Paeds Flashcards
Normal resp rate for: Term-3 mo 4-12mo 1-4yrs 5-12yrs 12yrs+
Term-3 mo: 30-60 4-12mo: 30-40 1-4yrs: 20 5-12yr: 16 12yrs+: 16
HR MET criteria for: Term-3 mo 4-12mo 1-4yrs 5-12yrs 12yrs+
Term-3 mo: <100 >180 4-12mo: <100 >180 1-4yrs: <90 >160 5-12yrs: <80 >140 12yrs+: <60 >130
Normal signs of respiration in young children (4)
Chest in-drawing
Periodic respiration (not constant rate) BUT NO APNOEA
Incr rates of resp
Definition of apnoea in newborns
No respiratory effort for greater than 20 seconds.
No respiratory effort for shorter periods of time may also be classified as apnoea if accompanied by cyanosis or bradycardia
Causes of the following types of tachypnoea:
• Expiratory wheeze (lower airway obstruction with asthma, bronchiolitis)
• Exhaling with a closed glottis (pneumonia)
• Stridor (upper airway obstruction)
• Effortless (DKA)
other
- Expiratory wheeze (lower airway obstruction with asthma, bronchiolitis)
- Exhaling with a closed glottis (pneumonia)
- Stridor (upper airway obstruction)
- Effortless (DKA)
Other: anaemia, fever, cardiac failure, CNS pathology
Most common causes of bradycardia
Hypoxia MOST COMMON
Bradyarrhythmia
Drugs
Causes tachycardia
Fever Pain, Anxiety Hypoxia, hypercarbia, Hypovolaemia Anaemia Arrhythmia, cardiac failure Seizures Drugs
Causes of hypotension with
- Wide PP
- Narrow PP
- Wide PP (120/20)
- PDA
- AR
- Thyrotoxicosis
- Anaemia
- Sepsis - Narrow PP (70/50, weak thready pulse)
- Hypovolaemia
- Haemmhoragic shock
- Severe dehydration
- AS, coarctation of aorta
24 hours of fever, lethargy and vomiting in child.
- primary diagnosis and management
Bacterial sepsis until proven otherwise!
- A: Protect airway (sit up/safety position;; NG tube; yankee sucker)
- B: Give O2 >5L/min
- C: Give Hartmann’s or saline
- BSLs
- Reassess
- ORder: Blood cultures, blood gas
- Prophylactic antibiotics
- Call reg and PET service
Lump in children - what are the 3 main differential categories?
- Congenital
- Inflammatory
- Cancer
What is exomphalos?
What about this kills babies?
Exomphalosis a weakness of the baby’s abdominal wall where the umbilical cord joins it. This weakness allows the abdominal contents, mainly the bowel and the liver to protrude outside the abdominal cavity where they are contained in a loose sac that surrounds the umbilical cord.
It is the evaporative heat loss leading to hypothermia that kills babies
What is the most common DDX for a lump on the eyebrow at birth
Treatment
Exoid dermoid cyst (developmental remnant)
Treatment is surgical excision
How do you treat strawberry naevi
Propranolol accelerates their complete regression (would go away on their own by ~5 years)
What are the signs of hydrocephalous in infants?
Macrocephaly
Sun setting eyes (can only see upper half of iris)
Bulging fontanelle
Seizures
Causes of hydrocephalous in infants - what is the most common?
Congenital
Acquired
- Most common is medullary blastoma in 4th ventricle
- intraventricular haemmhorage
- SA haemmhorage
- meningitis
- SC lesion/tumour
- Traumatic head injury
- premature birth
What are you worried about when you see an absent anal cleft?
Sacrococcygeal teratoma -> tumor on coccyx that eventually grows to fill out the anal cleft and can grow larger than the baby. Turns malignant peri-natally
What is the functional consequence of cleft palate in babies?
Swallowing and sucking difficulties (can usually swallow but not suck)
What is the significance of an enlarged Virchow’s node in children? What does it drain?
What differentials you think of ?
Virchow’s node only enlarged with cancers, not inflame conditions. Drains the thoracic duct.
Hodgkins (10-15 year olds) or Neuroblastoma (very young children)
What is the most common anorectal malformation in females?
Symptoms
REctovestibular fistula. Abnormal connection between vagina and the rectum.
Symptoms: Gas, faeces, pus passing through vagina
- Vulvar irritation, inflammation
- Gross smelling vaginal discharge
- Frequent UTIs
- Pain during sex if older
Clinical features of malrotation
Early signs
- Bilious vomiting (flour green)
- Poor feeding
Late signs include: PR bleeding, abdominal distention and tenderness
What causes malrotation?
Anatomical variation where base of mesentery is narrow which means DJ flexure and Ileocaecal flexure are next to each other, in RUQ which results in SHORT BASE OF MESENTERY and predisposes the mesentery to volvulus
With malrotation, at what point does venous and arterial supply become compromised and when is best to intervene?
- If mesentery twists 360deg, venous and lymphatic supply are compromised resulting in bile-stained vomiting. Surgical intervention here has good outcome.
- If gut rotates further, arterial supply can become compromised -> intestinal ischaemia and infarction
How do you diagnose malrotation?
What is the treatment?
Upper GI contrast study is gold standard - look for LOSS OF C-shaped duodenum to indicate malrotation
Or AXR changes: double bubble, gastric and proximal duodenal dilatation…
Urgent surgical referral and laparotomy -> LAdd’s procedure + appendicectomy
Child with bile stained vomiting - diagnosis
Malrotation +/- volvulus until proven otherwise
Non-bilious vomiting in neonates - differentials
Pyloric stenosis
Infection - Sepsis, Meningitis, UTI
Reflux
Overfeeding
Typical presentation of hypertrophic pyloric stenosis
PYLORIC STENSOSIS: Typically first born boys, with non-bilious projectile vomiting (vomit past their feet) after each feed who are HUNGRY after!
- family history of HPS
- visible gastric peristalsis
+/- palpable pyloric tumour (‘olive’) if stomach isn’t too distended
When does pyloric stenosis typically present?
Peak 3-6 weeks old
But can occur 10 days-11 weeks
What metabolic derangements do you see in pyloric stenosis and why?
Due to profuse vomiting -> losing water, HCL, NACL, K
Metabolic alkalosis
Hypochloraemia
Hypokalaemia
Normal serum na
Acidic urine (paradoxical change - kidneys conserve Na as compensation)
What is intussception and what generally causes it?
Invagination of proximal into distal bowel
- Peaks at 5-11 months
- Physiological/idiopathic cause is most common (hypothesised that as babies wean, new antigen exposure causes payer’s patches in terminal ileum to swell from inflammation and cause intussception)
Less commonly can be due to pathological lead points
Classic presentation of intussception
Crampy (intermittent, also known as colicky) Abdominal pain (infant pulls legs into stomach to relax abdo wall)
Vomiting
Bloody ‘red currant jelly’ stools (LATE sign)
Sausage shaped mass in RUQ and emptiness in RLQ.
What are ‘anatomic’ or ‘pathological’ lead points of intussception
Merkel’s diverticulum
Polyp
Vascular malformation
lymphoma
Complications of intussception if not treated early
Bowel obstruction,
Ischaemia, perforation, shock
How do you diagnose intussception?
Clinical suspicion -> US (‘target sign’) is first choice
or AXR (?soft tissue mass ?absence of gas in caecal region)
Treatment intussception
<48 hour history in otherwise stable child = air enema reduction
> 48 history or peritonitic/septic child = laparotomy
Treatment pyloric stenosis
Fluid rehydration therapy and electrolyte replacement
- 0.45% saline with 5% dextrose
- Add K when baby is urinating
Non-urgent surgical referral
Treatment exompathalous
Place baby in humidicrib wrapped in glad wrap (ensure blood supply of exposed bowel isn’t twisted/compromised)
NGT for GI decompression
Fluid resus
Urgent T/F to tertiary centre
DDX for acute scrotum (red, painful, tender scrotum)
Immediate management
- testicular torsion
- torsion of appendix testies
- epididymo orchitis
- idiopathic scrotal oedema
Urgent surgical referral ?surgical exploration
Classic presentation of appendicitis
Colicky periumbilical pain migrating to RLQ and becoming constant
Assoc w :
- anorexia
- fever
- nausea
- d&v
What are warning signs for appendicitis in kids?
abdo pain >24 hours
diarrhoea >24 hours
Infant preferring to lie still
Suspected peritonitis if child doesn’t allow abdo exam
What group most commonly have atypical presentations of appendicitis and how do you diagnose it?
Kids <5 yo
Adolescent girls
Need U/S diagnosis
- May need to do bloods (CRP, WCC), but bloods are NOT ROUTINE in kids.
Long term effects of diptheria infection
Toxin causes nerve and heart damage
Mortality 1/15
Long term effects of tetanus infection
Toxin causes nerve and muscle changes resulting in paralysis, convulsions
Mortality 1/10
Pertussis - effects of infection
Whooping cough. M&M highest in infants
Poliomyelitis - effects on infection
Febrile illness followed by paralysis in many (may become permanent)
Mortality 1/20
HIB - effects of infection
Systemic infection - meningitis, epiglottitis, bone and joint infections
Mortality 1/20
MMR
Measles encephalitis 1/2000, mumps encephalitis 1/200
Where to give vaccines to children?
• Children under 1
○ Anterolateral thigh (if 3 vaccines given at once, space injections 2.5 cm apart with third vaccine in other thigh)
• Children >1
○ Mid-deltoid region of upper arm
• NOT BUTTOCKS -> risk damage to sciatic nerve
Side effects of vaccines
- Local superficial inflammatory response -> redness, swelling at injection site
- Mild transient systemic SX (crying, irritability, mild fever, febrile seizures)
- Measles may be followed by mild, transient measles like illness (fever and brief rash 7-10s post immunisation)
- anaphylaxis is v rare
What extra vaccines what an aboriginal/torres straight islander child receive?
BCG
Hep A vaccine
Vaccines given at 2,4,6 months
DTPa (Diptheria, tetanus, whooping cough)
HIB
IPV (inactive polio vaccine)
HBV
PCV (13v pneumococcal conjucate)
RV (Rotavirus)
Vaccines given at 12 months
MMR (measles, mumps, rubella)
HIB
MenCCV
Vaccines given at 18mo
VZV (chickenpox)
MMR (measles mumps rubella)
DTP
Vaccines given at 4 years
DTPa (diphtheria, tetanus, pertussis)
Polio
Vaccines given at 10-15years
DTPa (diphtheria, tetanus, pertussis)
VZV (chickenpox #2)
HPV
Vaccines given at birth
HBV
Pattern of generalised seizure vs focal seizure
Generalised: wide spread all over brain, symmetric activity bilaterally
Focal: starts in localised area of brain, unilateral
What is another term for focal seizure that is commonly used and how is this further classified based on consciousness?
Partial seizure
- Simple partial seizure: consciousness intact (motor, somatosensory, visual/auditoary, autonomic, dysphasic)
-Complex partial seizure
(consciousness not intact)
How are generalised seizures further classified?
Tonic clonic
Absence
Myoclonic
Atonic, Tonic etc
Do generalised seizures affect consciousness? Motor systems?
Yes, always involve consciousness AND motor manifestations!
What is the definition of a seizure vs of epilepsy
Seizure:
Transient occurrence of signs and/or SX due to abnormal, excessive or hypersynchronous neuronal activity in cerebral cortex
Epilepsy:
Tendency to have recurrent unprovoked seizures (2 or more AFEBRILE seizures)
What types of seizures aren’t included in the definition of epilepsies?
