CHH Flashcards
Development - 6 weeks
Head control – 45⁰ when prone
Stabilises when sitting
Follows object to midline
Startles to loud noise
Social Smile
Development - 3 months
Head steady when in sitting position
Follows past the midline
Vocalises, coos and laughs
Spontaneous smile
Development - 6 months
Rolls front to back
Palmar Grasp/Transfers
Turns to loud sound, Babbles
Mouths objects, Holds a bottle
Development - 9 months
Stands with support
Pincer Grip
Bangs cubes
Responds to own name
Play’s Peek-a-boo
Holds/Bites food
Development - 12 months
Stands independently
Casts bricks
Mama/Dada
Waves/Claps
Drinks from a beaker with a lid
Development - 18 months
Walks (9-18 months)
2 Cube tower, scribbles
Vocab: 3-6 words, Understands nouns
Imitative play
Development - 24 months
Run, Kicks Ball
4 Cube Tower
Draws a vertical line
Vocab: 50 words
2 Words Together
Understands Verbs
Removes a garment
Development - 2.5 years
Jumps
Throw Ball over head
6 Cube Tower
Draws a Horizontal Line
Vocab: 6 Body parts
3-4 word sentences
Understands prepositions
Eats well with a spoon
Development - 3 years
Balance 1 foot, 1 second
8 cube tower, 3 brick bridge
Draws a circle
Uses Adjectives
Understands negatives
½ understandable speech
Eats with a fork/spoon
Puts on a t-shirt
Takes turns
Development - 4 years
Balance 1 foot, 3 seconds
Hops
Builds Steps (6 bricks) Draws a Cross
Understands Comparatives
Knows 4 colours
Sympathy, imaginative play
Dresses alone
Development - 5 years
Balance 1 foot 5 seconds
Heel-toe walk
Skips
Draws a Triangle & Person 6 parts
Understands Complex (3 part) instructions Counts to 5
Can play a board game
Brushes teeth
Uses a knife
Use of anti-pyretics
Either paracetamol or ibuprofen, but not normally both simultaneously
Generally only used if the child is distressed
Anti-pyretics will not prevent febrile convulsions
Febrile convulsions - when and why?
Ages 6 months to 5 years.
Usually due to infection or inflammation outside the CNS in an otherwise well child
Simple febrile convulsion
isolated, generalised, tonic-clonic seizure
Complex febrile convulsion
Complex if 1+ of:
- Focal onset/focal features
- Duration >15 minutes
- Recurs within 24h/same illness
- Incomplete recovery after 1 hour.
Febrile convulsions - management
- If cease before presentation – do not give drug treatment.
- If >5 mins – rectal diazepam/buccal midazolam.
Always check blood glucose if child is unconscious/is convulsing
How is suspected meningitis managed in the community?
Single dose of benzylpenicillin IV/IM and immediate transfer to hospital (call 999)
Abx in meningitis - <3 months
IV cefotaxime and IV amoxicillin (to cover listeria meningitis) and IV gentamicin
Abx in meningitis - >3 months
IV ceftriaxone
also IV gentamicin (only if probable sepsis)
Management of meningitis
Ideally blood cultures and LP before Abx (unless significant delay)
Start Abx
If probable or confirmed bacterial meningitis – dexamethasone, ideally with first dose of antibiotics
Supportive therapy - high flow O2, fluids, antipyrexials
Why is dexamethasone used in bacterial meningitis?
Decreased sequelae in pneumococcal meningitis and Haemophilus Influenzae meningitis.
No evidence of improved outcome or harm in meningococcus/viral meningitis.
UTI in children
= commonest bacterial infection of children.
Most commonly caused by E. coli.
Urgently admit if <3 months and UTI is suspected.
Older children may also need admission if at risk of serious illness.
When should a UTI be treated?
If leucocytes and nitrites (or just nitrites) are positive on urine dip
If good clinical suspicion of UTI
What should be done if only leucocytes or neither leucocytes/nitrites are raised on a urine dip?
Potentially look for other focus of infection.
Only treat UTI if high clinical suspicion
Follow-up for UTI
When is it appropriate to refer to a specialist?
If not improved after 24-48 hours, review treatment and diagnosis
Follow up result of any urine sent for culture and review antibiotics
Refer urgently to specialist if:
- Poor response to appropriate treatment
- History/clinical features suggest urinary tract obstruction
What age group is affected by bronchiolitis?
Birth – 2 years
BUT most common in 1st year
What causes bronchiolitis?
Viral cause - ~75% RSV
Can be bacterial superinfection in more severe cases
Management of bronchiolitis
- Close fluid management (IV/NG/oral)
- Oxygen to maintain sats
=> may need CPAP/high flow nasal cannula oxygen
~15% of patients will require admission to intensive care for intubation/ventilation
What groups of children are typically affected by viral-induced wheeze?
Age 6 months – 5 years
=> Most will “grow out of it” before school
Association between passive smoking and severe disease.
What can cause viral induced wheeze?
All respiratory viruses
Management of viral-induced wheeze?
Fluids
Oxygen to maintain sats
Salbutamol (10 puffs MDI or nebuliser):
=> Hourly or back-to-back initially
=> Stretch to 2-hourly as tolerated
=> Can discharge when at 3-4 hourly
What is more likely with an older child presenting with viral-induced wheeze?
The child is more likely to present with asthma later on
What age group is affected by croup?
6 months – 6 years
most common age 2-3
what causes croup?
Parainfluenza most common cause, but possible with all respiratory viruses.
Management of croup
Fluids, antipyretics
Aim to keep child calm
Oxygen to maintain sats
Single dose of oral dexamethasone (or nebulised budesonide)
Nebulised adrenaline if inadequate response to steroids
What age group is affected by pneumonia?
All paediatric age range
What causes pneumonia?
Strep. pneumoniae,
Staph. aureus,
H. influenzae,
Some cases are likely to be viral, but cannot be distinguished clinically
Management of pneumonia
Fluids, oxygen to maintain sats.
Amoxicillin 1st line if uncomplicated CAP (5-7 days)
Benzylpenicillin/Cefuroxime if IV treatment needed
Consider macrolide if no response to 1st line treatment at 48h
What causes otitis media?
50% viral cause
Bacterial causes include:
- S. pneumoniae
- H. influenzae
- S. pyogenes
- M. catarrhalis
- S. aureus
Management of otitis media
80% of cases resolve without treatment in ~4 days (regardless of cause)
Delayed Abx may be considered as this is as effective as immediate treatment
=> Amoxicillin – 5 days (clarithromycin if pen allergy)
when might immediate antibiotic treatment be considered in otitis media (instead of delayed Abx)?
in a systemically unwell child with fever, vomiting, pain for >48h and otorrhoea, and those with other comorbidities
What is the most common chronic illness affecting children?
Asthma
What is asthma?
An inflammatory condition, leading to reversible airway obstruction causing intermittent wheeze.
The airways narrow due to smooth muscle contraction and mucous hypersecretion
Symptoms of asthma
Cough, Wheeze, Breathlessness, Chest tightness
AND evidence of variability in airway obstruction
What are signs of poorly controlled asthma?
Increase in cough, SoB, wheeze
Difficulty walking/talking/sleeping
Reduced relief from/frequent use of SABA
What clinical features would increase the probability of a diagnosis of asthma?
Symptoms - frequent, worse at night/early morning, occur in response to triggers
Personal or family Hx of atopy
Widespread wheeze heard on auscultation
History of improvement of lung function in response to adequate therapy
What clinical features would decrease the probability of a diagnosis of asthma?
Symptoms with colds only, no interval symptoms
Isolated cough in the absence of wheeze/SoB
Dizziness/light-headedness/peripheral tingling
Normal PEF when symptomatic
No response to trial of asthma therapy
Clinical features pointing to alternative diagnosis
What PMHx may be relevant for asthma?
Atopy - hay fever, eczema
Recent URTI
What FHx may be relevant for asthma?
Atopy
Asthma
What SHx may be relevant for asthma?
Impact on daily activities/hobbies
Pets
Smoking
Parental smoking
Diagnosis of asthma
Normally based on history and examination
- PEF - looking for reversibility/diurnal variation
- Spirometry (only really from age 6+ due to technique)
- ?IgE/skin prick tests for allergens
- ?CXR to r/o other conditions
Non pharmacological management of asthma
trigger avoidance, breathing exercises
Pharmacological management of asthma
Step-wise approach - start with most appropriate therapy based on presenting severity
SABA as required, plus:
- very low dose ICS (or LTRA if <5 years)
- very low dose ICS plus LABA/LTRA
- consider increasing to low dose ICS
- Refer to specialist care for further therapies
Step up if using SABA >3 times per week.
