 6-12 months: Coloxyl drops or Lactulose (Actilax)
o Infants <6 months: Coloxyl drops
o Coloxyl + Senna senna is stimulant component and should be avoided unless
stools are soft
Disimpaction Regime
Children with severe constipation benefit from disimpaction before maintenance
treatment begins
Stop once rectal effluent is clear and switch to maintenance therapy
Rectal treatment with suppositories should be used only in cases of severe rectal pain or
distress related to faecal impaction
Inpatient management Macrogol/electrolyte solutions (Colonlytely or Glycoprep) 1-
3L/day via NGT at rate of 25ml/kg/hr normal maintenance fluids should be given in
addition to maintain hydration
Eosinophilic oesophagitis is some bullshit. It’s to do with TH2 predominance in the oesophagus that leads to esoinsinophilic response. I am not going to learn this, but what is the treatment?
Elimination diets guided by circumstantial evidence and food allergy test
results
o “6 food elimination diet” removing major food
allergens (milk, soy, wheat, egg, peanuts/tree
nuts and seafood)
o Elemental diet composed exclusively of an
amino acid-based formula
Topical and systemic corticosteroids have been used for
nonresponders and non-allergenic (primary EoE)
symptomatic and histologic remission rates ~90%
Remember, if it’s secondary to generalised atopy, then it can be associated with other allergies, which could need management by RAST testing etc.
6 food elimination diet: milk, soy, wheat, eggs, nuts, seafood)
Functional abdominal pain is a topic you need to know quite well. It affects 1-15% of children. COnstipation is sometimes associated, but it tends to be overdiagnosed as an aetiology. Describe some clinical features?
Psychogenic factors (eg: family, school issues) need to be considered in some cases.
Non-pharmacological measures (reassurance, relaxation, heat packs) can be tried.
Have pain almost daily
Not associated with meals or relieved by defaecation
Often associated with tendency towards anxiety and perfectionism symptoms often
result from stress at school or in novel social situations
Pain worst in mornings and prevents/delays children from attending school
It is described as being periumbilical!!
IBS is related, but it fits the ROME V criteria.
Remember when working them up, you must rule out any signs of more sinister disease, and this includes the IBD’s. Do a full workup with your history.
Ddx for recurrent abdo pain in kids?
Functional abdominal pain Irritable bowel syndrome Chronic pancreatitis Gallstones Peptic disease o Duodenal ulcer o Gastric Ulcer o Oesophagitis Lactose intolerance Fructose malabsorption Coeliac disease Inflammatory bowel disease o Crohn’s disease o Ulcerative colitis Constipation Obstructive uropathy Congenital intestinal malformation o Malrotation o Duplication cyst o Stricture or web Abdominal migraine Eosinophilic oesophagitis
How do you work up the recurrent abdo pain patient?
Recurrent abdominal pain can be worked up by:
Warning signs and complete history.
Determine the effect of the impairment i.e. are they missing school
FBC, ESR, Lipase, Urinalysis
Abdominal USS
Trial of 3 day lactose free diet.
Investigate as required.
Ways to differentiate functional from organic abdominal pain in a kid?
How do we manage?
Does it disappear at different times of the day?
Constipation can be a feature, but it’s overdiagnosed as a cause. Have they had any other symptoms pointing to an organic pathology?
Where is it located? Periumbilical is more likely to be functional, whereas specific locations with tenderness are more organic.
Child repeatedly kept home from school because of pain receives reinforcement and
withdraws from full social functioning
Increases anxiety and prolongs the course
Assist child in returning to normal activities immediately
o Instead of being sent home with stomach-aches child take short break from
class until symptoms abate
o Inform child and parents pain likely to be worse on day child returns to school
as anxiety worsens dysmotility and enhances pain perception
Fibre supplements may help manage symptoms of IBS
Probiotics and peppermint oil can be beneficial
Cognitive behavioural therapy, amitriptyline or SSRI may be helpful
When significant anxiety or social dysfunction persists consult mental health
professional
When do sickle cell and Thal present? g6pd?
tHEY PRESENT 4-6 months when the foetal haemoglobin goes away.
G6PD can present at birth with jaundice.
Write out a list of differnetials, and remember to aks about famly factors associated?
Drugs increasing risk of anaemia?