- Single seizure events
- Neonatal seizure
- Febrile seizures
- Acute symptomatic seizure (systemic illness, acute neurological insults)
Investigations for seizures in children
EEG (+/- video monitoring)
MRI if…
◊ Suspected underlying cerebral abnormality
◊ Significant developmental delay
◊ Abnormal neurological findings on exam
◊ History of prior ne◊ Poorly controlled seizures
CT only if suspected stroke, increased ICP, traumatic brain injury (never perform in otherwise well child)
Seizure mimics
○ Normal phenomenon
§ Sleep jerks
§ Tantrums
§ Inattention, day dreaming
○ Syncope and related episodes
§ Vasovagal
§ Breath-holding spells
§ Long QT syndrome
○ Parasomnias and related sleep disturbances
§ Night terrors, sleep walking, cataplexy, confusional arousals
○ Movement disorders
§ Tics, clonus, chorea, tremor
○ Behavioural and psychiatric disturbances
§ Mannerisms, psychogenic seizures, rage attacks
○ Migraine variants and NV episodes
§ TIA, complicated migraine, benign paroxysmal vertigo
How can absence seizures be provoked?
hyperventilation
what are febrile seizures often associated with?
What ARENT they associated with?
Mostly assoc w URTI/UTI/viral exanthema
Family history of seizures (30%) - same mutation in neuronal ion channel gene
Age-limited predisposition to seizures (mostly 5mo-2yrs)
NOT ASSOC W: CNS illness, prev afebrile seizure, incr mortality or later intellectual impairment
Medications for epilepsy
Sodium valproate
Carbamazepine
Lamotrigine
Ethosuximide
DDX for generalised tonic clonic seizure (and what you would expect for each on history)
Focal seizure becoming generalised
□ Preceding aura (note: NO aura with generalised TC)
□ Todd’s paresis (transient unilateral postictal weakness)
□ Focal neurological deficits on exam
□ HX of prior CNS illness/cerebral trauma
Syncope
□ Vasovagal setting
□ Brief duration with rapid recovery
Psychogenic seizure
□ Eye closure during seizure
□ Resistance to passive eye opening
□ Intermittent or waxing and waning motor activity
what broad category of seizure if there is limb jerking/head turning/stiffening that is UNILATERAL?
Focal seizure! Not generalised because must be in one hemisphere only.
What type (lobe?) of focal seizure often gets confused for absence seizure?
Temporal lobe epilepsy
What type of (lobe?) focal seizure features hyperkinetic autisms (tapping, cycling, running in place)
Focal lobe epilepsy
Treatment of generalised vs focal epilepsies
Generalised seizures: Sodium valproate
Focal: Carbamazepine
What is the best method of measuring temp in children and what is the upper limit of normal (degC)
Electronic thermometer in axilla
Axillary > 37.2C
What is the definition of PUO?
Fever without focus for >2 weeks
What are the 3 main causes of PUO
- infection (?encapsulated bacteria)
- autoimmune
- malignancy
What 3 main encapsulated bacteria infect kids
HIB
Strep pneumonia
Neisseria meningiditis
What do you do if a child comes in with a fever?
If child is : > 3months non toxic fever <14 days It is likely viral so DON'T do septic screen (possibly check urine ex: if <6 months) and review to ensure they don't deteriorate.
Otherwise they get a septic screen
What comprises a septic screen?
FBE, blood film
Blood and urine cultures
LP +/- CXR (if resp SX/signs)
What questions to ask on HX when a child comes in with fever
Localising symptoms: cough coryza headache photophobia diarrhoea, vomiting abdominal pain joint symptoms
Travel history
Sick contacts
Immunisation hx
SX, signs suggestive of a ‘toxic’ or unwell child
Lethargic Poor interaction Inconsolability Tachycardia, tachypnoea, Cyanosis, poor peripheral perfusion
Presentation of meningococcus
Rapid onset
Fever
Flu-like SX (malaise, lethargy, vomiting, headache, myalgia, arthralgia)
Confusion
Rash (petechial/purpura)
Photophobia
Neck pain/stiffness
Differentials for child presenting with fever and petechial rash (previously well, onset this am)
Meningococcus if unwell/shocked/toxic
Viral infection (enterovirus, influenza)
HSP
ITP
15 month old presents with a non-itchy blanching erythematous rash (not on face) following 3 days of sudden-onset high-grade fever and a single febrile seizure.
What’s your top differential? Treatment?
HHV6 (roseola)
No treatment required - self limiting.
Child presents with ‘slapped cheek’ rash on face and lacy rash on trunk and limbs following low-grade fever, malaise, or a “cold” a few days before the rash broke out.
Differential? Treatment?
Parvovirus B19
No treatment required bc is viral
+/- Paracetamol to bring down fever
What is a rare complication of parvovirus B19 infection in pregnant women?
How common is this?
If exposed to ParvovirusB19 in first half of pregnancy, baby can get fetal anaemia hydrops fetalis and fetal death (miscarriage)
Occurs in 5% of pregnant women infected with parvovirus
What are the clinical features of measles?
4 day infectious prodrome (3 Cs) preceding rash:
Cough, coryza, conjunctivitis
Fever
Koplik’s spots
Rash (red, blotchy, starts on the head and then spreads to the rest of the body) - lasts ~7d
2 year old with incomplete immunisations at creche with fever and cough, coryza, conjunctivitis progressing to descending, blotchy raised (papular) rash
- diagnosis
Measles
Management for measles
MMR vaccine (2 doses) within 72 hours of exposure if >9mo
IVIG if <9mo or >9mo but >72 hours post exposure
Differentials for diffuse erythematous rash (sunburn-like) in child
Toxic shock syndrome (Staph or strep) Scarlet fever/Invasive GAS Kawasaki disease Enteroviral infection Antibiotics
what is the most severe complication of measles?
Encephalitis -> fatal in 15%
What causes Scarlet fever?
Exotoxins from Group A Strep (pyogenies)
What infections does GAS cause?
Scarlet Fever Pharyngitis Toxic shock Necrotising fasciitis Acute rheumatic fever GN
Clinical presentation of scarlet fever
Exudative tonsillitis +/- pharyngitis
Confluent erythematous sunburn-like rash
Strawberry tongue
Circumoral pallor
Treatment of scarlet fever
Penicillin (oral) - to treat GAS
What infectious agents cause toxic shock syndrome?
Exotoxins from staph aureus and strep pneumonia and strep progenies
Features of Kawasaki disease
Fever>5 days (unresponsive to antibiotics)
Polymorphous rash
Bilateral non-exudative conjunctivitis
Mucus membrane changes (oropharynx injected, strawberry tongue, swollen lips)
Swollen erythematous hands and feet with eventual desquamation
Unilateral cervical lymphadenopathy >1cm
Treatment of kawasaki disease
IVIG and low-dose aspirin
Complication of kawasaki disease
Coronary artery disease (aneurysm)
Higher risk of IHD
Features of infectious mononucleosis (glandular)
FEVER Exudative pharyngitis Tonsillitis Lymphadenopathy Splenomegaly Palatal petechiae Rash
Management of mono
None
Steroids only if airway obstructed due to tonsillar enlargement
What is TTN?
RF?
Tachypnoea of the newborn (TTN) = wet lung
retention of fetal long fluid
□ C-section without labour -> ‘Cold’ c-section = no maternal hormone surge hasn’t caused resorption of fluid yet
□ Breech delivery
□ Male sex
□ Birth asphyxiation
□ Heavy maternal analgesia
characteristic CXR for TTN
Coarse streaking w fluid in fissures
Mx TTN
most babies settle in 24-48 hours with minimal handling and cot O2.
CPAP if acidotic, low sats, working hard to breathe.
Signs of resp distress in a newborn
○ Tachypnoea (>60breaths/min)
§ In response to incr CO2 in order to breathe out and decr the CO2
○ Expiratory grunt
§ Produced by exhalation against a partially closed glottis in order to increase PEEP and therefore keep alveoli open
§ May be interpreted as crying or moaning
○ Recession of intercostal spaces and suprasternum; in drawing of subcostal margin
§ Due to the increased resp effort generating more negative intrapleural pressure which sucks in the softer/more compliant chest wall during inspiration
○ Nasal flare
§ Flare during inspiration decreases airway resistance
○ Central cyanosis
§ Note - polycythaemic babies will appear cyanosed at relatively high O2 sats but babies with low Hb will not appear cyanosed until saO2 is v low.
○ Deranged temperature control
○ Low O2 saturation
Ix for resp distress in a neonate
BSL CXR FBE, blood film, UEC Blood culture VBG
What is infant RDS? Another name for it?
Who gets it (RF)?
Treatment?
= hyaline membrane disease
§ Occurs in pre-term infants due to surfactant deficiency in the alveoli
Mx:
Empirical abx because looks similar to sepsis!
CPAP
If need more, intubate and give surfactant (need intubation).
Characteristic CXR appearance of RDS/HMD
Hypo aeration, diffuse ground-glass appearance, air bronchograms
RF for meconium aspiration?
Post-term (>40 weeks)
Births involving fetal distress
what is the pathophys behind meconium aspiration syndrome?
Aspiration of substances leads to obstruction, atelectasis and chemical and mechanical pneumonitis
RF for neonate sepsis
Maternal GBS positive
Maternal fever
Prolonged rupture of membrane (>=18 hours)
Signs of pneumothorax
Most sensitive is transilluminator Tracheal deviation Chest asymmetry Unequal expansion Decr breath sounds unilaterally Resp distress
Abx coverage for neonatal sepsis (what bugs are you worried about?)
Gentamicin (listeria, e coli, HIB)
Benzyl-penicillin (GBS)
Differentials for resp distress
TTN/wet lung HMD/RDS Meconium aspiration syndrome Sepsis pneumothorax congenital pneumonia Cardiac (VSD, PDA, transposition, pulm HTN) Anatomical - although not usually in neonatal period (laryngomalacia etc) Drugs ?
RF for pneumothorax in neonates
Being on CPAP
Resp distress
Mx for MDS
NO evidence for suctioning airways
(UNLESS baby is floppy or has no/inadequate respirations then it is reasonable to suction under direct vision using laryngoscope)
Septic workup
CPAP if needed/intubation
metabolic disturbances causing apnoeic episodes in premmies
Hypoglycaemia, hypocalcaemia, hypo/hypermagnesaemia
Define apnoea in neonates
§ No air flow occurs for >=20sec
§ No air flow for >=10sec + bradycardia or desat
General management of Respiratory distress in neonates
Observation - admit to neonatal nursery, incubator
Monitor vital (HR, RR, saO2)
Septic workup (FBE, blood film, blood cultures, CXR, vBG)
Empiric antibiotics (gent and benpen)
IV fluids (10% dextrose at 60ml/kg daily)
Advice from senior physician!
Additional resp support (CPAP, intubation)
Definitions for
- term
- pre term
- post term
- term: ≥ 37 completed weeks’ gestation
- preterm: < 37 completed weeks’ gestation
- post-term: > 42 completed weeks’ gestation
Definitions for
- LBW
- VLBW
- appropriate weight for gestational age
• low birth weight (LBW): < 2500 g
• very low birth weight (VLBW): < 1500 g
- appropriate weight for gestational age; between 10th and 90th percentiles
3 things to look for on GI when examining a baby
- pink (well perfused)
- no incr WOB (resp effort)
- active, good tone
when is bronchiolitis most common?