What is defined as complete control of asthma?
- No daytime symptoms
- No night-time waking due to asthma
- No need for rescue medication
- No asthma attacks
- No limitations on activity, including exercise.
- Normal lung function (FEV1 and/or PEF >80% predicted)
- Minimal side effects from medication
Actions of Salbutamol
Relieve acute breathlessness by relaxing bronchial smooth muscle
Duration of action = 3-6 hours (maximum effect at 30mins)
Side effects of salbutamol
Palpitations, tremor
Vasodilatation,
Hypokalaemia,
Muscle cramps
What would you expect to see on the U&Es of a patient on back-to-back salbutamol nebs?
hypokalaemia
Actions of inhaled corticosteroids
Provide control of the disease by reducing airway inflammation
Symptoms alleviated after ~3-7 days from initiation
When are ICS considered in asthma?
Any child who is:
- Using SABA ≥3 times/week
- Symptomatic ≥3 times/week
- Waking one night a week
- Aged 5-12 years with an exacerbation requiring oral steroids in the last 2 years
Adverse effects of ICS
Local - oral candidiasis, hoarseness, infections
Systemic - growth restrictions, osteoporosis, acute adrenal crisis
Use of LABAs in asthma
Limited evidence for use <5 years, and not licensed for <4 years
Added on to therapy with ICS (not used alone)
Why should a LABA only be used alongside inhaled steroids?
LABA alone causes increased risk of asthma-related death
Use of LTRAs (e.g. montelukast) in asthma
Reduce inflammation and hyper-responsiveness
Regular preventative therapy – alternative to/in addition to ICS
Less effective than ICS alone or ICS plus LABA in children >5
Rare adverse event: Churg-Strauss syndrome
Churg-Strauss syndrome
= a rare form of systemic vasculitis:
eosinophilia, vasculitic rash, worsening pulmonary symptoms, cardiac complications peripheral neuropathy
What are the issues around using aminophylline/theophylline in managing asthma?
Narrow therapeutic range – target plasma levels between 10-20mg/L.
Side effects within therapeutic range – nausea, headache, insomnia, palpitations, arrythmias
At toxic levels – arrythmias and seizures
Indications for use of oral steroids in asthma
- Acute exacerbation – 3-5 days short course
2. Chronic severe asthma – when response to other drugs is inadequate (high dose ICS continued to reduce oral dose).
Stopping oral steroids used for asthma
can be stopped abruptly, UNLESS:
- Course >3 weeks
- Already on maintenance oral corticosteroids
- Repeated short courses.
Use of monoclonal antibody (e.g. Omalizumab) in asthma
s.c. injection every 2-4 weeks depending on the patient’s IgE level and weight
Reduces the steroid burden for the patient, without increasing the risk of adverse events
mAb forms complexes with free IgE and prevents its interaction with these receptors
What is important to remember when prescribing salbutamol
State the dose, frequency, and max number of doses in 24h explicitly to the child/parents
“as required drug” in a hospital drug chart
route - inhaled or via nebuliser
What is important to remember when prescribing ICS
Prescribe by BRAND!
Important to put brand name and dose
regular prescription on drug chart
What is important to remember when prescribing a LABA
regular prescription on drug chart
Often in combination inhalers (e.g. seretide)
Do not initiate in rapidly deteriorating asthma
Initiate at a low dose and check effect before increasing – review effect regularly
Benefits of using a spacer in asthma
- Remove the need for coordination – tidal breathing is effective.
- Reduce risk of oral infection from ICS
- Suitable for managing mild/moderate exacerbations.
Stepping down asthma treatment
Review regularly and titrate steroids down if possible.
Do not step-down treatment if ongoing symptoms and needing reliever, or if they have had a recent exacerbation
If there is symptom control - reduce ICS dose slowly
(e.g. by 25-30% every 3 months)
Severe asthma exacerbation
SpO2 <92% PEF 33-50% Tachypnoea Tachycardia Audible wheeze Accessory muscle use
Signs/symptoms suggesting a life-threatening asthma attack
SpO2 <92% PEF <33% RR reduced (exhaustion) Tachycardia Silent chest Cyanosis Altered consciousness/confusion
Life-threatening asthma exacerbation - “CHEST”
Cyanosis Hypotension Exhaustion Silent chest Tachycardia
Mild-moderate Asthma exacerbation - management
Admission if poor response
SABA via spacer (up to 10 puffs every 2 mins)
Consider PO prednisolone
Moderate-severe Asthma exacerbation - management
Admission
O2 via mask (if sats <94%)
SABA via nebuliser (if on O2)
PO prednisolone 20mg
life-threatening Asthma exacerbation - management
Initially
- Urgent admission
- O2 (if sats <94%)
- SABA + ipratropium via nebuliser (every 20-30 minutes)
- PO prednisolone / IV hydrocortisone
If no improvement:
- Contact PICU for review
- IV treatments – magnesium, aminophylline
- Blood gases
When can a patient be discharged after admission for an asthma exacerbation?
May be discharged when off nebulisers and >4 hours between inhalers:
- Continue SABA PRN
- Continue prednisolone PO for 3-5 days.
GP follow-up in 48 hours
What is the difference between normal saline and Hartmann’s solution?
Hartmann’s is considered to be more “physiological” than Normal Saline as it contains other electrolytes in concentrations similar to plasma.
Both are distributed in the intra-vascular and interstitial spaces, making them useful for both resuscitation and fluid maintenance.
How to calculate fluid requirements in children?
First 10kg weight => 100 mL/kg OR 4 mL/kg/hour
Second 10kg weight => 50 mL/kg OR 2 mL/kg/hour
All additional Kg weight => 20 mL/kg OR 1 mL/kg/hour
Which solutions should be used for maintenance fluids in children?
Isotonic crystalloids that contain sodium in the range 131-154 mmol/L must be used as first line maintenance fluids and for resuscitation, commonly used with 5% glucose
AVOID fluids with low/no saline
Why should fluids with no/low saline be avoided for maintenance fluids in children?
Children are more prone to dilutional hyponatraemia than adults
Increased ADH production during illness causes retention of water, and thereby increased risk of dilutional hyponatraemia
Monitoring for IV fluids
Check U&Es at least daily (every 4-6 hours if abnormal)
Assess fluid balance (input vs output) and hydration status
Check blood glucose at least every 12 hours
If hyponatraemia symptoms – check U&Es, glucose and serum osmolality immediately
Dilutional Hyponatraemia
the most common electrolyte abnormality seen in patients on IV fluids
Predominantly neurological symptoms – seizures, drowsiness, confusion.
Hyponatraemic seizures (usually generalized tonic-clonic) are a medical emergency
Recognising hyponatraemia
Na+ of 130-135 is often asymptomatic
Na+ <130 is mainly neurological symptoms:
- Headache
- N+V
- Lethargy, irritability
- Hyporeflexia
- Decreased conscious state
- Seizures
- Dry, inelastic Skin
- Apnoea
How much potassium should be added to IV fluids?
If K+ serum level is in range when starting fluids, aim to give about 1mmol/kg/day
=> split across fluid bags and then adjust according to U&Es
If K+ serum level is unknown when starting fluids – give with caution/avoid until serum level known and urine output established
How can you recognise dehydration in a child?
Gold standard = acute weight loss
Normally just estimated clinically:
3 groups to consider:
- No clinically detectable dehydration
- Clinical Dehydration
- Clinical Shock – ~10% dehydrated.
What features might suggest clinical dehydration?
Tachycardia
CRT >2s
Decreased skin turgor
Tachypnoea
What features might suggest clinical shock in a dehydrated child?
Weak pulses CRT >3s Decreased skin turgor Hypotension Decreased consciousness Very tachycardic
Management of a child who is clinically dehydrated
ORT 50ml/kg over 4 hours PLUS maintenance fluid (via NG tube if needed)
Use IV fluids if child deteriorates despite ORT/persistent vomiting of anything given PO or NG tube
Management of a child who is clinically shocked
Sodium chloride 0.9% 20mL/kg IV bolus
=> repeat if remains shocked
=> refer to PICU if shocked after 2nd bolus
One shock resolved, commence IV deficit replacement
Attempt to stop IV fluids early, with gradual introduction of ORT during IV fluids.
What is the size of an IV fluid bolus in a child?
20 mL/kg
Oral Rehydration Therapy
Dioralyte – 1 sachet in 200ml.