G6PD, SPherocytosis, ellipitocytosis, Diamond-Blackfan, Sickle cell anaemia, Thal
Nitrofurantoin and antimalarials
Penicillins (haptens causing complexes and destruction)
Chemo
Phenytoin
When do you admit for an anaemia?
If suspect it’s a serious disease
Hb <60g
Haemolysis
Needs transfusion
Management of iron def anaemia?
If dietary history is strongly suggestive of iron-deficiency
o Modify diet (increase red meat, chicken, fish, pulses, green vegetables; limit cow’s
milk consumption to 500 ml/day)
o Give iron supplementation (if Hb < 100g/l or low ferritin).
o Arrange follow-up to ensure appropriate response to treatment.
Iron supplementation - aim for 2-6 mg/kg/day (higher doses for severe anaemia should be
given tds to avoid gastric irritation)
o Ferro-Liquid 6mg/mls 0.3-0.45 mls/kg/day
o Ferrous sulphate spansules contain beads that can be sprinkled onto food for
lower doses, shouldn’t be crushed or chewed
o Ferro-Gradumet SR tablets for children who can swallow them whole
Transfusion rarely required (e.g. cardiac failure, urgent surgery required)
Definition of LBW or Macrosomia?
What is normal weight gain for babies?
Describe the normal weight gain for a pregnant woman.
Management of overwight in pregnancy/
Macrosomia is over 4000g, but LBW is under 2500 grams.
150-200g in first 3 months per week, then 100-150g after that is a normal weight gain for a baby per week.
11.5 - 16 kg is a normal range of weight gain for a pregnant woman, and it changes based on their BMI. Brydie says that it’s 12kg.
However, want them gaining less than this if they are GDM or obese (something like 5-9 kg). Thus, you don’t want them to go and lose weight, because that’s dangerous for the
Diagnostic pitfall of thal alpha?
Need HbA2 of more than 3.5% and needs to be pathological. Also, it may not be elevated if the patient also has an iron deficiency. Therefore, you need to offer the patient iron supplements to boost their Hb production before you diagnose.
Discuss the presentation of anaemia in the newborn infantg versus in the frirst few days of life:
At birth: heart failure, pallor or shock. Possible causes: haemolytic disease of newborn, tearing/cutting of umbilical cord
during delivery, abnormal cord insertion, communicating placental vessels,
placent praevia/abruption, nuchal cord, incision into placenta, internal
haemorrhage (liver, spleen, intracranial), α-thalassaemia, congenital
parvovirus/hypoplastic anaemias, twin-twin transfusion in monozygotic twins
If it’s in the first few days, most frequently haemolytic disease of the newborn. Other causes: haemorrhagic disease of newborn, bleeding from improperly tied
umbilical cord, large cephalohaematomas, intracranial haemorrhage, subcapsular
bleeding from liver/spleen/adrenals/kidneys
o Detected by rapid decreases in haemoglobin or haematocrit
Discuss anaemia of prematurity:
Occurs in low birthweight infants 1-3 months after birth.
Clinically manifests as pallor, poor wieght gain, decreased activity, tachypnoea, tachycardia, and feeding problems.
It is usually due to repeated phlebotomy, shortened RBC survival, rapid growth and physiological transition from foetal haemoglobin to neonatal. PaO2 goes up but sats reduce due to the lower affinity.
Delayed cord clamping (30-180 seconds) with infant held below the placenta is a good way to prevent, but this should not be done as substitute for resus as they are an increased risk of PPh.
What are the fluid compartments you need in hydrops faetalis?
It’s 2 or more of skin, pleura, pericardium, placenta, peritoneum or amniotic fluid.
DDX for childhood obesity? How would you assess?
Lifestyle: high calories or low exercise
Genetic: Prader Willi, Turner’s, Down’s
Endocrine: hypothyroid, Cushing’s, GH deficiency, PCOS, hypothalamic lesion
Look at their growth charts etc and do a full physical examination looking at the features above. Ask all around their lifestyle, and puberty for Turner’s/ neck lumps in the thyroid (low thyroid)
What is obesity for Kids under 2?
97th percentile: babies tend to be fat. ALSO REMEMBER THEY JUST CALL IT OVERWEIGHT! It’s not obesity in this age group.