Up to 2 years of age
In winter/rainy season
Risk factors for bronchiolitis
Maternal smoking, pre-term delivery, chronic lung disease of prematurity, allergy, CHD, immunodeficiency
common causative agents of bronchiolitis
VIRAL always Rhinovirus #1 cause of mild bronchiolitis RSV #1 cause of SeVere bronchiolitis HRV Parainfluenza, influenza A/B Adenovirus
SX and signs of Bronchiolitis
Low grade fever § Tachypnoea § Mild dry cough § Expiratory wheezing § Hyperinflation § WOB § Fine inspiratory crackles § Difficulty feeding if severe
Mx of bronchiolitis
○ Mx - supportive (O2, fluids, nutrition)
What is the most common cause of wheeze in the first 2 years of life?
Viral bronchiolitis
Complications of Pertussis (whooping cough)
who is most at risk?
Apnoea, severe pneumonia, encephalopathy, death
Most at risk is <6mo
Clinical signs and investigations : Pertussis
§ Prodrome of a few days: nasal discharge and mild dry cough
§ Cough becomes more pronounced and characteristically ‘whoop’ing
§ +/- severe vomiting and subconjunctival haemorrhages
§ Apnoea in young infants
Ix: nasopharyngeal specimen: immunofluorescent Ab, culture
Treatment of pertussis
§ Admission for supportive therapy
§ Macrolide antibiotics if early in course of disease or v severe Sx
§ Treat household contacts
§ Contact precaution (until 5 days of antibiotics or illness for 3 weeks)
Most common causes of viral pneumonia in kids
parainfluenza influenza RSV Human metapneumovirus (HMV) Adenovirus Human rhinovirus
What does an x ray of viral pneumonia look like?
CXR: patchy, widespread bilateral infiltrates rather than lobar involvement
Clinical présentation of viral pneumonia
Dry cough
Fever
LOA
Complications of HIB
Epiglottitis
Meningitis
Risk factors for HIB
Age <5yo Indigenous Lower SES Male sex Congenital and acquired immunodeficiency
Causative agents of bacterial pneumonia
- Strep pneumonia most common by far!
- Staph aureus
- Mycoplasma pneumonia
- HIB
Less common causes:
- Group A beta haemolytic strep (pyogenies)
- Klebsiella
Presentation of pneumococcal pneumonia
Typical CXR findings
fever sob pleuritic CP wet cough tachypnoea grunting nasal flaring Reduced expansion, dull to percussion, reduced breath sounds, bronchial breathing on affected side
CXR: lobal opacification although can be patchy
What antibiotics to use for pneumococcal pneumonia?
Penicillin and third gen cephalosporin
lung complications of pneumonia
what clinical features are the same, and what are different?
Pleural effusion
Pneumothorax
same - tracheal deviation
and reduced breath sounds
different - stony dull percussion and bronchial breathing above effusions.
what is the typical CXR appearance of mycoplasma pneumonia?
Central peribronchial opacification
Extensive opacification of 1+ lobes
Air bronchograms
Presentation of staph pneumonia
□ Shorter acute HX than other forms of pneumonia (acute onset, rapid course) □ Appears more toxic □ High fever □ Marked tachypnoea □ Significant resp distress □ Non-specific chest signs
Complications of staph pneumonia
LARGE pleural effusions Empyema Tracheal deviation Abscesses Air leaks (pneumothorax)
Antibiotics for staph pneumoniae
IV flucloxacillin and third generation cephalosporin (cefotaxime)
Vancomycin if MRSA suspected
RF for staph pneumonaie
Low SES
Indigenous b/g
Examples of ACYANOTIC heart defects
1. L->R shunt VSD PDA ASD AVSD
2. Obstructive heart defects Pulmonary stenosis Aortic stenosis Coarctation of aorta Hypoplastic L heart syndrome
Presentation of a VSD
Depends on the size
1. Small: pan systolic murmur @ L sternal edge rad to axilla BUT ASYMPTOMATIC at birth bc pressures between L and R heart are equal
- Large: left heart dilatation leads to displaced apex, parasternal heave
- SX of HF occur after lungs open up and L sided pressures > R.
(poor feeding, FTT, tachypnoea, incr WOB, hepatomegaly)
Note: L heart dilatation occurs because L heart has to work harder to generate the same CO w shunt present.
what are the 2 most common types of CHD in kids?
- VSD
2. PDA
What are SX of heart failure in a newborn?
tachypnoea
SOB and sweating when feeding
Failure to thrive
Incr WOB
Long-term complications of VSD
® Progressive AR if shunt is located close to aortic valve (aortic leaflets sucked/prolapses into defet due to high-velocity L->R flow)
Pulmonary HTN due to Increased pulmonary pressures (L-> R shunt)
What causes the ductus arterioles to close? when does this occur?
Closes in first 1-7 days post birth due to decreased circulating PGE2 and increased paO2, as well as muscle contraction
What can cause the ductus arteriosus to fail to close?
Prematurity
Congenital malformation
What is the treatment for a PDA in a premature infant?
Indomethacin or other NSAIDs (inhibit PGE2 to promote ductal constriction and closure)
Why do you treat small PDAs and how? How does this differ from treatment of large PDAs?
Small PDAs are treated to prevent endocarditis rather than to treat symptoms or complications. Via transcatheter duct occlusion.
Large PDAs need surgical ligation .
How do PDAs present?
Small PDAs generally asymptomatic. May have continuous murmur at upper L sternal edge.
Large PDAs present with L heart dilatation (displaced apex beat, parasternal heave) and progressive SX of heart failure.
+ Bounding pulses
+ Apical mid-diastolic murmur
What investigations do you do if you hear a murmur in a baby?
CXR
ECG
ECHO is diagnostic
Where do most ASDs occur?
fossa ovale (central part of atrial septum)
How do ASDs present?
Small ASDs go undetected (low pressure gradient across atria)
Large ASDs rarely symptomatic in childhood
-may cause Atrial arrhythmias in adulthood, and reduced exercise capacity
Because L->R shunt causes R heart enlargement ->
- parasternal heave
- ES murmur in pulmonary region with fixed splitting of A2 and P2
What might an ECG of ASD show?
partial RBBB
What is the treatment for ASD and when is it indicated?
Indicated if patient has RH enlargement
Transcatheter or surgical closure
Which congenital heart defect is most assoc w down syndrome?
AVSD
How does AVSD present?
Partial AVSD - behaves physiologically and symptomatically like ASD
Complete AVSD - presents like severe VSD (FTT, feeding difficulties, tachypnoea, WOB)
Treatment of AVSD
almost always needs surgical closure
What is the most common type of Acyanotic obstructive heart defect?
What type of murmur is associated?
Pulmonary Stenosis
Ejection systolic @ L upper sternal edge
Radiating to back
Ejection click earlier than with AS
A2 and P2 widely split
how does pulmonary stenosis present?
usually asymptomatic in children and infants
Mild is benign, non-progressive finding
Severe can lead to heart-failure
What causes AS in children usually.
What type of murmur?
Bicuspid aortic valve
ES murmur over aortic area + radiation to carotids
Ejection click later than PS
Less splitting of A2 and P2 than PS
How might AS present in kids
ES murmur
Apical heave due to LV hypertrophy
Gradual progression of SX (syncope, angina, dizziness on exertion, sudden death)
Severe cases, HF evident at birth
When do you treat AS in kids? How?
If symptomatic or ECG changes w exercise
Balloon valvuloplasty (trans-acth) or aortic valvotomy (surgical)
what is coarctation of the aorta?
What can it result in?
Stricture at distal part of aortic arch (max obstruction site close to aortic end of Ductus arteriosus)
Can lead to severe cardiac failure in newborns with oliguria and acidosis
When does cardiac failure onset in newborns with coarctation of aorta?
How might this present on exam?
When ductus arteriosus closes because then there is NO blood flow to the rest of the body.
Diminished/absent femoral pulses
unequal BPs between L and R arm
Treatment of coarctation of aorta
surgical repair as early as possible!!
CXR findings of severe coarctation of aorta
Cardiomegaly
Pulmonary congestion
Abnormal appearance of aortic knuckle
Rib notching (due to enlarged IC arteries bypassing obstructed segment of aorta)
If a newborn has coarctation, what else might you expect?
other congenital heart defects such as :
VSD
PDA
valvular abnormalities
How does hypo plastic L heart syndrome present?
What is it?
§ Infants present w severe cardiac failure or shock within first few days of life
□ All periph pulses diminished or absent
Small left ventricle (hypoplasia) - Underdevelopment of left heart + valves (often assoc w severe MS and AS)
What is hypo plastic left heart syndrome always associated with
always assoc w PDA otherwise they would have died. Necessary to keep systemic circulation maintained
(R->L shunt due to R ventricular blood shunting via PDA into aorta )
Complications of Hypoplastic left heart syndrome
95% die within first few weeks of life if untreated
Neurodevelopment impairment if children survive due to marked hypoxia and cyanosis in early days of life
Treatment for Hypoplastic left heart syndrome
Immediate: PGE1 keeps PDA patient initially, until
SURGERY can be performed.
If untreated 95% die in first few weeks of life.
Examples of cyanotic heart defects
The 4 Ts:
- Tetralogy of ballot
- Transposition of great arteries
- Tricuspid atresia
- Truncus arteriosus
what is the most common cyanotic heart defect? What is it commonly assoc with?
tetralogy of fallot?
Syndromes -down syndrome
What is the tetralogy of fallot and what 4 things comprise it?
Obstruction to RV outlfow tract + septal defect below obstruction such that blood can flow from RV to LV (R->L shunting)
§ 4 anatomical defects: □ Overriding aorta □ RV hypertrophy □ Pulmonary stenosis □ VSD
Clinical picture of tetralogy of fallot
Kids:
Gradual, delayed development of cyanosis
Delayed exercise tolerance, finger clubbing, growth retardation
Development of compensatory polycythaemia
Babies:
‘tet’ spells: cyanosis more obvious when baby is upset, crying
(Baby may go floppy, lose consciousness)
What do you suspect if a baby becomes cyanosed only when upset and crying, and on one occasion goes floppy and loses consciousness during such an episode?
What do you do to manage this?
Tetralogy of fallot
Treatment - soothe the baby
Treatment for tetralogy of fallot in kids?
get older kids to squat to incr systemic vasc resistance and reduce R->L shunting
Surgical closure of VSD and repair of PS
what type of murmur do you hear, if any, in tetralogy of fallot and what is this due to?
Ejection systolic murmur over pulmonary region due to PS (not VSD)
What changes would you see on CXR with tetralogy of fallot?
Normal heart size; ‘boot shape’ (upturned apex), reduced lung vascularity (fields look blacker)
What is transposition of great arterities?
§ Aorta and pulmonary arterty connected to wrong side of heart and as a result venous blood is directed straight through into systemic circulation
§ 2 parallel circulations result with
® Systemic venous deoxy blood flowing through R heart back into aorta
® Pulmonary venous oxy blood flowing through L heart back into pulm circulation
What does survival depend on with transposition of great arteriess?
§ Survival depends on mixing of blood between circuits via foramen ovale, ductus arterosus or septal defect
Clinical presentation of transposition of great arteriess?
® Cyanosis present at birth and generally progresses gradually
® +/- metabolic acidosis from tissue hypoxia
® No murmur
CXR findings for transposition of great arteriess?
mildly hypertrophied heart w contour ‘egg on its side’, increased pulmonary vascular markings
Treatment for transposition of great arteriess?