- Under 5 years – aim for 50mL/kg over 4 hours, plus maintenance volume.
- Over 5 years – 200mL after each loose stool (in addition to normal fluid intake)
How to calculate IV fluid replacement
if shocked, then add 100 ml/kg to maintenance and give over 24 hours
if not shocked, add 50 mL/kg to maintenance and give over 24 hours
Fluid choice for resuscitation vs replacement
Resuscitation – isotonic crystalloid without glucose.
Replacement – isotonic crystalloid with glucose.
HYPERtonic dehydration
How is this caused?
Presentation?
How is it corrected?
Na+ >150
Can occur through severe, acute water loss.
More commonly occurs by parents making up feeds incorrectly
Child often hungry, but few signs of dehydration. Skin can be “doughy” and metabolic acidosis present.
Aim for correction over 48 hours and fall of <0.5 mmol/L Na+ per hour.
HYPOtonic dehydration
Na+ <130
Usually dilutional
Child lethargic and skin dry/inelastic
Give maintenance fluids plus deficit as calculated, checking U&Es every 4 hours.
how should hypertonic dehydration NOT be managed?
DO NOT manage hypertonic dehydration with fluid with no sodium – rapid drops in serum sodium causes a relatively high CSF sodium, attracting water into the CSF (can be fatal).
How is the foetal circulation different to “normal” circulation?
- Left atrium pressure is low, as little return from the lungs
- Right atrium pressure is high, as it receives all systemic blood (including from placenta).
- RA pressure keeps foramen ovale open, and blood flows from RA to LA.
- Blood also bypasses lungs by flowing through the ductus arteriosus.
How does the foetal circulation change at birth?
Decreased pulmonary resistance => more blood into LA => increased LA pressure
Loss of placental circulation => decreased RA pressure
Foramen ovale closes
Ductus arteriosus closes within the first few hours/days
What are “duct-dependent lesions?”
In severe left-sided obstructions, blood flow through the ductus arteriosus is critical for survival.
There will be a dramatic deterioration when the duct closes
=> Tetralogy Of Fallot, TGA, HLHS, aortic stenosis/coarctation
Congenital heart disease - Holes
atrial septal defect (ASD)
ventricular septal defect (VSD)
Atrioventricular septal defect (AVSD)
Congenital heart disease - pipes/valves
Patent ductus arteriosus (PDA)
Aortic/pulmonary stenosis
Coarctation of the aorta
Congenital heart disease - CYANOTIC diseases
Transposition of Great Arteries (TGA) Tetralogy of fallot Hypoplastic left heart Tricuspid Atresia Pulmonary Atresia
How can congenital heart conditions present?
- Antenatal cardiac USS diagnosis (at 20 weeks)
- Detection of a heart murmur
- Heart failure
- Cyanosis
- Shock and collapse
Innocent heart murmurs
30% of children will have at some point (often during febrile illness/anaemia)
= Soft, Systolic, Sternal Edge, Asymptomatic, No thrills and normal CXR/ECG
Presentation of atrial septal defect
Child will generally be fairly well
Often presents when the child visits the GP for another reason and a murmur is heard = EJECTION SYSTOLIC murmur (split S2)
Why are ASD/VSDs and PDA not cyanotic diseases?
Left-to-right shunt => no cyanosis
Atrial septal defect - Investigations
ECG - potentially partial RBBB/right axis deviation
CXR - pulmonary oedema, cardiomegaly
Is patent foramen ovale an ASD?
It is a normal variation of the anatomy
Fairly common and goes unnoticed.
Atrial septal defect - Management
Usually no urgent treatment required
Can close spontaneously
Keyhole or surgical procedure to close it at ~4 years
What is the most common congenital heart defect?
VSD
2nd most common = coarctation of aorta
When is a VSD normally found?
- Identified as incidental finding at 6-week baby check (by that point the right-sided pressure has come down and the murmur will be audible)
- Failure to thrive.
What type of murmur occurs with a VSD?
= Pansystolic
The volume of the murmur does not correlate well with the size
Ventricular septal defect - Investigations
ECG – Right axis deviation and biventricular hypertrophy.
CXR – pulmonary oedema, cardiomegaly
Ventricular septal defect - Management
Can resolve spontaneously
Surgery to fix at <1 year.
What is Maladie de Roger ?
A very small VSD
=> High pitched squeaking sound
What is Eisenmenger’s Syndrome?
Long standing left-to-right shunt (e.g. untreated VSD) causes right ventricular hypertrophy
Eventually this leads to reversal of the shunt to a cyanotic right-to-left shunt.
Incidence of Eisenmenger’s is decreasing - earlier diagnosis and management
What genetic condition is strongly associated with AVSD?
Trisomy 21
90% of AVSDs will be in children with Down’s
What type of murmur occurs with an AVSD?
= Pansystolic murmur
Atrioventricular septal defect - Investigations
ECG – superior (north-west) axis
CXR – pulmonary oedema, cardiomegaly
Atrioventricular septal defect - Management
Surgery <6 months
Patent Ductus Arteriosus
= Failure of duct closure by 1 month after estimated date of delivery (not pathological if pre-term).
Blood flows from the aorta to the pulmonary artery (i.e. a left-to-right shunt)
Presentation of PDA
Normally asymptomatic
Can have heart failure and pulmonary hypertension if duct is large
What type of murmur occurs with PDA?
A continuous, “machinery-like” murmur
Patent Ductus Arteriosus - Investigations
Echo – shows patent duct
CXR and ECG – usually normal
Patent Ductus Arteriosus - Management
Ibuprofen
Surgical tying
Closure with coil/occlusion device
What is aortic Stenosis?
What can it be associated with?
= Narrowed/deformed aortic valve
Can be associated with bicuspid aortic valve, Turner’s Syndrome
When does aortic stenosis normally present?
If Critical – shortly after birth with collapse
If Mild – chest pain on exercise
Presentation of aortic stenosis
Inadequate cardiac output leads to shock presentation:
- Globally poor peripheral pulses
- Tachypnoea
- Mottled/grey appearance
Aortic stenosis - on examination
loud ejection systolic murmur,
Right sternal edge (2nd ICS) radiates to the carotid arteries
Aortic stenosis - Investigations
ECG – left axis deviation, left ventricular hypertrophy
What is pulmonary stenosis?
What can it be associated with?
= Narrowed/deformed pulmonary valve.
Can be associated with Noonan’s Syndrome and William’s syndrome
Pulmonary stenosis - on examination
Murmur – ejection systolic murmur at left sternal edge
RV heave
Pulmonary stenosis - Investigations
ECG – RV hypertrophy
What is coarctation of the aorta?
What can it be associated with?
= narrowing of the aorta,
usually distal to the branches supplying the upper limbs
Can be associated with bicuspid aortic valve and Turner’s syndrome
How does coarctation of the aorta present?
Affects lower limbs, not upper limbs – Absent femoral pulses
Lack of blood flow to the rest of the body => renal failure/gut ischaemia
Can cause back up of flow into LV, eventually causing cardiac failure
Coarctation - on examination
ejection systolic murmur, heard between shoulder blades
Coarctation - management
Resuscitation
Cardiac catheterisation – balloon or stent
What is transposition of the great arteries?
Aorta connected to the RV, and pulmonary artery connected to the LV.
=> Incompatible with life, unless blood can mix.
There will be CYANOSIS when ductus arteriosus closes (around day 2)
transposition of the great arteries - on examination
Cyanosis without tachypnoea.
One loud, single 2nd heart sound.
May be a murmur if another defect is present, but often no murmur.
transposition of the great arteries - Investigations
Echo – visualise abnormalities
ECG – usually normal
CXR – “egg on a side” outline of heart, increased pulmonary markings
transposition of the great arteries - Management
Maintain duct patency – prostaglandin analogue
Balloon atrial septostomy – create hole in atrial septum to allow blood mixing.
Arterial switch procedure – pulmonary a. and aorta transected and switched, performed <4 weeks.
What are the four cardinal features of Tetralogy of Fallot?
- Large VSD
- Aorta overriding the ventricular septum (receives blood from both ventricles)
- Sub-pulmonary stenosis (= RV outflow obstruction)
- RV hypertrophy (as a result of RV outflow obstruction)
what genetic condition can Tetralogy of Fallot be associated with?
DiGeorge Syndrome
Tetralogy of Fallot - On Examination
CYANOSIS in 1st week
=> Variable – can have pink/blue fallot
Loud, harsh ejection systolic murmur (VSD and PS)
Clubbing (older children)
Tetralogy of Fallot - Investigations
Echo – shows cardinal features
CXR – small, “boot-shaped” heart
ECG – RV hypertrophy
Tetralogy of Fallot - Management
Maintain duct patency
Surgery at 6 months – close VSD, relieve RV outflow obstruction.