Management suggestions for obesity
- Explain long-term consequences of obesity
- Implement nutritional changes and exercise aimed at changing lifestyle not weight, eg.
Implement ‘fun’ activities, decrease sugar intake, improve lunchbox and portion sizes - Involve entire family, set as priority
- Seek dietetic advice if necessary
- Decrease TV and screen time, don’t eat in front of TV
- Underlying syndromes and endocrine causes are rare but these involve different
management approaches
Differentials for jaundice in a newborn?
<24 hrs:c Haemolytic disease of the newborn, infection (GBS sepsis), and RBC defect
24-72 hours of life: physiological (immaturity of bilirubin), infection (sepsis), polycythaemia (delayed clamping), concealed haemorrhage, or increased enterohepatic circulation (secondary to bowel obstructions)
72 hours: Congenital jaundice, sepsis, hypothyroid, biliary atresia, neonatal hepatitis or a1 deficiency, RBC defects
Jaundice management? What about conjugated?
Management
Unconjugated Hyperbilirubinaemia
- Discharge instructions:
o Sunlight exposure not recommended
o Arrange early follow-up with GP to ensure adequate oral intake,
especially if:
<3 days old
Exclusively breastfed
Bilirubin level is borderline for requiring treatment
- Phototherapy converts bilirubin into structural isomers that are lipophilic and
excreted into bile without undergoing glucuronidation
o Monitor weights and electrolytes daily
o Correct dehydration
o Recheck bilirubin 6 hours after initial test
o Ensure eyes are protected
- Exchange transfusion transfusion of blood volume
o Only carried out in tertiary
facility
If it’s conjugated, refer to surgery lol.
Generalised swelling mnemonic?
Nephrotic syndrome, nephritic syndrome, allergic reaction / anaphylaxis, heart failure, malnutrition, other causes of hypoalbuminaemia like protein losing enteropathy.
Features of anaphylaxis?
Features:
o Resp: tongue swelling, stridor, hoarse voice, tingling throat, cough,
wheeze, dysphagia
o Other: pale/floppy, palpitations, tachycardia, hypotension, ALOC, nausea,
vomiting, diarrhoea, generalised pruritus, urticaria, angioedema, collapse
- Diagnosis: clinical, no Ix required
- Management:
o 0.01ml/kg of 1/1000 adrenaline (max 0.5ml) IMI lateral thigh, repeat
after 5 minutes if not improving
o Generally: <6yo = 150mcg (0.15ml); 6-12yo = 300mcg (0.3ml); >12yo =
500mcg (0.5ml)
Nephrotic and Nephritic syndrome: how do we differentiate?
Proteinuria, oedema, urine output, GFR, metabolic findings, casts.
Proteinuria is >3.5g/ day in nephrotic. Oedema is featured due to low albumin, and polyuria, increased GFR, dyslipidaemia (high cholesterol) and lipiduria due to urinating out LCAT and LPL. They are also hypercoaguable, and they have protein casts.
Nephritic syndrome: non selective proteinuria, oedema (due to RAAS - salt retention), oliguria, decreased GFR and increased CR, BUN (reduced urea creatinine ratio), hypertension, protein casts and red cell casts.
Non prolif vs prolif glomerulonehritis:
Non prolif is minimal change, membraneous, focal segmental
Prolif is IgA nephropathy, Membranoproliferative, rapidly progressive, post infectious (PSGN).
Types of nephrotic?
90% is idiopathic, and 85% of this is minimal change. 15% is focal segmental glomerulosclerosis.
10% is due to congenital, henochschonlein, SLE etc.
Proteinuria, hypoalbuminaemia and oedema are the classic features that often follows an URTI.
How do we work up these nephrotic patients?
Is it mild moderate or severe oedema? Mild is just peri orbital or scrotal/ labial, moderate is pitting on the limbs or sacrum, and severe is gross limb, ascites, pleural effusions.
If they have features or rash, it’s likely not nephrotic. Thus rule out nephritic.
Acute complications are hypovolaemia, infection (from cellulitis, peritonitis) and thrombosis.
Investigate with a dipstick, microscopy of urine.
Do FBC, UEC, LFT, C3/4, ANA, serum lipids, coags screen, hep B (causes membraneous).
How do we manage nephrotic syndrome?