® Balloon atrial septostomy (intra-cath) to forcefully create an ASD as an emergency procedure to improve systemic arterial O2 sat
® Surgical correction = arterial switch (transection and re-anastamosis of great arteries to appropriate ventricle)
® Perform within first few weeks of life so you don’t get atrophy of LV
Complications of kawasaki disease
risk of coronary artery aneurysms, myocardial ischemia or infarction
What is myocarditis caused by and what are potential complication(s)?
Treatment?
Triggered by common viral infection, is immune-mediated
Compl: CCF, arrhythmias
Treatment: supportive +/- IV IG or immunosuppressives
What is the risk with long QT syndrome?
At risk of ventricular tachyarrhythmias (VT or VF) with sudden urges in adrenergic drive (exercise, morning alarm), which can lead to sudden death.
Runs in family. ask about fam HX of sudden death
Treatment: anti arrhythmic drugs, auto defib. implant
Treatment for heart block
® Positive chronotropic agent (isoprenaline)
® OR Positive Inotropes
® Implantation of temporary or permanent pacemaker
What are shockable rhythms?
VT and VF?
How might SVT present? What do you see on ECG?
Babies - mild distress w tachypnoea and poor feeding.
Kids - complain of palpitations
ECG shows Wolf-Parkinson White syndrome (rapid regular tachycardia 200-300bpm with narrow QRS)
Treatment for SVT
Vagal manoeuvres (valsalva) or IV adenosine to terminate an acute episode
DC cardioversion if haemodynamically compromised
When might you pick up heart block in a baby?
Uncommon but may pick it up on routine antenatal assessment (monitoring /ECG) w fetal bradycardia <60bpm
pathophys of RHD
What can it lead to?
Autoimmune: host immune response to strep Ag -> attacks heart, synovial membranes, other tissues (mainly damages heart VALVES)
Can cause myocarditis, pericarditis leading to reduced ventricular function (CCF) and arrhythmias, and mitral and aortic stenosis/incompetence
How does RHD present?
Follows acute rheumatic fever (strep infection of throat or tonsils)
- Polyarthtiris, large joints
- Carditis - NEW ONSET MURMUR
- Sydenham chorea
- Transient truncal skin rash (erythema marginatum)
- Skin nodules over bony prominences
- Fever
Causes of nephrotic syndrome
Idiopathic (90%)
- minimal change disease (85%)
- FSGS (15%)
Non-idiopathic (10%)
- HSP
- SLE
- Membranoproliferazive GN
- Membranous nephritis
- Congenital nephrotic syndrome
What are the key features of nephrotic syndrome?
Heavy proteinaemia
Oedema
Hypoalbuminaemia
Hyperlipidaemia
Note: may get some haematuria and FSGS can cause HTN.
Don’t generally get renal impairment
Key features of nephritic syndrome
Haematuria
Acute fluid overload
Hypertension
Renal impairment
Complications of nephrotic syndrome
Hypovolaemia
Infections
Thrombosis (haemoconcentration and loss of antithrombin in urine)
Signs of renal impairment
Oliguria
Increased plasma creatinine
Deranged UECs
Potential results of acute fluid overload
oedema
pulmonary oedema
CCF
When do you investigate isolated haematuria?
isolated haematuria is common and usually benign when there is no history of kidney disease.
Further investigations only if it occurs in 3 diff specimens over period of 2-3 weeks
Causes of nephritic syndrome
Idiopathic hypercalciuria ( excessive urinary calcium excretion)
Thin basement membrane disease (benign familial haematuria)
Proliferative glomerulonephritis (IgA nephropathy, post-strep GN, SLE, HSP)
What is post-strep glomerulonephritis caused by and what is the typical presentation?
Group A beta haemolytic strep (progenies)
○ Follows 7-14 days after group A beta haemolytic strep throat infection or 3-6 weeks following strep skin infection
Presents w: MACROSCOPIC haematuria acute fluid overload (facial and leg oedema +/- papilloedema) HTN Lassitude, fever, loin pain
Mx of post-strep GN
Oral penicillin for 10 days
If fluid overloaded: fluid restrict, low salt diet, frusemide
Dialysis if urea >50-60mmol/L, or hyperkalaemia or pulmonary oedema not controlled by diuretics and fluid restriction
electrolyte changes in renal failure
Incr: K, phosphate, Mg, urea, creatinine, H
Decr: Na, Ca
Metabolic acidosis
What is the clinical picture of IgA nephropathy
Macroscopic haematuria (haematuria often occurs at same time as intercurrent viral infections)
May present as acute renal failure with gross oedema and HTN
May be asymptomatic
Changes expected on positive SLE bloods
§ Serum C3 low
§ ANA, anti-dsDNA positive
Protein in urine can be normal in many kids. At what time doing a alb: creatinine spot test would you expect to see abnormally elevated results.
First morning void (Should be negligible if normal).
In normal kids with no pathology, incr protein secretion occurs during the day, NOT overnight
How does minimal change disease typically present
Children <10 Generalised oedema (facial puffiness, peripheral oedema, ascites)
NORMAL BP and renal function
30% have microscopic haematuria
Normal C’ levels
Treatment for nephrotic syndrome
Steroids
Fluid restriction and low salt diet if fluid overloaded +/- albumin
Complication of ascites
Spontaneous bacterial peritonitis (infection with encapsulated bacteria such as klebsiella, pseudomonas, e coli, staph aureus, strep pneumonia)
When would you suspect FSGS in a kid with nephrotic syndrome
What is the prognosis?
If they are steroid and/or immunosuppressant resistant
If they have multiple relapses
Prognosis is poor - 60% progress to ESKD over 10 years.
Investigations for atopy
Skin prick testing is first line (needs specialist referral)
Serological testing (lower specificity and sensitivity)
What is cystic fibrosis?
Autosomal recessive disorder common in caucasian population caused by defect in CF transmembrane conductance regulator gene which codes for a Cl channel present on epithelial cells of the conductive airways and GIT
How might cystic fibrosis be diagnosed?
Neonatal screening
Meconium ileus
Positive sweat test ([Cl]>40)
In adulthood, presentation with pseudomonas pneumonia or male infertility (due to bilateral absence of vas deferens)
What is the pathophys behind cystic fibrosis
Defective or absent Cl channel means that Cl is not getting pumped into secretions which would normally draw water in to thin secretions out, so as a result secretions are abnormally viscous.
Thick meconium can get stuck and lead to meconium ileum (emergency!
Ciliary dysfunction and damage due to thick mucus build up
Leads to mucus buildup and inflammation and recurrent infection in lungs initially.
Recurrent infections and mucus buildup lead to bronchiectasis
Leads to thickened pancreatic secretions that block exocrine secretion from pancreas. protein and fat aren’t absorbed -> poor weight gain, FTT, Steatthorea.
Over time pancreas is damaged from backed up enzymes and can lead to acute or chronic pancreatitis. Eventually leads to pancreatic endocrine dysfunction leading to insulin-dependent diabetes
Bugs that kids with cystic fibrosis are particularly prone to
Staph aureus (GP) and pseudomonas (GN)
Chronic complications of Cystic fibrosis
Bronchiectasis from recurrent/chronic lung infections.
Respiratory failure and death
Nasal polyps
Digital clubbing
Infertility in men due to bilateral absence of vas deference
Pancreatic failure
Liver disease
Growth delay
Osteoporosis
Urinary incontinence
4 domains of development
○ Gross motor
○ vision and Fine motor
○ Social, emotional, daily living
○ Communication, language, hearing
What are the 3 common features of all kids with cerebral palsy
□ Deformity, contracture, hip dislocation
□ Tone and/or movement disorder
□ Spasticity, dystonia, chorea etc
NOT all kids w CP have intellectual disability!
What should all kids w possible developmental delay/behavioural and attention difficulties get done (Inx-wise)?
Formal hearing and vision testing
speech assessment
What does HEADSS stand for?
Home Education Activities (hobbies etc) Alcohol • A lot of kids your age start experimenting w drugs and alcohol - have you ever tried any alcohol, or drugs?
Drugs
Sex/sexuality
• Are you involved in a romantic relationship??
Suicide
when do solids get introduced?
between 4 and 6 months
when should babies be sleeping through the night by?
3-6 months .
When to refer to speech and audiology assessment for a child with ‘language’ delay?
<50 words at 2yo or no 2 word combinations at 2yo
Doesn’t understand simple instructions without gesture
When to refer to speech and audiology assessment for a child with ‘language’ delay?
<50 words at 2yo or no 2 word combinations at 2yo
Doesn’t understand simple instructions without gesture
What are the 3 realms of problems that kids w Autism have?
- problems w socialisation
- problems w communication
- repetitive or obsessive behaviours
What is the mean IQ ?
IQ: mean 100 w SD of 15
Differentials for developmental delay
○ Deprivation/abuse
○ Neurodegenerative disorder
○ Unrecognised epilepsy
○ Severe sensory or developmental disorders (ASD, ADHD, cerebral palsy)
○ Cultural differences, mental health disorders, ill health, refusal to participate
○ Movement difficulties
what is the screening for down syndrome?
§ 1st and 2nd trimester serum markers
□ Low alpha-fetoprotein and pregnancy associated plasma protein A
□ High chorionic gonadotrophin levels
□ Low blood oestriol levels
§ US findings - nuchal thickening, characteristic malformations
characteristic dysmorphic features of down syndrome
§ Hypotonia
§ Eyes slated, epicanthic folds, brushfield spots
§ Tongue appears large
§ Ears small and poorly formed
§ Hands broad, simian crease (single palmar crease)
Gap between first and second toes
Diagnosis of down syndrome
Microarray or FISH (genetic testing showing trisomy 21)
Common co-occurring malformations with Down syndrome
§ Congenital heart disease (tetralogy of fallot, AVSD etc)
§ GI malformation (duodenal atresia, imperforate anus, Hirschsprung disease)
Pathological Causes of constipation in kids
SC lesions Spina Bifida Intestinal neuropathy (Hirschsprung's) Cow milk protein intolerance Coeliac disease Cystic fibrosis Metabolic (hypothyroid, hypercalcaemia) Pyloric stenosis, malrotation +/- volvulus, incarcerated inguinal hernia Cerebral palsy Drugs
Causes of delayed passage of meconium
Cystic fibrosis Malrotation +/- volvululus Fistula Imperforate anus Down Syndrome Hirschsprung's
Functional causes of constipation in kids
Physiological/functional
- withholding behaviour
- pain
- anxiety
- diet
- dehydration
- change in lifestyle (weaning onto solids, toilet training, starting school)
What is fecal incontinence associated with?
- Painful or frightening event assoc w defecation in early childhood
- Limited attention or learning disability
- Nocturnal enuresis/urinary incontinence
- Constipation (overflow)
Management of constipation in kids
- Change behaviour (toilet sits, position on toilet, stool diary)
- Diet - incr fluid and fibre, healthy diet
- Education
- Disimpaction if there is significant impaction that they are unlikely to pass
- Laxatives
Regular review and monitoring
What are the mechanisms of action of the following laxatives:
- Paraffin oil
- Senna
- Coloxyl
- Movicol
- Osmolax
- Colonlytely
- Paraffin oil - lubricant/softener
- Senna - stimulant
- Coloxyl - Softener
- Movicol - osmotic
- Osmolax - osmotic
- Colonlytely - osmotic
Exam and Ix for constipation
Exam
- Neurological lower limb motor and sensory (neurological/spinal abnormalities)
- Abdominal exam (faecal masses?)
- Height, weight (FTT)
- Spine and external exam of anal region (sacral teratoma, spina bifida, imperforate anus)
Ix - none unless SX continue despite behavioural modifications and laxative therapy, then look into pathological causes
what is the most common cause of constipation in kids?