Treatment of hyper-cyanotic “TET spells”
- Knees to chest, sedation, pain relief (morphine)
- O2 +/- ventilation
- IV propranolol (to relax RV)
- IV fluids
What are TET SPELLS?
= worsening of right-to-left shunt
During exertion/crying/agitation causing increased pulmonary resistance
Causes cyanotic episodes
If severe = drowsy, seizures, death.
What is hypoplastic left heart and how does it present?
= underdeveloped left heart (including aorta).
Often detected antenatally so symptoms are prevented, but symptoms can be:
- Profound acidosis and CV collapse
- Weakness of all peripheral pulses
Hypoplastic Left Heart - management
Norwood procedure (3-stage surgery)
Cardiac Failure in children - signs and symptoms
What is an important differential to consider?
Signs and symptoms:
- Failure to thrive
- Breathlessness (especially when feeding)
- Sweating when feeding
- Ventricular Heave
- Backlog of pressure – crackles on lungs, big liver
Differential – SEPSIS!
Management of cardiac failure
Diuretics, inotropes, treat cause
Supraventricular Tachycardia - signs/symptoms
= HR 250-300bpm
Signs/Symptoms:
- Dizziness, palpitations, chest pains, SoB
- Tachyarrhythmia (abnormal, fast HR)
- Heart failure (pulmonary oedema, increased RR)
- Hydrops fetalis (abnormal fluid accumulation), causes intrauterine death.
Supraventricular Tachycardia - Investigations
- ECG – 250-300bpm and narrow QRS (P-waves often hidden)
- Echo – to r/o structural problem
Supraventricular Tachycardia - Management
- Acute:
• Circulatory and respiratory support
• Carotid sinus massage/ice pack on face (successful in ~80%)
• IV adenosine (induces AV block)
• Electrical cardioversion with synchronised defib shock. - Maintenance:
• Flecainide or Sotalol
• Radiofrequency ablation/cryoablation
What is myocarditis?
What causes it?
= Inflammation of the myocardium
Usually due to infection, but also drug reaction/ chemicals/ radiation
Common viral causes = parvovirus, influenza, adenovirus, rubella, HIV
Myocarditis - signs/symptoms
Fever/malaise
Non-specific Sx of heart failure: SoB, cough, chest pain, oedema, pallor
Myocarditis - Management
Usually resolves spontaneously
Diuretics, ACEi, Beta blocker (carvedilol)
Severe cases may need heart transplant
What is Subacute Bacterial Endocarditis?
Most common cause in children?
Biggest risk factor in children?
= Slowly developing infection of the endocardium.
Alpha-haemolytic strep is the most common cause in children
Congenital heart defects are a BIG risk factor (especially VSD, PDA, coarctation)
Subacute Bacterial Endocarditis - symptoms
Fever, malaise and a NEW murmur
Also:
- Anaemia/pallor
- Arthritic/arthralgia
Subacute Bacterial Endocarditis - signs
Microscopic haematuria
+/- splinter haemorrhages
+/- Osler’s nodes, Janeway lesions, Roth spots
Subacute Bacterial Endocarditis - Investigations
Blood cultures (before starting Abx)
Echo – visualise vegetations
Bloods – anaemia, increased ESR/CRP
Urine dip – microscopic haematuria.
Subacute Bacterial Endocarditis - Management
Abx
=> high dose IV penicillin + gentamicin for 6 weeks
when is the neonatal period?
<28 days
When is a child considered pre-term?
Born <37 weeks
When is a child considered post-term?
Born >42 weeks
What is considered low birthweight?
<2500g
What is considered very low birthweight?
<1500g
What is considered extremely low birthweight?
<1000g
Respiratory Transition in the newborn
Alveoli will transition from fluid-filled to air-filled in order to survive without the placenta.
- Fluid resorption starts before birth through lymphatics and circulatory system.
- Some fluid is squeezed out during labour.
- Breathing is stimulated by cold/touch/light and loss of placental gas transfer.
Babies take large, deep breaths (crying).
To keep the lungs open, you need to overcome the surface tension in the alveoli (surfactant is needed for this).
Positive end-expiratory Pressure (PEEP)
= the pressure in the lungs (alveolar pressure) above atmospheric pressure, that exists at the end of expiration
Extrinsic/Applied PEEP
applied by a ventilator
= used for most mechanically ventilated patients to prevent end-expiratory alveolar collapse
Intrinsic/Auto PEEP
caused by incomplete exhalation
=> causes air trapping (hyper- inflation).
Develops commonly in hyperventilation, obstructed airway or increased airway resistance
What are causes of respiratory distress in neonates?
Respiratory Distress Syndrome
Meconium aspiration Syndrome
Infection
Pneumothorax
Congenital Causes
Transient tachypnoea of newborn (TTN)
Meconium aspiration Syndrome
Distress causes the baby to inhale meconium, which is toxic to the lungs.
Meconium is present at delivery
RFs - post-term delivery
What are the potential issues associated with prematurity?
Respiratory Distress Syndrome
Chronic lung disease
Retinopathy of prematurity
Intracranial haemorrhage
Long-term neurodisability
Temperature control (hypothermia)
Infection
Hypotension
Patent Ductus Arteriosus
Bradycardia
Metabolic problems (Hypoglycaemia, Hypocalcaemia, Metabolic bone disease of prematurity)
Feeding difficulties
Necrotising Enterocolitis
GORD
why is intracranial haemorrhage a problem in pre-term infants?
The pre-term brain is very susceptible to bleeding
What is early-onset sepsis?
What organisms usually cause it?
Sepsis that starts near the time of delivery
Group B Streptococcus (Strep agalactaie)
E. coli
H. influenzae
Listeria monocytogenes
Group B strep infection of the newborn
= most common cause of neonatal infection (sepsis/meningitis/pneumonia)
Infection is prevented by giving antibiotics >2 hours before delivery
Infection is treated with benzylpenicillin and gentamicin
Investigations in suspected sepsis in a newborn
The “sepsis screen”:
- Blood culture
- Urine – SPA/clean catch
- Lumbar puncture
- CXR
- FBC, CRP
Why would a child need IV maintenance fluids?
if NBM or not taking enough orally
What is a risk with 0.9% saline that is less of a risk with Hartmann’s solution
0.9% saline has increased risk of hyperchloraemia
How do you calculate a child’s fluid deficit ?
Deficit (mL) = % dehydration x bodyweight (kg) x 10
“Bottom shufflers”
replacement for crawling
Child may not have tolerated tummy time therefore less development of arms, neck and back.
what are the developmental red flags?
No responsive smile by 8 weeks
Not achieved good eye contact by 3 months
Not reaching for objects by 5 months
Not sitting unsupported by 9 months
Not walking unaided by 18 months
Not saying single words with meaning by 18 months
No two/three word sentences by 30 months
What are the neurodevelopmental conditions?
- ADHD
- ASD
- Intellectual disability
- Cerebral palsy
- Attachment disorders
- Mood disorders
- Anxiety Disorders
- Impulse control disorders
What is ADHD?
What factors are needed for a diagnosis?
Inattention and hyperactivity/ impulsivity
Occurring <12 years and lasting >6 months
Occurring in 2 settings (e.g. home and school)
Interfering with social, academic or occupational functioning
Not explained by another disorder (e.g. oppositional defiant disorder)
Often also difficulties with emotional regulation and executive function
Epidemiology of ADHD
M>F 4:1 in childhood
50% of children with ADHD will have ADHD as an adult
=> M:F 1:1 in adulthood
Strong genetic component (multiple genes)
What FHx of ADHD increases the risk of a child having it?
1st degree relatives 4-5x more likely to have ADHD
10-fold risk among siblings of individuals with combined type
ADHD - pathophysiology
Linked to dysregulation of dopamine + noradrenaline in the brain
=> Dopamine involved in reward, risk-taking, impulsivity, mood.
=> NA involved in attention, arousal, mood
Pharmacological Rx of ADHD
1st line = methylphenidate (Equasym/Concerta/Ritalin)
=> MOA: blocks dopamine and noradrenaline transporters to increase the concentration within synapse
Taken around breakfast time; covers school hours
Prolonged action preparations available for home symptoms later in the day
What are the side effects of methylphenidate used in ADHD?
How are these prevented/managed?