Management:
- Admit to hospital on 1st presentation
- Manage oedema:
o No added salt diet, daily weights and urine dipsticks
o Strict fluid balance
o IV 20% albumin with frusemide if intravascular volume depletion of
severe symptomatic oedema - Prophylaxis against complications:
o Penicillin V (phenoxymethylpenicillin) 125mg/dose 12 hourly (<5yo) or
250mg/dose 12 hourly (>5yo) until oedema subsides
o Ranitidine 2-4mg/kg/dose 12 hourly (max 150mg) or PPI as prophylaxis
against prednisolone induced gastritis - Prednisolone:
- 60 mg/m2 per day as a single dose (max 60 mg/day) for 4 weeks. Then:
- 40 mg/m2 alternate day (max 40mg) for 4 weeks
- 20 mg/m2 per alternate day for 4 weeks
- 15 mg/m2 per alternate day for 4 weeks
- 10 mg/m2 per alternate day for 4 weeks
- 5 mg/ m2 per alternate day for 4 weeks
- Note: this is treatment for 1st episode, relapse treatment is same but each
dose is for 2 weeks - Family education:
o Prognosis: 80% of idiopathic glomerulonephritis will respond to steroids
BUT 80% have a relapse and 50% have frequent relapses
o Teach how to test urine protein each morning and document for
nephrology appointments
o After remission, still test urine daily for 1-2 years for relapse (defined as
3+ protein for 3 consecutive days)
Approach to the nephritic syndrome?
IgA nephropathy has an association with Coeliac just remember.
Ask about the features and examine for them, particularly looking for asystemic features of a rash, fever or arthritides.
Urine: dipstick, microscopy (haematuria), spot protein creatinine ratio
- Blood: FBC, UEC, LFT, C3 & C4, ANA (SLE), anti-DNase B & ASO (PSGN)
- Kidney biopsy
We do biopsy these, but not nephrotic.
- PSGN: penicillin, potentially diuretics depending on level of HTN, low-sodium &
low-protein diet initially - IgA nephropathy: observation but if significant use corticosteroids
DDX for a faint, fit or funny turn? (unique to kids)
Think about hyperventilation or febrile convulsions.
Discuss febrile convulsions: what are they?
Convulsion in child between 6 months to 6 years, in the setting of an acute febrile illness,
without previous afebrile seizure, significant neurological abnormality and no CNS
infection. 3% of healthy children get these.
Differentiate between a simple and a complex febrile convulsion?
Classification:
- Simple: generalised, tonic-clonic seizures <15 minutes that do not recur within same
febrile illness
- Complex: have one or more of the following
o Focal at onset or during seizure
o Duration >15 minutes
o Recurrence within same febrile illness
o Incomplete recovery within 1 hour
Complications:
- Febrile status epilepticus: >30min duration
How do treat febrile convulsions?
Acute Management:
- Reassurance
- Paracetamol for pain, note that it does not decrease chances of febrile seizures
- When necessary treat as per afebrile convulsion guidelines
Counselling to parents:
- During the seizure:
o Nothing can be done to stop seizure
o Stay calm
o Place child on soft surface
o Do not restrain or try and cool down
o Watch what happens and time it, record if possible
- Call 000 if:
o Lasts more than 5 minutes
o Child doesn’t wake up afterwards
o Child looks very sick afterwards
o Educate on what makes a complex febrile seizure and when to bring to ED
- After the seizure:
o Loosed tight clothing and roll on side if necessary
o Don’t allow child to be by themselves if they are in a dangerous area, eg. Around
water or dangerous objects
o Otherwise go about usual routine with more regular monitoring of child
o No need to try and reduce fever, it is natural response of body to infection
o Ensure all who care for child are aware of what happened
o If in hospital, only discharge if CNS infection ruled out and seizure action plan
provided
- Follow-up:
o Increased risk of having another febrile convulsion
o Most kids who don’t have any long-term consequences
o Normally grow out of them by 6 months
What is the guthrie card?
Thyroid, PKU, Immunotrypsinogen (CF), sickle cell, galactosaemia and random bullshit.
Prophylactic antibiotic coverage for surgery?
Cephazolin and metronidazole for small bowel. For the biliary it’s just cephazolin.
For colorectal surgery it’s metro + either cephazolin or gent.
Triple therapy is only if they’re really crook.