Functional at >95% cases
Causes of vomiting in neonates
Systemic infx/sepsis
Bowel obstruction (anal atresia, duodenal atresia, Hirschsprung, meconium ileus w CF, incarcerated inguinal hernia)
Hypoglycaemia
Malrotation +/- volvulus
UTI/renal disease
Adrenal insufficiency (congenital adrenal hyperplasia, w ambiguous genitalia in females)
Causes of vomiting in infants
infection lesions of GIT (malrotation, strangulated inguional hernia, pyloric stenosis) GORD Coeliac Gastroenteritis Intussception (3-12mo)
Causes of vomiting in older kids
Migraine headache
Sepsis
Intracranial neoplasm (morning vomiting and headaches)
Acute appendicitis and peritonitis (>5yo)
Poisoning
Psychological (anxiety, stress)
SX and Treatment of overactive bladder
SX - frequency, incontinence, bed wetting, HOCKERING posturing
+/- fecal incontinence
often resistant to alarms and desmopressin, persisting beyond 10yo
Treatment - regular toiling program + anticholinergic (oxybutynin)
Investigations for urinary incontinence
U/S KUB (?Structural abnormality)
Uroflow (filling or emptying problem?)
Post-void U/S (?Residual volume)
Treatment of monosymptomaatic NE
Alarms worn at night
Wetting diary
Desmopressin (synthetic ADH/vasopressin analogue) - used for those who ave not responded or are unsuitable for alarm. Child should NOT drink overnight (risk hyponatraemia)
Treatment of polysymptomatic NE
Alarms
Treat constipation/fecal incontinence and exclude UTI
Anticholinergics (oxybutynin)
Frequent, regular voiding
Causes of daytime wetting without NE
Urge incontinence (overactive detrusor muscle) - urgency, freq, posturing, wetting
Dysfunctional voiding (lack of coordination between detrusor and bladder neck activity w poor relaxation of external sphincter during voiding) ASsoc w high residual volumes, upper tract dilatation MX- teach pelvic floor/sphincter relaxation and optimal voiding techniques
Neurological - neurogenic bladder (large of expressible bladders +/- NE ) Urological pathology (fistula, ectopic ureter) - constant rather than episodic bladders, may have NE too
Risk factors for DDH
Female
○ Breech presentation
○ Positive family history of DDH
Oligohydramnios
Detection of DDH
O/E and Inx
§ Ortolani - detects dislocated hip reducing during exam
§ Barlow - detects dislocating or subluxing during exam
§ Positive tests are ones in which ‘clunk’ is felt (click/popping)
§ Other signs to look for:
□ Discrepancy in leg length
□ Asymmetrical thigh skin folds (also present in 25% normal babies)
○ Ix: ultrasound <6months
X-rays > 6 months
Treatment for DDH
What happens if not treated early?
Tx: Pavlik harness.
If not treated early, hip joint develops abnormally and open or closed surgical reduction is required
What is DDH?
spectrum of disorders of hip instability producing subluxation or dislocation and imaging features of poor acetabular development
Commonest organisms for meningitis
<2 years old
§ Group B strep (pyogenes)
§ E coli and other GNB
§ Listeria monocytogenes
>2 years old § above § Strep pneumoniae § Neisseria meningitis § HIB (in unimmunised children)
Commonest organisms for encephalitis
Viruses
- Enterovirus
- HSV
- Other herpes (EBV, CMV, HHV6, VZV)
- Arbovirus
Bacteria, fungal, parasite causes RARE
Exam features of meningitis
Full fontanelle
+/- neck stiffness
Purpuric rash suggests meningococcal septicaemia
Signs of encephalitis
Altered conscious state, focal neurological signs
interpretation of CSF
for viral vs bacterial meningitis
Bacterial Neutr=100-10000 (higher) Lymph<100 (lower) protein >1g/L (higher) glucose <0.4
Viral Neutr<100 (lower) Lymph 10-1000 (higher) Protein 0.4-1g/L (lower) Glucose normal
MX of meningitis
- encephalitis
Meningitis
-Bacterial
<2mo: IV Cefotaxime and benpen
> 2mo: IV ceftriaxone +/- dexamethasone (reduces risk of hearing loss)
Enceph:
viral -> acyclovir
Analgesia
Admission if bacterial meningitis or IV hydration required (bolus if shocked -> 2/3 maintenance)
Monitor:
- Neurological obs
- BP readings
- Weight and HC
- UEC to monitor for electrolyte abnormalities whilst on IV fluids
what does AVPU stand for?
A Alert V Responds to voice P Responds to pain - Purposefully - Non-purposefully - Withdrawal/flexor response - Extensor response U Unresponsive
age range for epidiymitis
1) Only occurs immediately after birth (times when you have surges of androgens which open the vas) or in 14 + year olds
what is the anatomical variant that predisposes boys to testicular torsion?
‘Bell-clapper testes’ - anatomical variant where the testes hangs on longer mesentary than usual so more prone to twisting (within tunica)
How long do you have to save the testes from infarct with testicular torsion?
Have 6 hours with testicular torsion to save the testes from infarct
What is another name for idiopathic scrotal oedema and what is it’s typical presentation?
Allergic cellulitis
Bilaterally red swollen skin w surrounding skin also red (inflammation not contained by tunica vaginalis)
Often caused by flea bite on groin
Often presents in middle of night, quick onset (<4-6h)
MX of idiopathic scrotal oedema
Conservative - self limiting within 1-2 days
DDX
Left hemiscrotum is enlarged and blue - painless hard lump within scotum of a baby
Ix?
Most commonly due to torsion of testes in utero
DDX: testicular tumour
Ix: Inguinal exploration to distinguish
Enlarged non-erythematous right scrotal mass
DDX
How else might this present?
Cancer - probably rhabdomyosarcoma of cremaster muscle (cancer of spermatic cord)
May also present as lower urinary tract SX -haematuria +/-urinary retention
Primary vs secondary head injuries
Primary:
- Contusion vs contre-coup
- Axonal shearing
- Injury to intracranial blood vessels (extradural/subdural/SA haematoma/intraventricular bleed etc)
- Recognise patterns of injuries and blows to consciousness
Secondary
- Seizures
- Hypoglycaemic state
- Brain hypoxia, hypercarbia
- Cerebral oedema -> Raised ICP
Assessing a burns victim
ABCDE
Airway
- cervical spine needs demobilisation
- ensure patent airway (+/- adjuncts +/- intubation)
Breathing
- O2 via mask, highest flow possible
- RR and SaO2
- Expose chest for chest trauma/burns, observe chest movement (if burns are restricting chest expansion, consider escharotomy)
Circulation + haemorrhage control
- Pulses, CRT
- IV fluid resusc
- Elevate limbs if there are circumferential burns (may restrict perfusion) +/- escharotomy
Disability
- AVPU
- Pupil size, symmetry, response
Exposure
- Minimise heat loss (warm room, blankets, cover wound, Baer hugger)
- Expose fully, remove everything
- Burn assessment (depth, % TBSA)
Management of a burns victim
Dressing (clingfilm/paraffin/acticoat) Tetanus status Fluids (use TBSA% as guide) Analgesia Tubes (NGT +/- IDC if TBSA >10% +/- intubation)
What is the most common cause of newborn jaundice? Why?
Physiological jaundice
- As a foetus, unconjugated bilirubin is excreted by placenta. During transition to hepatic conjugation and excretion, all infants have raised bilirubin to some degree.
When is newborn jaundice always pathological
If it occurs within first 24 hours after birth (suspect haemolysis or sepsis)
Conjugated hyperbilirubinaemia
Why does physiological newborn jaundice occur?
- Incr RBC turnover (t1/2 less) - incr unconj bilirubin load
- Defective hepatic uptake
- Decr efficiency of conjugation (lower UDPG levels)
- Breast milk jaundice (factors in milk cause incr enteric absorption of bilirubin)
Mx of newborn jaundice
- Observe/watch
- Blue light phototherapy (converts bilirubin into water-soluble form that can be excreted in bile and urine)
- Exchange transfusion (replace baby’s blood w donor blood to decr bilirubin levels rapidly)
SBR Levels at which these are performed are determined using standard hospital monogram
Abi if sepsis suspected
When do you use a lower SBR threshold for phototherapy and exchange transfusion?
Premature
Asphyxiated infant
Ill or haemolysing infant
How long should physiological jaundice last?
~1 week, with peak SBR levels at 3 days in term babies.
Peak at 1 week in preterm babies
Causes of pathological jaundice
- Haemolytic
- Incr Haem load (haemorrhage, polycythaemia, swallowed blood)
- Impaired hepatic uptake and conjugation (Gilbert, hypothyroid, drugs etc)
- Mixed (prematurity, sepsis, infants of diabetic mothers, asphyxia)
Complication of jaundice
kernicterus (neuronal death caused by toxic unconjugated bilirubin crossing the BBB) -> manifests as bilirubin encephalopathy
Can lead to death or survival with cerebral palsy (neurodevelopment impairment)
Haemolytic causes of jaundice
Immune
- ABO and Rh blood group incompatibility
- Drug-induced
Acquired
- bacterial sepsis
- congenital intrauterine info
Hereditary
- G6PD deficiency
- Hereditary spherocytosis
What is the genetic underpinnings (at risk group) for G6PD deficiency
X linked
Mediterranean
Asian ethnic groups
DDX - asymmetrical scrotum
When is this most obvious?
- Varicocoeal if bag of worms appearance (Most obvious when patient is vertical rather than horizontal)
- Undecended testes
- Cancer
- torsion of testes or appendix testis
- Hydrocoeal (although may be bilaterally swollen, giving dumbbell appearance)
What side are variocoeals more common and why is this?
Left side
Because pampiniform plexus in scrotum becomes enlarged due to impaired drainage
How do you diagnose a hydrocoeal?
Tx?
Transilluminates
No treatment required
Sx of benzo poisoning
CNS depression (drowsy, coma)
REsp depression
Hypotension
Mx benzo poisoning
Observation - vitals, sats, RR (intubation, IV fluids, inotropes if necessary)
Call POISONS, get help from consultant, ICU
Urine drug screen (benzos)
Antidote - flumazenil - not generally used. only under discussion from specialist.
+/- Social work/department of Human Services referral
DDX depressed conscious state in a 2.5 year old
Ingestion/poisoning (drugs/alchohl/pesticides/poisons/medications such as benzos, opioids)
Head trauma
Sepsis/meningitis
How do you evaluate paracetamol levels?
Serum paracetamol levels at 4 hours post ingestion (testing any earlier doesn’t help)
Pain management in kids (and what is the pain score)
- mild
- moderate
- severe
- mild (pain score 1-3)
- Oral panadol (20mg/kg loading dose then oraly 15mg/kg q4h as req)
- Oral panadeine (15mg/kg/dose q4h paracetamol and codeine)
- Oral ibuprofin (helps bring down swelling, use if they are eating and drinking)
- distraction/bheavioural techniques - Moderate (pain score 4-7)
- Intranasal fentanyl and midaz (helps w anxiety)
- Codeine once pain has settled to mild/moderate - Severe (pain score 8-10)
- SC Morphine 0.15mg/kg/dose q4h
- IV morphine, titrated 4 hourly
What does bilirubin bind in the blood?
Albumin
Things to ask on HX when assessing a jaundiced baby
Family history:
- spherocytosis
- G6PD/ethnicity
- Previously jaundiced children
- splenectomy
- haemolytic anaemia
Antenatal HX:
- blood group
- maternal diabetes
Birth HX
Trauma - bruises/cephalhaematoma/ventouse extraction
What is the blood volume of a newborn baby?