- Suppression of appetite, causing impaired growth (good breakfast, 3 meals + snacks; monitor weight + height)
- Hypertension (monitor BP)
Non-pharmacological Rx of ADHD
ADHD medication is unlikely to have significant impact on behaviour without parenting support and access to behavioural management advice
What 3 areas are impaired in autistic spectrum disorder?
- Social & emotional interaction
- Imagination and flexibility of thought
- Social communication and language
May also have sensory difficulties (inc. touch, noise, light, smell, movement, food textures)
Autistic Spectrum Disorder - epidemiology
- Incidence – 1 in 100
- M>F 4:1 (but may be under-recognised in girls)
- Strong genetic component
- Can be a component of other conditions (e.g Rett syndrome, Fragile X, tuberous sclerosis, Down Syndrome, William Syndrome and many others)
Autistic Spectrum Disorder - management
No pharmacological Rx for autism itself (though melatonin may help with sleep disturbance)
Management centred around behavioural strategies, parental support and optimising environment to allow development
Intellectual disability
Affects ~1% of population
Variable severities of disability
Characterised by deficits in intellectual functioning (e.g. communication, learning, problem solving) and adaptive behaviour (e.g. social skills, routines, hygiene)
IQ testing to quantify intellectual impairment
Mild <70
Moderate <50
Profound <35
Severe <20
Intellectual disability - management
- Identification of co-existing medical conditions
- Family support
- Behavioural support
- Educational support
Educational, Health and Care Plans
A legal document
Describes a child’s educational, health and social care needs.
Details extra help that will be provided to meet those needs and how that help will support the child to achieve what they want to in their life.
Normal Pubertal Onset in F and M?
Girls – before age 8 is early, after 13 is late
Boys – before age 9 is early, after 14 is late.
How is bone age classically identified?
By an X-ray of the left wrist
Surgical assessment of acute abdominal pain
All patients require a full history and examination.
Girls - include a gynae history and pregnancy test if pubertal.
Boys - requires a testicular examination as it is a source of referred pain.
Management of acute abdominal pain
Most management plans will include analgesia, nil by mouth, IV access, bloods, fluids and imaging if necessary
Idiopathic abdominal pain
accounts for 30-40% of referrals to paediatric surgery,
It is a diagnosis of exclusion and requires careful review
Very common causes of acute abdominal pain
Gastroenteritis Acute appendicitis UTI Constipation Mesenteric Adenitis
Less common causes of acute abdominal pain
Strangulated Hernia Intussusception Pancreatitis Intestinal Obstruction Lower Lobe pneumonia DKA Henoch-schonlein Purpura
Rare causes of acute abdominal pain
Haemophilia Lead poisoning Acute porphyria Sickle-cell anaemia Herpes Zoster
What is the most common reason for acute surgical intervention?
Appendicitis
What is the typical presentation of appendicitis if the appendix is located in RIF, anterior to bowel?
- obvious RIF tenderness, guarding, rebound tenderness.
- In this position the diagnosis is typically easy to make and made early as it is the anterior peritoneum that is inflamed, and the symptoms localised.
What is the typical presentation of appendicitis if the appendix is located in RIF, posterior to bowel?
- Vague deep tenderness, can have guarding, may develop mass or perforation before diagnosis.
- This is a hard diagnosis to make and often delayed in presentation.
- The posterior peritoneum is inflamed and/or psoas muscle (giving the child the desire to limp to alleviate the pain).
- Few anterior abdominal wall signs.
What is the typical presentation of appendicitis if the appendix is located in the pelvis?
- Vague suprapubic tenderness, with no guarding.
- PR exam may illicit tenderness or a mass.
- Possible to have urinary/bowel symptoms due to irritation of these structures.
- Commonly perforated as it is hardest to diagnose and present late.
- Few anterior abdominal wall signs.
Management of suspected appendicitis?
Bloods and IV fluids,
Urine dip,
Good analgesia - Paracetamol and IV morphine if needed.
Consider NG tube,
Consider antibiotics
Contact the relevant on call surgical team.
=> the mainstay of treatment is surgery
What is the average morbidity from appendicitis?
10%
due to post operative collections, prolonged stay, wound infections, adhesional obstruction.
when are most abdominal wall defect discovered?
in antenatal scans
What is gastroschisis?
A congenital defect of the abdominal wall, usually to the right of the umbilical cord insertion.
Abdominal contents herniate into the amniotic sac, usually just involving the small intestine but sometimes also the stomach, colon and ovaries.
There is no covering membrane.
What is a risk factor for gastroschisis?
Any associated conditions?
More commonly seen with younger maternal age
Commonly an isolated anomly however, it may be associated with Arthrogryposis
Gastroschisis - acute management
careful fluid balance, IV antibiotics and placing lower half of body in a protective bag.
=> Prevent temperature and fluid losses as well as reducing infection risk.
What is Exomphalos?
A congenital abnormality in which the contents of the abdomen herniate into the umbilical cord through the umbilical ring.
The viscera, which often includes the liver, is covered by a thin membrane consisting of peritoneum and amnion
Are any conditions associated with exomphalos?
Commonly associated with other abnormalities, therefore examination and investigation for genetic abnormalities may be required.
=> Associations with trisomy 13, 15 and 18 as well as Beckwith Wiedemann syndrome are well documented.
Exomphalos - acute management
- Careful fluid balance
* IV antibiotics.
What is the estimated blood volume of a child?
= 80 mL/kg
What is the estimated weight of a child?
< 9 years = 2 x (age +4)
> 9 years = 3 x age
What might be considered a better fluid bolus in trauma?
10 mL/kg as there is a risk of disturbing a potential clot and exacerbating further bleeding.
Managing blood loss
Blood replacement:
- give type specific blood as a bolus and then reassess to see if more is required.
- When type specific blood isn’t available then O negative blood is adequate.
Before blood products are available then saline 0.9% is a good resuscitation fluid
What is intussusception?
Where does it normally occur?
= a type of bowel obstruction, normally occurs in the ileocaecal region
occurs when one segment of the bowel invaginates into another segment just distal to it, the venous blood flow is restricted, swelling occurs and it becomes stuck. This causes obstruction.
Intussusception - presentation
Pain (80-90%):
- Often colicky in nature
Vomiting (90%):
- Will often progress to becoming bile stained.
Abdominal mass (70%) - Sausage shaped mass in RUQ
Lethargy/hypotonia (70%)
- a non-specific symptom.
Shock
Altered Stool (55%): - “Redcurrant jelly” stools (a late sign)
What are the 3 “food signs” of intussusception?
Sausage-shaped mass in RUQ
Donut sign on USS
Redcurrent jelly stools
Causes of intussuception
Idiopathic, Meckel's diverticulum, Polyps, Peutz-Jegher's, Tumours, Inflamed appendix, Foreign body, Peyer's patch hypertrophy.
Intussuception - management
A-E Assessment – stabilise the child.
Surgical involvement is necessary – air reduction enema +/- laparotomy.
Congenital Diaphragmatic Hernia
when the normal diaphragm process is incomplete and the bowel herniates through and into the thoracic cavity.
This pressure can then stop the lung buds from being able to form into normal lungs (the earlier it occurs, the more impact it has on the developing lung)
When is the diaphragm normally fully formed during foetal development?
by 20 weeks, along with gut and lung formation
Do left or right sided diaphragmatic hernias have a better prognosis?
Left sided have a better prognosis than right sided (due to the solidity of the liver on the right side preventing the development of lung).
Can a congenital diaphragmatic hernia be detected on antenatal scans?
Mostly, yes
Congenital diaphragmatic hernia - management
Early recognition
intubation without bag and mask ventilation (to not inflate the stomach) and to watch and wait for the first 48 hours.
If the child is stable enough after this period of time then they will have the defect repaired surgically through either a lateral thoracotomy of through an abdominal approach.
Oesophageal Atresia / TOF
= incorrect development of the oesophagus so that the lumen is no longer patent.
As part of this anomaly the oesophagus can make an incorrect attachment to the trachea and create a tracheo-oesophageal fistula.
Can oesophageal atresia / TOF be identified antenatally?
Less well identified antenatally
often suspected when a newborn child either wont feed, vomits, has lots of salivary secretions and/or respiratory distress
Management of oesophageal atresia / TOF
Surgical intervention is performed to reconnect the two ends of the oesophagus and allow feeding to commence,
However when a child is unstable the most pressing issue is to disconnect the fistula.
=> Both procedures are typically performed through a right lateral thoracotomy.
Common causes of Neonatal Bowel Obstruction
Hirschsprung’s Disease
Necrotising enterocolitis
Less common causes of Neonatal Bowel Obstruction
Small bowel atresia Imperforate anus Duodenal atresia/stenosis Malrotation with volvulus Meconium Ileus
Duodenal atresia
= narrowing of duodenum
Can have different types ranging from a narrowed lumen to several discrete atretic segments with separated blood supply.
bile stained vomit in duodenal atresia
If the atresia occurs prior to the midpoint of the second part of the duodenum then the vomiting won’t be bile stained.
=> This can sometimes delay the diagnosis by several days and result in a very sick child.
Duodenal atresia - management
- resuscitate the child
2. intervene to remove the atretic segment and try and restore bowel continuity
Small Bowel Atresia
= narrowing of small bowel
This can be caused by thrombo-embolus, volvulus or intussusception
Small Bowel Atresia - management
and outcome?
- resuscitate the child
- intervene to remove the atretic segment and try and restore bowel continuity.
=> Sometimes this isn’t possible and a stoma is formed.
If the child loses a significant portion of bowel then they may never be able to absorb enough nutrients and have a life dependant on total parenteral nutrition
what is necrotising enterocolitis?
Inflammation and necrosis of intestinal tissue
More common in premature babies
Results from immature guts not being able to stop translocation of gut flora.
Can cause sudden and dramatic deterioration and death
Necrotising enterocolitis - management
Early recognition => triple antibiotic therapy and NBM
Surgical intervention may be required to remove non-functional bowel and restore continuity or create a stoma.
what is Hirschsprung’s disease?
Caused by defective nerve growth into the myenteric plexi of the bowel.
It can effect a small section of the bowel or the whole of the digestive tract.
=> the extent of the disease has a direct effect on severity of symptoms and time of diagnosis
How does Hirschsprung’s disease present?
How is it diagnosed and managed?
delayed passage of meconium and episodes of enterocolitis.
Dx is made via a rectal biopsy.
Mx - often requires removal of the non-functional bowel and to restore continuity prior to potty training age
Meconium ileus
born with very thick meconium and are unable to pass it
Commonly the child will pass the meconium (sometimes requiring a washout) and the symptoms will resolve.
One must think about the possibility of cystic fibrosis as a cause of thickened meconium and consider testing for it.
Where can testicular pain be referred to?
the abdomen
Testicular Torsion
Occlusion of the testicular blood vessels will affect the viability of the testis unless prompt action is taken.
It is more frequently seen in the left testis
Torted Hydatid of Morgagni
A small embryological remnant at the upper pole of the testis.
Torsion of the hydatid is of no consequence in itself except that it presents a similar picture to torsion of the testis.
The pain is usually less severe and of a longer duration than a torted testis.
Occasionally the torted hydatid may be palpable or visible as a ‘blue dot’ in the scrotum.
If in doubt, then one must explore surgically.
Torted Epididymal Cyst
This is a smooth, small fluid filled swelling that slowly develops in the epididymis.
They are often painless, but the affected testis sometimes ache or feel heavy.
It is not clear what causes cyst development, but they tend to be more common in middle aged men.
Epididymo-Orchitis
Inflammation of the epididymis and/or testis.
It is usually due to infection, most commonly from a urinary tract infection or a sexually transmitted infection.
A course of antibiotics will usually clear the infection. Most people make a full recovery without complication.
Idiopathic Scrotal Oedema
A self-limiting condition characterised by marked oedema +/- erythema.
Important to recognise to prevent unnecessary surgical exploration.
Most common under the age of 10.
Unknown aetiology.
Tends to resolve in 3 - 5 days.
Reassurance and analgesia are the mainstays of treatment
Trend of eGFR in children
Low in newborns
Rises rapidly in 1-2 years.
Trend of plasma creatinine in children
Increases throughout childhood with height and muscle
DMSA scan
Static scan of renal cortex
Shows functional defects (e.g. scars), can help to give differential function between the two kidneys.
!! Can give false positives if done within 3 months of UTI.
What are congenital abnormalities of the kidneys?
- Renal Agenesis
- Multicystic Dysplastic Kidney (MCDK)
- Polycystic Kidney Disease (PKD)
- Horseshoe/Pelvic Kidney
- Duplex Kidney
- Posterior Urethral Valves
What is bilateral renal agenesis?
What does this lead to?
= absence of both kidneys
Results in oligohydramnios, due to no foetal urine.
Complications: FATAL potter syndrome.
What is Potter Syndrome?
= physical characteristics that can occur due to oligohydramnios
- distinctive facial features
- skeletal abnormalities
- lung hypoplasia
What is Multicystic Dysplastic Kidney (MCDK)?
What are the complications and management?
Caused by failed union of ureteric bud and renal mesenchyme.
Results in non-functioning kidney with variably sized fluid-filled cysts and narrow ureter.
Complications: Potter syndrome if bilateral.
Management: often no Tx needed, sometimes nephrectomy if remain large.
What is Polycystic Kidney Disease (PKD)?
How is it inherited?
What are the complications?
Always bilateral, but some/normal renal function is maintained.
Results in enlarged kidneys with separate, discrete cysts.
Either autosomal dominant or autosomal recessive.
Complications – HTN, haematuria, renal failure.
What is Horseshoe Kidney?
What are the complications?
Lower poles of the kidney are fused at the midline.
Complications – increased risk of obstruction/infection
what is Duplex Kidney?
what are the complications of this?
Either 2 renal pelvises or 2 complete ureters for 1 kidney
Complications – reflux in lower ureter, ectopic drainage/prolapse of upper ureter
What are Posterior Urethral Valves?
What are the complications?
How is this managed?
Abnormal flaps of tissue/membranes grown in the urethra, obstructing drainage from the bladder.
Complications:
- Hydronephrosis
- Small, dysplastic, non-functioning kidney
- Reduced amniotic fluid leading to Potter Syndrome
Mx: cystoscopic ablation of valves
What is the most common cause of bladder outlet obstruction in male newborns?
Posterior urethral valves
How might UTI present in an infant?
NON-SPECIFIC
Fever Vomiting Lethargic/irritable Poor feeding/FTT Jaundice Sepsis Offensive urine
How might UTI present in a child?
Fever Abdo/loin pain Frequency/accidents Dysuria/haematuria Lethargic Vomiting/anorexia Offensive urine
Pyelonephritis/upper UTI in children
Fever >38o
+ bacteriuria
+/- loin pain
Cystitis/lower UTI in children
bacteriuria WITHOUT systemic Sx
“Atypical” UTIs in children
- Severely ill/sepsis
- Poor urine flow
- Abdo/bladder mass
- No Tx response within 48h
- Increased creatinine
- Non-E.coli organism
- FHx of urinary tract abnormality
UTI - important points to gather from Hx?
- Exact symptoms
- Antenatal scan results
- What is the urinary stream like?
- Voiding history in general
- Bowel habit
- Drinking habits
- Previous episodes?
UTI - important points to gather from examination?
- Appears well/unwell?
- Fever?
- Any spinal lesion/ lower limb neurology?
- Any palpable bladder or kidneys?
- Is blood pressure normal?
Urine dip specificity/sensitivity for UTI
Nitrites = specific (+ve result = likely UTI)
Leucocytes = sensitive (-ve result = unlikely UTI, but +ve result may be other cause [e.g. other febrile illness or balanitis/vulvovaginitis])
When is urine MC&S required in children with ?UTI ?
ALWAYS required unless nitrites AND leucocytes are negative on urine dip
UTI - when are further investigations required?
Only if recurrent/atypical UTIs
USS – shows structural abnormalities, renal defects, obstruction
DMSA – for scarring/VUR/obstruction
UTI - Management
If <3 months – URGENT HOSPITAL ADMISSION
=> IV Abx
If >3 months with upper UTI/pyelonephritis:
=> PO Abx for 7-10 days
If >3 months with lower UTI/cystitis:
=> PO Abx for 3 days
Causes of vesicoureteric reflux
Familial – 30-50% risk if 1st degree relative
Bladder pathology – neuropathic bladder, urethral obstruction, post-UTI
Types of vesicoureteric reflux and their management
Mild – reflux into ureter only
=> usually resolves within the first few years of life
Severe – reflux into kidney
=> prophylactic Abx, surgery
vesicoureteric reflux - investigations
MCUS – shows dilated ureters and direction of flow (diagnostic – shows grade of reflux)
MAG3 – shows direction of flow.