10ml/kg
so around a can of coke’s worth in a term 3.5kg baby!
What is breast milk jaundice?
Hormones in breast milk (+ added affect of constipation) result in increased enterohepatic circulation so more bilirubin is absorbed back into blood rather than being excreted.
Normal and physiological
What is the most common haemolytic cause of newborn jaundice?
What is the most severe cause?
ABO incompatibility
Mother is usually type O with baby type A
Rh disease is more severe
How do you test for blood group incompatibility in jaundiced babies?
Direct coombs test
- strongly pos in Rh disease
- negative or weakly pos in ABO incompatibility
What is
Gal-1-P UT deficiency leads to build up of Galactose which is toxic
Newborn baby is jaundiced and has pale poos. what do you suspect and how do you investigate this?
why is it important to treat early?
Biliary atresia
US of liver/biliary tree to investigate for obstructive causes
Investigate within 6 weeks otherwise results in irreversible liver damage
Risks associated with ABO incompatibility
Fetal hydrops
Jaundice -> kernicterus/bilirubin encephalopathy
Causes of short stature (3) and how is bone age related to chronological age in each?
is the growth velocity normal or abnormal in each?
- Familial Short Stature (bone age = chronological age)
Normal growth vel. - Congenital Delayed Growth (bone age < chronological age)
Normal growth vel. - Pathological (endocrine PICNICS)
Abnormal growth vel.
Pathological causes of delayed growth
Endocrine PICNICS
Endocrine - hypothyroid, GH deficiency, Cushing’s disease, adrenal insufficiency
Psychosocial
Iatrogenic - exogenous steroids, spinal
Chronic disease - GI (coeliac, IBD); renal (CKD, RTA), cardiac (CHD), JIA, tumour
Nutritional disease
Intrauterine growth restriction
Chromosomal - Turner syndrome, Down syndrome, Prader Willi
Skeletal abnormalities
Types of allergies
IgE mediated
Non-IgE mediated
HX for allergies
Quality - specific symptoms experienced
Severity of SX
- medical req to control SX
- medical visits and hospitalisation
- ICU admissions
- interference w sleep, sport, play
Timing: seasonal, perennial, episodic; immediate onset or delayed?
Context: triggers
Any HX of anaphylaxis
SX of anaphylaxis (Severe allergic reactions)
Children vs young kids
MUST have resp involvement or involvement of 2+ body systems
- difficult/noisy breathing
- Drooling
- SOB, resp distress, cough, wheeze, hoarse voice, clearing throat, swelling/feeling of tightness in throat
- Dizziness or collapse
+/- drooling, Angio-edema/swelling of lips, tongue, hives/urticaria
- Young kids: pale and floppy
SX of mild to moderate allergic rxn
Swelling of lips, face, eyes
Hives/welts
Tingling mouth
Abdo pain, vomiting
Action plan for mild to moderate allergic Rxn
Mild to moderate:
- Stay with person and call for help
- Locate epicene adrenaline autoinjector
- Give other medications if prescribed (+/- H2 antag for SX relief of pruritus +/- oral steroid tablets for bronchospasm)
- phone family/emergency contact
- watch for any ONE of the signs of anaphylaxis indicating resp involvement
Action plan for severe allergic Rxn
Severe
- Lay person flat
- Give epicene adrenaline auto injector (pull of blue safety cap, place orange end against mid-thigh and push down hard until you hear a click -> hold for ten sec, then remove epipen and massage the spot). Can be given through clothing.
- Phone ambulance 000
phone family/emergency contact
- Further adrenaline doses can be given if no response after 5 min if you have another auto injector available
WHEN IN DOUBT GIVE ADRENALINE (and always give adrenaline before inhaler if in doubt as to whether it is anaphylaxis or asthma)
What are the investigations for allergy?
Ig E mediated:
Skin prick testing: positive if welt >3mm
Serology: measure allergen-specific Ig-E levels (more expensive and lower sensitivity and specitifiy but widely available)
Both in conjunction with clinical history
Non-IgE mediated and/or IgE mediated:
Food challenge is gold standard but only perform at RCH (controlled environment)
When is immunotherapy indicated as treatment for allergies?
For IgE-mediated inhalant or venom allergic disease only
Rhinoconjunctivitis as main indication
Atopic diseases
Eczema (Allergic dermatitis)
Asthma
Allergic rhinoconjunctivitis (hayfever)
Anaphylaxis
What might you see on exam of someone with allergic rhino conjunctivitis?
- Mouth breathing
- Inferior nasal turbinates pale and swollen
- Clear nasal discharge
- Conjunctivitis -itchy, red eyes w incr lacrimation
Causes of failure to thrive (5)
-
MAY BE PSYCHOSOCIAL so take thorough social hX
- blunts GH response - Inadequate intake
- Neglect
- Low SES
- Poor diet - micronutrient deficiencies
- inability to suck/swallow - Inadequate digestion, absorption
- coeliac
- CMPA
- CF
- pancreatic, cholestatic issue
- Giardiasis
- Diabetes - Incr metabolism
- Carcinoma
- Hyperthyroid
- Chronic disease (resp, cardiac, renal, GI) - Prenatal issues
- prematurity
- maternal illness/drugs/smoking
- IUGR
- chromosomal abnormalities
Investigations for short stature/FTT
Bone scan
Bloods: FBE, UEC, LFTs
- TFT, coeliac serology
- Nutrition: CMP, Fe, vit D, B12, folate, IGF
MX for short stature
- education/reassurance
- change diet
- treat any underlying pathology
- +/- GH therapy
- psychosocial support
How might pain present in a neonate? vs young child
Tachycardia Tachypnoea Restless/writhing/squirming Irritable Poor feeding
Young child: miserable, crying/screaming, lack of function, can verbalise pain
What is a smegma?
Combination of desquamated skin cells, skin oils and moisture collects around the clitorus or under the foreskin of males.
Looks like localised collection of pus but there are no signs of inflammation and it is normal in toddlers due to the foreskin separating gradually from penis between ages of 2 and 5!
Ballinitis presentation
Aetiology?
- Red, swollen, painful penis, often presenting in middle of night.
- Common in 1-3 year old during period of separation of foreskin
- Infection by e. coli or candida in pockets between inner layer of foreskin and penis (where smegma form)
Treatment and prevention Ballinitis
Treatment: high dose topical antibiotics (eye ointment) squirted under foreskin every 2 hours until it’s fixed (clears in 4-6 hours)
Prevention: wash regularly in salt water (cooking salt in bath)
What is parafimosis?
Treatment
Foreskin trapped behind corona forming tight band of constricting tissue which causes venous obstruction and swelling of glans
Treatment: urological emergency! Manipulation of glans within foreskin under laughing gas
What is phimosis?
When is treatment warranted and what is treatment?
What are complications if not treated?
Inability to retract the skin covering the head (glans) of the penis
May appear as a tight ring or ‘rubber hand’ of foreskin around tip of penis, preventing full retraction.
Can be physiological (self-resolves around 5-7 years of age) or pathological (due to scarring, infection, inflammation).
If there is ballooning of foreskin during urination/difficulty urinating, or infection, treatment (topical steroids +/- circumcision) may be warranted.
Complications: renal failure due to complete obstruction of urinary tract
What is hypospadias?
What is treatment?
Developmental condition where the meatus isn’t at the tip of the penis. Instead, the hole may be any place along the underside of the penis.
The meatus (hole) is most often found near the end of the penis (“distal” position) (80%), often occurring with dorsal hood of foreskin and chordee
Tx: urological surgery within 6 weeks
What is chord
What is associated with?
Tx?
Penis curves up or down at junction of head and shaft of penis, most obvious during erection
Can be assoc w hypospadias
Tx: surgery in infancy
What is epispadius?
What is it associated with?
URethra opens in top of penis rather than the tip
Assoc w dorsal chordee (penis curves up) and rarely with bladder exstrophy
When do you intervene surgically in an umbilical hernia
If it persists beyond 2 years of age (under 2 years it should resolve spontaneously)
What is the most common cause for boys needing renal transplant in childhood?
Posterior urethral valve (developmental abnormality)
Leads to urinary obstruction -> renal failure
Systemic effets of anorexia
Hypotension
Arrhythmias
Long QT
Decr grey matter (reversible)
Decr bone density - growth delay/arrest
Hypothermia
Delayed/interrupted puberty
Long term effects on sexual/reproductive health
Treatment anorexia
CBT
Maudsley family based treatment
Features of ADHD
Developmental problem w deficits in:
- Inattention
- Impulsivity
- Overactivity
Tx:
- Stimulant medication (ritalin)
- Psychosocial/behavioral strategies involving positive parenting, teachers, counselling
When does ODD typically present and what os the risk of not treating it?
Tx?
Typically surfaces at primary school but can be younger
May progress to conduct disorder if untreated
Tx: psychological strategies
- Assess current motivation to change
- CBT
- Family interventions
IgE vs non-IgE mediated allergies
IgE mediated:
- Sx appear within 1-2hrs but typically within min
- Sx: hives, urticaria, angeioedema, resp distress
ex: tree nuts, raw egg
Non-IgE mediated
- T cell mediated
- Sx appear >2 hours after ingestion
- Sx: GI and skin related (vomiting, diarrhoea)
- ex: cow’s milk allergy, soy milk, rice, FPIES
How is a skin prick test conducted?
Allergen introduced under epidermis
Measure wheel at 15min
Controls: histamine (expect pos) and saline (expect neg)
Wheal => 3mm above saline control is positive result
Indications for food challenge
– Non-IgE mediated
– IgE mediated BUT low suspicion of allergy
w uncertain history w +ve SPT/RAST (serum specific IgE)
w OR good history w -ve SPT/RAST
High risk groups for anaphylaxis
□ HX anaphylaxis
□ Multiple food and drug allergies
□ Poorly controlled asthma
□ Underlying lung disease
What is FPIES
Type of non-IgE mediated food allergy
Food protein induced enterocolitis syndrome
- occurs in infants and young children
- profuse vomiting and diarrhoea 2-4 hours after first exposure to allergen
Mx of allergic rhinitis
Avoidance/ reduction measures
Drugs: oral antihistamines (end gen), intranasal corticosteroids (fluticasone)
Allergy immunotherapy
What are the 4 types of child abuse?
Physical Emotional Neglect Sexual \+/- family violence witnessing
What do you do if you suspect child abuse?
Mantatory reporting if you have reasonable grounds to suspect it is causing harm to child and parents have failed or are unlikely to protect them.
Look up number to call on child protection website.
‘Child FIRST’ referral
What sort of injuries might indicate child abuse?
Bruising (esp on buttox, ears and peri-orbital)
Posterior rib fractures and epicondylar fractures from shaking
DDX midline neck lump in a child
- thyroglossal cyst (will elevate on protrusion of tongue and swallowing)
- Thyroid lump
- Thymus lump
Features of psoriasis in children
- Appearance
- Location
- Complication(s)
□ Deep salmon red colour, silver scaly plaques
Commonly on extensor surfaces, scalp, nails, umbilicus
In childhood get more post-strep guttate pattern on trunk
Complications: arthritis (1/10)
What is tinea and what is it’s typical appearance?
Tinea is ringworm. fungal infection.
Typical appearance is spreading ring rash
What virus causes roseola?