USS – shows abnormalities/obstruction
Complications or presentation of vesicoureteric reflux
Incomplete bladder emptying = risk of UTI
Intrarenal reflux = risk of pyelonephritis
High voiding pressures = transmitted back to kidneys, damaging renal papillae.
What is enuresis?
= involuntary micturition
Primary nocturnal enuresis
= “Bed wetting”
- Common – 10% at 5 years, 5% at 10 years.
- Need to R/o underlying cause
- Mx – encourage child/reward system, etc.
Daytime enuresis
= Lack of bladder control during the day in a child old enough to be continent (3-5 years)
Causes of daytime enuresis
Lack of attention to bladder sensation Detrusor instability Bladder neck weakness Neuropathic bladder UTI Constipation Ectopic ureter
Daytime enuresis - Ix
Neuro exam (gait, sensation, reflexes)
Spinal X-ray
Urine MCS
Bladder USS/urodynamic studies
Daytime enuresis - Mx
Treat underlying cause.
Anti-cholinergics (to decrease bladder contractions)
Star charts, bladder trainings, “damp alarms”, etc.
Secondary/onset Enuresis
= Loss of previously achieved continence.
Causes of Secondary/onset Enuresis?
Emotional upset (most common) UTI Osmotic diuresis (DM, sickle cell, chronic renal failure)
Secondary/onset Enuresis - Ix
Urine dip - ?DM, ?UTI
Urine osmolality
USS renal tract
Nephrotic Syndrome
= Inflamed basement membrane allows passage of proteins into nephron.
- Heavy proteinuria (>200mg/day)
- Hypoalbuminaemia (<25g/L)
- Oedema – periorbital, legs, scrotal/vaginal
Can be either Steroid-sensitive or Steroid-resistant (rare)
Cause of nephrotic syndrome?
The cause is unknown, but may be 2o to systemic disease (e.g. HSP, SLE, infections, etc)
Clinical features of nephrotic syndrome
- Periorbital oedema – especially on waking
- Leg, ankle, scrotal/vulval oedema
- Ascites
- Breathless (due to pulmonary oedema)
- Frothy urine (proteinuria)
Nephrotic Syndrome - investigations
- Urine dip – protein
- FBC, ESR/CRP
- U&Es, creatinine, albumin
- Urine MCS
- Complement levels
- Throat swab/anti-strep
- Hep B & C Screen
- Malaria screen
Management of steroid-sensitive nephrotic syndrome
Corticosteroids (8 weeks PO prednisolone)
• Tx resistant cases need renal biopsy
• Frequent relapses need high maintenance dose steroids
Fluid balance
Abx Prophylaxis (loss of Ig leads them susceptible to infection)
Refer to specialist if atypical features
Management of steroid-resistant nephrotic syndrome
Fluid Balance
• Restrict intake of water and salt
• Diuretics, ACEI, NSAIDs
Haematuria - glomerular
Brown Urine, deformed RBCs, protein
CAUSES:
- Acute/chronic glomerulonephritis
- IgA nephropathy
- Familial nephritis
- Goodpasture’s Syndrome (anti-basement membrane)
Haematuria - non-glomerular
Red urine, no protein
CAUSES: Infection Trauma (to genitals/urinary tract/kindeys) Stones Tumours Renal vein thrombosis Sickle cell disease Bleeding disorders
Haematuria - investigations
For all patients with haematuria:
- Urine dip & MCS
- FBC, ESR/CRP, platelets, clotting screen
- Sickle cell screen
- U&Es, creatinine, calcium, phosphate, albumin
- USS KUB
For suspected glomerular haematuria:
- Complement levels (often low)
- Anti-DNA antibodies (present in vasculitis)
- Throat swab + Antistreptolysin O/ Anti-DNAse B
- Hep B/C Screen
What is Nephritic Syndrome?
What are the clinical features?
Inflammation causes increased glomerular cellularity, which restricts blood flow and decreases filtration.
- Haematuria (>10 red cell casts)
- Oliguria (<0.5-1 mL/kg/hour)
- Proteinuria (>3.0g/day)
Clinical features:
- Oedema (especially periorbital)
- HTN, causing seizures.
Causes of Nephritic Syndrome
Post-infection (often streptococcal) Vasculitis (HSP, SLE, Wegener granulomatosis) IgA nephropathy Membranoproliferative glomerulonephritis Goodpasture Syndrome
Nephritic Syndrome - management
Maintain fluid and electrolyte balance
Treat infection if present
If rapid decrease in renal function – renal biopsy, immunosuppression, plasma exchange.
Post-infective Nephritis
Occurs 7-21 days after a sore throat or skin infection
Low complement, raised ASO/Anti-DNAse B
Henoch-Shonlein Purpura - pathophysiology
= Increased circulating IgA and IgG form complexes that deposit in organs (e.g. kidneys, skin, joints)
Henoch-Shonlein Purpura - Clinical Features
- Palpable purpuric rash – symmetrical over buttocks and extensor surfaces/ankles
- Arthralgia and periarticular oedema
- Colicky abdominal pain
- Glomerulonephritis – micro/macroscopic haematuria
- +/- fever and malaise
Henoch-Shonlein Purpura - risk factors
- 3-10 years
- M>F (2:1)
- Winter
- Preceding URTI
Henoch-Shonlein Purpura - Management:
- Normally self-resolved in 6 weeks
- Analgesia
- Corticosteroids – only if severe gut/joint involvement
- Follow-up for 1 year if renal involvement to ensure no CKD
IgA Nephropathy
“Berger’s Disease”
Similar pathology to HSP (IgA vasculitis), but ONLY affects the kidneys.
Glomerulonephritis
= Group of diseases causing immune-mediated inflammation of the glomerulus (increased permeability)
Causes nephrotic/nephritic syndrome
SLE - cause, RFs, Sx
involves dsDNA autoantibodies, decreased complement
Risk factors – adolescent girls/young women, Asian/afro-Caribbean
Symptoms - haematuria and proteinuria, malar rash, malaise, arthralgia
What is AKI?
What are the causes?
= a sudden, potentially reversible drop in renal function.
= Oliguria <0.5 mL/kg
PRE-RENAL
=> hypovolaemia, circulatory failure
RENAL
=> vascular/tubular/glomerular/interstitial
POST-RENAL
=> congenital/acquired obstruction
AKI - management
- Correct fluid and electrolyte balance / any metabolic acidosis
- TREAT CAUSE:
- Pre-renal - Urgent IV fluids and circulatory support
- Renal - depends on cause
- Post-renal - urine drainage
AKI - indications for dialysis
- Failed conservative Mx
- Hyperkalaemia or hypo/hypernatraemia
- Severe acidosis
- Pulmonary HTN/oedema
- Multi-system failure
What is Haemolytic uraemic syndrome (HUS)?
A triad of:
- Renal Failure
- Thrombocytopaenia
- Microangiopathic haemolytic anaemia (damaged RBCs due to small vessel occlusion)
Typical vs. non-typical Haemolytic uraemic syndrome
95% “typical” (diarrhoeal) – good prognosis
5% “atypical” (non-diarrhoeal) – poor prognosis
Pathogenesis of Haemolytic uraemic syndrome
Secondary to gastroenteric infection (diarrhoeal prodrome) with verocytotoxin-producing E. coli 0157:H7
Toxin causes intravascular thrombogenesis in renal endothelial cells
Clotting cascade becomes activated.
Platelets are consumed and haemolytic anaemia occurs.
Haemolytic uraemic syndrome - investigations
- FBC – low Hb, low platelets, fragmented blood film
- U&Es
- Stool culture
Haemolytic uraemic syndrome - management
- Supportive – manage fluid balance
- Dialysis and plasma exchange
- Follow-up – for persistent proteinuria, HTN, progressive CKD
CKD in children
CKD = progressive loss of renal function
Very rare in children (~10 in 1 million)!
Causes of CKD in children
- Structural malformation
- Glomerulonephritis
- Hereditary neuropathies
- Systemic diseases
- Unknown
Clinical features of CKD in children
- Anorexia, lethargy
- Polydipsia & polyuria
- Hypertension
- Bone deformities
- FTT, poor/delayed growth (despite high GH levels)
- Anaemia (unexplained, normocytic)
CKD - management
Management with specialist paediatric nephrologist and MDT
Aim = to prevent metabolic complications and allow normal growth & development.
- Diet – supplements, ?NG tube/gastrostomy
- Prevent renal osteodystrophy – calcium and phosphate restriction, vitD supplements
- Fluid and electrolyte balance
- Anaemia – recombinant EPO
- Hormone abnormalities – recombinant human GH.
Dialysis and transplantation for end-stage CKD.