Human Herpes Virus 6 and 7
Systemic complications of port-wine stain birth
CCF
Brain PHACES
Hypothyroid
Possible causes of hair loss in kids
Alopecia Areata (autoimmune hair loss in patches)
Tinea Wapitis (focal hair loss w underlying scaly erythematous lesions)
Treatment of atopic eczema
Face - topical hydrocortisone and steroid-sparing medications (weaker)
Body - topical methylprednisilone (stronger)
Regular emollients
Treat secondary infection (ex: staph)
Identify and remove any potential allergens and irritants
Treatment of psoriasis (3)
- Topical
- Keratolytics (salicylic acid) if scaly
- Steroids
- Emollients
- Vitamin D and A (retinoids) - Phototherapy in older kids not responding to steroids
- Systemic (difficult, severe, resistant cases)
- Retinoids (vit A)
- Methotrexate
ABCs of a paediatric behavioural history
- red flags of each
Antecedent (trigger)
- Red flags: no clear/reasonable trigger, occurring in multiple environments
Behaviour
- Red flags: developmentally inappropriate, regression, multiple concerning behaviours
- ASK SPECIFICALLY ABOUT: eat, sleep, play*
Consequences (what happens after; how does this affect the child and those around them and functioning)
- Red flags: harmful to self and others, affecting functioning of child and/or family
What do you suspect if a baby has a massively distended abdomen AT BIRTH
- hasn’t passed meconium
- vomiting bile
What if they were only distended a day or 2 after birth?
Distended at birth: think meconium ileum in a child w F
Distended a day or 2 after birth: think
- distal bowel obstruction (anorectal anomalies/imperf anus)
- hershsprung’s disease (rectal stimulation will give sudden gush of merconium)
What condition is duodenal atresia associated with? How would this present?
30% risk of down syndrome w duodenal atresia
Bowel obstruction WITHOUT distended abdomen (empty hypogastrium with distended epigastrium dye to duodenal/jejunal obstruction)
in a nutritionally deficient baby (thin, pale, ribs visible)
Classic x-ray finding of duodenal atresia
Double bubble sign
- distended stomach and duodenum separated by pyloric valve
(Have complete closure of portion of lumen of duodenal so get ballooning of lumen proximal to this)
What is hirschsprung’s disease?
A form of megacolon occurring when part or all of large intestine have no ganglion cells therefore are in constant state of contraction, causing distal bowel obstruction
Presentation: failure to pass meconium within 48 hours od devilry
+/- abdo distension, vomiting, explosive stools following rectal stimulation, bloody diarrhoea
What do you suspect in a baby who is unable to swallow and is constantly dribbling/drooling saliva?
How do you examine for this?
Oesophageal atresia
(drooling baby until proven otherwise)
Passing catheter through mouth and seeing how far it travels will establish whether oesophagus is non-patent or not
What BMI percentile cut off qualifies as FTT?
Overweight?
Obese?
<5th centile: FTT
85-95th centiles: overweight
> 95th centile: obese
Features of turner syndrome
XO karyotype
- Short girl relative to family
- Pubertal failure
- Webbed beck
- hearing, renal defects
- CHD, HTN
Endocrine causes of short stature
Hypothyroid most commonly (elevated BMI, constipation, sluggish behaviour etc)
Cushing’s disease (GC excess) - elevated BMI
GH deficiency
What is a form of skeletal dysplasia and how is this generally picked up?
Achondroplasia (dwarfism)
- Autosomal dominent, picked up antenatally on ultrasound
Red flags for investigating short stature
abnormal growth velocity
signs of chronic disease on systems review/exam
abnormally short for family
<1st centile
Obvious dysmorphic/syndromic features
What is the definition of failure to thrive?
Failure to thrive is being <3% for weight or dropping 2 or more percentile tracks
what are the three main complications in kids of renal failure?
Anaemia
Metabolic bone disease (renal osteodystrophy and hyperparathyroidism)
Poor growth
what is haemolytic uraemia syndrome?
microangiopathic
What is the most common cause of AKI?
Pre-renal cause (hypo perfusion due to septic shock, hypovolaemia, haemmhorage, severe dehydration etc)
Which electrolyte reflects water balance in the body?
[Na] w normal range 135-145mmol/L
[Na] high: dehydrated
[Na] low: over-hydrated
What is a severe complication of SiADH?
Around what [Na] does this occur?
Water retention from ADH release -> Cerebral oedema -> raised ICP -> hyponatraemic encephalopathy and brainstem herniation
Occurs around [Na] 120 in kids
What are the clinical signs of dehydration and what % body weight of fluid is lost with each?
- Mild
- Moderate
- Severe
Mild (<4%)
-none
Moderate (4-6%)
- delayed cap refill
- increased RR
- mildly decr tissue turgor
- sunken eyes and fontanelles
- oliguria/decr wet nappies
Severe (>=7%)
- cap refill >3sec
- mottled skin
- irritable, decr conscious state, hypotensive
- deep, acidotic breathing
- decr tissue turgor
How do you evaluate fluid status in a child?
Daily weights (Loss of body weight in g = estimated fluid deficit in ml)
Fluid charts (daily intake and losses)
Daily UEC and BSL monitoring
Clinical signs
When replacing a fluid deficit, over how long should you replace that deficit?
Over 24 hours
UNLESS they are hypo or hypernatraemic, then replace over 24-72 hours
Why is NGT preferred over IV rehydration in kids?
Less likely to cause electrolyte imbalances
What fluid do we use for rehydration in children and neonates?
Children: normal saline with 5% dextrose
Neonates: normal saline with 10% dextrose
What is the 4/2/1 rule of fluid resus?
When might you stray from this and why?
First 10kg body weight: 4ml/kg/hr
Second 10kg: 2ml/kg/hr
Over 20kg: 1ml/kg/hr
1/2 or 2/3 maintenance for kids w severe illness due to SiADH causing fluid retention (meningitis, encephalitis, head trauma, surgery, resp issues)
What can happen if serum [Na] changes too rapidly?
Cerebral oedema, seizures and permanent brain damage
Central pontine myelinosis occurs as a consequence of a rapid rise in serum tonicity following treatment in individuals with chronic, severe hyponatremia
What referral(s), if any, would you give a chid w school-based learning and behaviour problems?
Educational psychologist to test:
- Vision
- Hearing
- Cognitiion
When do you refer for speech therapy and audiology assessment?
<50 words at 2yo
No 2 word combinations at 2.5yo
No understanding of simple instructions without gesture
Differentials for an irritable baby who is sleeping poorly
Colic
GORD/physiological reflux
Poor maternal/child relationship
Cow’s milk protein allergy
Features of colic
PURPLE CRYING Peaks at 6-8 weeks Unexpected Resists soothing Pain-like face Long-lasting (crying for >5 hours a day at times) Evening (sleep deficit is at peak)
When might a child have lactose intolerance?
Never BORN with lactose intolerance - all kids under 3 have high levels of lactase.
They may only have it secondary to coeliac, IBD, giardiasis, CMPA which destroy the intestinal brush border which attaches to lactase
What may the presentation of CMPA be?
What are the rates of resolution?
Regurgitation, vomiting after feeds
Stool changes (diarrhoea/constipation, blood)
Skin/eczematous rash
FHX atopy
50% resolve by 1yo; 80% by 3yo
Management of physiological reflux in infants
Raise head of head
Thicken formula
Omeprazole is just a bandaid - decreases acidity but doesn’t prevent reflux.
What is the character and location of a pulmonary flow murmur?
Pulmonary area +/- radiation to axilla
Soft blowing ejection systolic murmur
Systolic murmurs in kids
ejection vs pan systolic
Ejection:
- innocent pulmonary flow murmur
- AS
- PS
- Bicuspid aortic valve
Pan systolic:
- MR
- VSD
Diastolic murmurs in kids
Early
Mid
Late
Early:
- AR
- Pulmonary Regurg
Mid
- MS
- Large VSD
Late
- MS (with atrial contraction)
What does APGAR stand for?
Appearance (colour) - pale or blue/body pink extremities blue/pink
Pulse rate - absent/<100/>100
Grimace (reflex irritability) - none/some/vigorous, cry
Activity (tone) - floppy/some flexion/good flexion
Respiratory rate - apnoeic/irregular/active crying
Where do you place the SaO2 probe on neonates and what does this represent?
R hand or wrist
= pre ductal pulse oximetry
When is peak surfactant produced in babies and below what age is it not enough to keep alveoli patent?
Peak at 37 weeks (term)
Not enough surfactant to keep alveoli open below 32 weeks
risk factors for hypoglycaemia in neonates
Maternal/gestational diabetes
Delay in feeding
Preterm
Growth retarded and sick infants
What affect does prematurity have on the kidneys?
Kidneys are unable to reabsorb phosphate which results in demineralisation of bones in order to increase serum [Ph]
How do you test for bone disease of prematurity
Mx?
Ix: test blood ALP and urine Phosphate levels
Mx: Ph and Ca supplements
When do you expect each of the following shunts to close:
- Ductus venous
- Foramen vale
- Ductus arteriosus
- Ductus venosus
- Over 3-7 days - Foramen ovale
- Functionally closes in first few breathes of life (but is not fully closed in 50% children by 5yo) - Ductus arteriosus
- 3-4 days in 95% term babies
Causes of apnoea in premies
- Apnoea of prematurity is most common in otherwise well bubs (caffeine as Mx)
- Infection (empirical antibiotics until infx is ruled out!)
- lung disease
- hypoxia
- academia
- drugs
- metabolic disturbances (hypoglycaemia, hypocalcaemia, hyper/hypomagnasaemia)
- Intracranial haemmhorage
- polycythaemia w hyperviscosity
- Necrotising enterocolitis
- CHD (PDA)
RFs for prematurity
1/2 of premature births don’t have RFs
- Maternal factors
- previous preterm
- extremes of maternal age
- low pre-pregnant weight/malnourished
- acute illness
- pre-eclampsia/eclampsia
- previous miscarriage or termination of pregnancy
- HX infertility
- IVF - Fetal factors
- fetal anomalies
- polyhydramnios - Placenta and membrane difficulties
- Social
- Low SES
- psychological stress
- Alch, drugs, smoking
Complications of prematurity (acute)
Resp
- RDS/HMD
- apnoea of prematurity
Cardiac
-PDA
Neurological
- intraventricular haemmhorage
- periventricular leukomalacia
- Cerebral palsy
Hepatic
- Hypo/hyperglycaemia
- Jaundice
Renal
- Bone disease of prematurity
- electrolyte imbalances (hypo/hypernatraemia, hyperkalaemia, metabolic acidosis)
GI
- feeding difficulties
- NEC
Infection due to immature immune system
Temp instability
Late/chronic effets of prematurity
Delayed growth (usually catch up
Retinopathy of prematurity
Chronic lung disease of prematurity
Neurodevelopment delay (CP, blindness, deafness)
Most common cause for IUGR?
placental compromise
Gross Motor milestones
Head lag minimal at 6-8 weeks
Rolling at 3-5 mo
Sitting at 6 months
Crawling at 9 mo
Walking at 12 mo
Jumps BY 3 years
Balances on one foot BY 4.5 years
Red flag for gross motor
Not walking by 18mo
Fine motor milestones
Palmar grasp by 6mo
Inferior pincer by 9mo
Pincer grip, stacks 2 cubes ~ 12mo
Handedness 18mo
Spontaneous scribbling by 2years
Imitates vertical line by 3 years
Copies face/ladder by 4.5 years
Social and daily living skills milestone red flags
No interest in other children/help w dressing at 24 months
NO interactive play with peers at 3 years
No imaginative role play by 4 years
Paracetamol overdose treatment in kids
- If dose ingested is possibly >10g or >200mg/kg, start NAC
- measure paracetamol concentration 4 hours post-ingestion
- If above treatment threshold, continue NAC
- repeat paracetamol concentration, UECs, LFTs on completion.