Ideally child gets transplant before dialysis is needed.
Normal RR, HR, SBP in neonates <28 days
RR - 50-60
HR - 110-160
SBP - 50-70
Normal RR, HR, SBP in infants <1 year
RR - 30-40
HR - 110-160
SBP - 70-90
Normal RR, HR, SBP in children <5 years
RR - 25-35
HR - 95-140
SBP - 80-100
Normal RR, HR, SBP in children >12 years
RR - 20-25
HR - 80-120
SBP - 90-110
Normal RR, HR, SBP in children >12 years
RR - Adult
HR - Adult
SBP - 100-120
Paediatric A-E Assessment
- General condition
- Airway
- Breathing
- Circulation
- Disability
- Exposure/ENT
- Temperature
Need to assess systems for:
- Effort
- Efficacy
- Effects on other systems
A-E Assessment - airway and breathing
- Effort – RR, WOB, accessory muscles, recessions, added sounds, respiratory distress
- Efficacy – talking, air entry, SaO2 (>92%)
- Effects – skin colour, conscious level
Mx - Open and maintain airway, 5 initial rescue breaths, 100% high flow O2, Anaesthetist involvement for intubation
A-E Assessment - circulation
- Heart – rate, rhythm, pulse
- Blood pressure – hypotension (late sign)
- Capillary refill (<2 seconds)
- Peripheral temperature, colour
Mx - Chest compressions if needed, IV access, bloods,, catheterise, consider inotropes
A-E Assessment - disability
- Level of consciousness (AVPU / GCS)
- Pupils – size, reactivity
- Posture and tone
- Blood glucose!
A-E Assessment - exposure/ENT
- Rash, injuries, bruises
- Pain
- ENT exam
- Temperature
Causes of shock
Hypovolaemic
=> Bleeds, burns, fever, V&D, urinary losses
Distributive
=> Sepsis, intestinal obstruction
Obstructive
=> Cardiac tamponade, PE, tension PTX
Cardiogenic (rare)
=> Myocarditis, congenital heart disease)
Clinical signs of shock
Early: • Tachypnoea, tachycardia • Cap refill >2s • Decreased skin turgor, sunken eyes/fontanelles • Mottled, pale, cold skin • Oliguria (<0.5 – 1 mL/kg/hour)
Late:
• Hypotension, bradycardia
• Metabolic acidosis
• Depressed cerebral state
Shock - management
- FLUID RESUSCITATION = priority
- 0.9% saline bolus (20 mL/kg)
- 2nd bolus if necessary - If no improvement, then involve PICU
Septic Shock
Features of shock, plus:
- Fever, lethargy
- Poor feeding
- +/- purpuric rash (meningococcal sepsis)
Septic Shock - management
- Fluid resuscitation
- IV Abx ASAP (Ideally after cultures)
Keep reassessing, further support if needed
what is Anaphylaxis?
What are the causes?
= life-threatening hypersensitivity reaction (IgE) with rapid onset airway and circulatory problems.
Food allergy (85%), Insect stings, Drugs, Latex
Features of anaphylaxis
Difficulty breathing/swallowing Stridor +/- wheeze Swollen face/tongue Urticaria Pale, clammy
SHOCK may develop
What are some differentials of anaphylaxis?
DDx – asthma, panic attack, septic shock
Anaphylaxis - management
- IM ADRENALINE 1:1000 – repeat in 5 mins if no improvement.
=> Adult and child >12 years = 0.5 mL
=> Child 6-12 years = 0.3 mL
=> Child <6 years = 0.15 mL - A-E assessment
- Steroids and Antihistamines
=> Hydrocortisone and Chlorpheniramine - Monitor - pulse oximetry, ECG, BP
What is the dose of adrenaline used in anaphylaxis ?
IM ADRENALINE 1:1000
Adult and child >12 years = 0.5 mL
Child 6-12 years = 0.3 mL
Child <6 years = 0.15 mL
DKA - clinical features
- Polyuria & Polydipsia
- Weight loss
- Abdominal pain
- Vomiting
- Tachypnoea
- Confusion
DKA - management
- A-E Assessment
=> Severity of dehydration
=> Evidence of acidosis (e.g. hyperventilation/Kussmaul breathing)
=> Assessment of conscious level - Initial investigations
=> Blood gas (pH), blood glucose, ketones, U&Es, ECG - IV fluid resuscitation and ongoing rehydration
=> Estimate dehydration and slowly rehydrate
=> 0.9% saline (10 mL/kg over 1 hour) - Insulin therapy and potassium replacement
=> 0.1 unit/kg/hour of insulin
Why is potassium replacement given alongside insulin therapy in DKA?
Insulin therapy causes a shift in potassium, which can cause hypokalaemia, so KCl given to replace potassium
What is the rate of insulin infusion for DKA?
0.1 unit/kg/hour of insulin
What is there a risk of when correcting fluids/sugar too rapidly?
How would you recognise this?
Risk of CEREBRAL OEDEMA
Sx:
headache, convulsions, abnormal posture, rising BP/falling pulse, poor respiratory effort, irritability/drowsiness, focal neurological signs, falling GCS, papilloedema, falling O2 sats.
How is cerebral oedema managed?
Inform senior immediately
Check blood glucose and r/o hypoglycaemia as a cause of neurological symptoms.
Mx: hypertonic saline/mannitol, reduce IV intake, transfer to PICU
Alcohol poisoning - effects
Hypoglycaemia
Coma
Respiratory Failure
Alcohol poisoning - management
Check blood alcohol levels
Monitor blood glucose
Ventilatory support
Acid/alkali poisoning - effects and management
Inflammation and ulceration of GI tract
Mx - Early endoscopy
Ethylene Glycol (anti-freeze) poisoning - effects
Tachycardia
Metabolic acidosis
Renal failure
Ethylene Glycol (anti-freeze) poisoning - management
Antidote – Fomepizole
Haemodialysis
Paracetamol poisoning - effects
24-48 hours: abdo pain, vomiting
3-5 hours: liver failure
Paracetamol poisoning - management
Measure plasma paracetamol conc.
IV N-acetylcysteine
NSAID poisoning - effects
N&V, drowsiness, blurred vision, tinnitus
Hyperventilation
Acute renal failure
NSAID poisoning - management
Measure plasma conc.
Rapid BM, blood gas, creatinine, FBC, ECG
Supportive Tx (fluids, dialysis, etc.)
There is no antidote!
Iron poisoning - effects
Initial: V&D, haematemesis, melaena, gastric ulcers
Latent period
6 hours later: drowsy, coma, shock, convulsions, liver failure
Iron poisoning - management
Measure serum iron levels
IV Deferoxamine (acts by chelating the iron)
Methadone poisoning - management
Activated charcoal within 1 hour
IV Naloxone
Methadone poisoning - effects
Drowsiness, mitosis, vomiting
Tachypnoea/apnoea leading to respiratory acidosis
TCA poisoning - effects
Tachycardia, arrythmias
Dry mouth, blurred vision
Agitation, confusion, convulsions
Respiratory Depression
TCA poisoning - management
Ventilatory support
IV Sodium bicarbonate (if arrythmia / severe metabolic acidosis)
Diazepam (if convulsions)
General management of overdose/poisoning
- Identify agent and amount taken
- Can activated charcoal be used to decrease absorption?
=> Only if <1 hour
=> Ineffective for iron and pesticides - Investigations:
=> FBC, renal and liver function, ECG, ABG - Administer antidote:
=> If available/toxicity high enough - Supportive Tx:
=> Ventilatory support, IV fluids, etc.
What is Status epilepticus?
Seizure >30 minutes
OR
Successive seizures over 30 minutes with no recovery in between
Status epilepticus - management
- A-E Assessment
- Open and maintain airway
- High flow oxygen
- Glucose to r/o hypoglycaemia
- Confirm it is an epileptic seizure (Hx, features, etc.) - Manage Convulsions
- IV lorazepam (again 5 mins later if no improvement)
- IV phenytoin
- Anaesthetist - intubation and PICU
what is an Apparent Life-Threatening Event?
= a frightening combination of symptoms (most common in <10 weeks).
- Apnoea
- Colour change
- Altered muscle tone
- Choking/gagging
Causes of Apparent Life-Threatening Event
- No cause identified (50%)
- Upper airway obstruction
- Infections (URTI)
- Seizures
- GORD
- Cardiac arrythmia
Apparent Life-Threatening Event - management
- Detailed Hx and examination
- Admission to hospital (basic investigations and overnight monitoring)
- Discharge if normal and no high risk features.