Main infectious agents of cellulitis
Ix
Mx
S aureus and Strep progenies (consider HIB in unimmunised children <5yo)
Ix: blood cultures
Mx: Flucloxacillin po or IV if fever, rapid progression
+/- ceftriaxone to cover HIB if unimmunised, <5yo
What is Prader-willi syndrome?
Behaviourial/developmental disability featuring food seeking, ODD and OCD, mild features of ASD as children
- incr risk of psychosis, T2DM, OSA, scoliosis as adults
Excessive appetite and lack of satiety -> risk of obesity
Genetic - loss of paternally expressed genes
Features of autism
- Problems w socialisation
- poor eye contact
- difficulties w gestures
- not responding to name
- failure to socialise w others - Problems w communication
- limited use of language
- no imaginative play or social imitative play - Repetitive or obsessive behaviours
- repetitive play
- inflexible, repetitive use of language
- unusually obsessions w inflexible and limited interests
- self-stimulating behaviours (toe walking, hand flapping, jumping in place, making sounds, grinding teeth etc)
What is ‘croup’?
Presentation
Aetiology
MX
Laryngotracheobronchitis
Presentation: barking cough +/- stridor on exertion (at rest = severe)
Aetiology: Parainfluenza
Mx: supportive treatment for most kids
- If stridor at rest, single dose of oral DEX then Observe for half an hour post steroid administration. Discharge once stridor-free at rest.
- If severe: O2, IM/IV dex, neb adrenaline, intubation or tracheostomy
If good improvement, observe for 4 hours post adrenaline. Consider discharge once stridor free at rest.
If deterioration/no improvement, give further adrenaline and consider admission or transfer as appropriate.
Complications of viral URTIs
- Otitis media
- Acute sinusitis
- Bacterial superinfection
- Progression to LRTI (bronchitis, croup, bronchiolitis, pneumonia)
- Asthma exacerbation
What are the bag bugs you have to watch out for that can cause pharyngitis?
Defining features
- EBV
- exudative tonsillitis assoc w cervical lymphadenopathy and generalised flu-like SX - HSV-1
Mucosal ulceration - Enteroviruses (Coxsackie A/B, echoviruses)
- assoc w oral ulcers and rash - Strep throat (pyogenies)
- exudative tonsilitis, strawberry tongue, widespread erythematous rash, tender enlarged cervical lymph nodes, high fever
Presentation: bilateral swelling, tenderness, pain in parotid glands
What is the diagnosis?
Mumps.
Most common causative agent of acute otitis media.
What would you see on ear exam?
How do you treat?
Strep pneumonia most common (H. influenza and moraxella catarrhalis)
See red bulging TM, presence of middle ear fluid
Analgesics. Limited value in treating w antibiotics as pain resolves in 2-7days
Maintains of MX of URTIs
- self-limiting and don’t require pharm. intervention unless they are complicated
- influenza and pneumococcal vaccine as prevention
- reduce exposure to tobacco smoke
- hygiene to reduce transmission rates
Features of asthma
SX
Signs
SX:
Wheeze and SOB
Responsive to salbutamol
Chest tightness, coughing (worse at night and in morning)
Signs:
- tracheal tug, WOB
- prolonged exp. phase
- exp wheeze
- tachypnoea
- decr RR and absent wheeze, decr breathe sounds in severe asthma
Asthma management plan (and what features define each stage?)
- mild
- moderate
- severe
- critical
1 dose salbutamol: 6 puffs if <6yo or 12 puffs if >6yo
- mild: 1 dose salbutamol and review after 20min. If good response, D/C on salbutamol PRN. Poor response, treat as moderate
- Moderate (incr WOB, disrupted sentences, tachycardia): Salbutamol 1 dose every 20min for 1 hour. review 10-20 min after 3rd dose to determine freq of next dose.
O2 if saO2<92% - Severe (agitated/distressed, marked WOB and limitation of speaking ability): Salbutamol 1 dose every 20min for 1 hour -> if responding, incr time between doses. If not responding, continue dosing even 20min.
+ o2 as above.
+/- atrovent via MDI/spacer every 20min for 1 hour only.
+/- IV Mg sulfate
+/- IV aminophylline - Critical (silent chest, confused/drwosy, no talking)
- O2
- Continuous nebuliser salbutamol
- Nebulised iprotropium (3x in 1st hour only)
- IV methylpred
- IV Aminophylline and MgSulfate
+/- ICU admission
+ 3 days oral pred with each (2mg/kg `day 1 then 1mg/Kg day2,3)
Signs of salbutamol toxicity?
Tachycardia, tachypnoea, metabolic acidosis. Can occur with both IV and inhaled therapy. Lactate commonly high.
Stridor
-differentials
- Inx?
Acute
- most common acute cause in kids is CROUP
- retropharyngeal abscess
- peritonsillar (quinsy) abscess
- laryngeal trauma
Persistent
- laryngomalacia most common cause of persistent stridor
- subglottic stenosis
- subglottic haemangioma
INX: only if stridor is persistent with an expiratory component (severe) = bronchoscopy
Differentials for wheeze
Since birth:
- airway malacia (tracheomalacia or bronchomalacia)
Gradual onset SX
- Asthma
- Recurrent viral-induced wheeze
- Cystic fibrosis
- Cardiac causes
Sudden onset SX
- LRTI (bronchiolitis, viral pneumonitis, bacterial bronchitis)
- Inhaled foreign body
RF for TB infection
Emigrants from developing countries Low SES Indigenous Immunodeficiency <5yo
Chronic cough DDX and first line IX
Asthma
Viral or bacterial URTI or LRTI
Cardiac (pulm HTN, pulm oedema)
Bronchiectasis (CF, primary ciliary dyskinesia, immunodeficiency, foreign body etc)
Aspiration
Chronic/less common infx (Tb, pertussis, mycoplasma, atypical pneumonia)
Interstitial lung disease (rheumatic diseases, cytotoxic, drugs, radiation)
GOR
Psychogenic
FIRST line Ix: CXR and spirometry if >6yo
Presentation of bronchiectasis
□ Chronic moist or productive cough, WORSE in mornings
□ Clubbing
□ Chest wall abnormalities (hyperinflation, pectus carinatum)
□ Inspiratory creps
Mx of cystic fibrosis
- Antibiotics to reduce bacterial colonisation and biofilm formation of resp tract
- Physio to promote mucociliary clearance
- Vaccines: pneumococcal and influenza
- High energy diet and pancreatic supplements (Creon)
- Vitamin and salt supplements
+/- lung and liver transplants at end-stage
DDX diarrhoea
Osmotic
- IBS
- Laxatives
Secretory
- Gastro (ETEC, cholera)
Inflammatory
- IBD
- Surgical (appendicitis, interception)
- Sepsis, UTI
- NEC
Motility
- Hyperthyroid
- Diabetic neuropathy
Malabsorption
- Coeliac
- Cystic fibrosis
- Giardia
- CMPA
Red flags for diarrhoea
SX of Dehydration (dizzy, decr urine output, lethargic)
Prolonged diarrhoea
Blood in stool
Systemically unwell
FTT
Bilious commits
Acute abdo (severe abdo pain and tenderness)
When do do a renal U/S for kids w UTIs
If <6mo: U/S during acute infection if atypical UTI or recurrent UTI OR within 6 weeks if responds to treatment within 48 hrs
If >6mo: U/S during acute infection if atypical UTI only OR within 6 weeks if recurrent UTI only . If responds to treatment within 48 hrs no need for imaging.
Features of atypical UTIs
- Seriously ill/septicaemia
- Poor urine flow
- Abdo or bladder mass
- Raised creatinine (deranged renal fun)
- Failure to respond to Ab treatment within 48 hours
- Non-ecoli isolated
Acute management of UTIs
<3mo: IV antis
> 3mo, pyelo/upper UTI: PO cephalosporin or augmentin (7-10days)
> 3mo, cystitis/lower UT: PO cephalosporin, trimethoprim (3 days)
Causes of non-blanching rashes
Viral most common (but higher % bacterial than w blanching rashes) - enterovirus, influenza
N. Meningitidis Other bacteria (Strep pneumonia, HIB)
HSP, ITP, DIC
Leukaemia
Mechanical trauma
Causes of blanching rashes
VIRAL most common cause Enterovirus Adenovirus Coxsachie virus Rhinovirus RSV Measles Parvovirus B19 (itchy) Bacterial - toxic shock syndrome
How does parvovirus cause fetal anaemia?
bone marrow suppression which decr production of erythrocytes
what about fevers can cause febrile convulsions?
Rate of temp rise rather than the degree of temperature itself
Steven Johnson syndrome results due to what causes?
what is the classic presentaiton
Flu-Like symptoms as prodrome followed by red/purple rash that spreads and forms blisters (skin, mucous membranes, genitals, eyes)
Main cause: mycoplasma infection
- drug reactions (anti epileptics)
-
Causative agents of osteomyelitis/septic arthritis
Management?
Staph aureus #1!!
Strep pyogenies and haemophilus influenzae
Mx:
- REFER TO ORTHO for aspiration +/- athrotomy and washout
- IV fluclox
- Elevate and immobilise limb
Rule of 2s of Meckel’s diverticulum
2% population 2:1 male:female 2 feet above ileocecal valve 2 inches long 2% patients develop complications over lifetime, typically before age of 2.
How can mocker’s diverticulum present?
Abdo pain (Related to bowel obstruction, Meckel's diverticulitis or perforation) GI bleeding SX of bowel obstruction
What does a high reticulocyte count indicate?
Low reticulocyte count?
® Incr -> indicates marrow response to ?haemolysis
® Decr -> indicates lack of marrow response -> ? Deficiency in necessary iron or vitamins OR ? Inability to respond (marrow aplasia or infiltration)
Causative agents of osteomyelitis/septic arthritis
Management?
Staph aureus #1!!
Strep pyogenies and haemophilus influenzae
Mx:
- REFER TO ORTHO for aspiration +/- athrotomy and washout
- IV fluclox
- Elevate and immobilise limb
Rule of 2s of Meckel’s diverticulum
2% population 2:1 male:female 2 feet above ileocecal valve 2 inches long 2% patients develop complications over lifetime, typically before age of 2.
How can meckel’s diverticulum present?
Abdo pain (Related to bowel obstruction, Meckel's diverticulitis or perforation) GI bleeding SX of bowel obstruction
What is HUS?
STEC (also known as VTEC) infection can cause bloody diarrhoea, fever, abdo pain, vomiting and sometimes haemolytic uraemic syndrome. Infection usually results from consuming contaminated food or water, or from contact with infected animals or people.
HUS is a severe condition characterised by kidney failure, bleeding and anaemia. It can sometimes be fatal. -> bruising/petechial rash (low Plts), haemolytic anaemia, reduced consciousness, reduced urination, HTN, seizures.
Definition of failure to thrive
Infant’s weight below 3rd centile or >2SD below population mean
Weight crossing 2 major centile lines with time
Risk factors for FTT
Prematurity
IUGR
Causes of FTT
What 2 are most common
Reduced intake (most common)
- Inadequate caloric intake (poor feeding etc)
- Psychosocial
- maternal depression/poor maternal-child bond
- difficulties at home
Incr metabolism
- Chronic or intercurrent illness, infections (UTI, Thyroid, CF, CHD, CRF, chromosomal, atopy, Tb, HIV etc)
Reduced nutrient absorption
- Coeliac
- CMPA
- IBD
What are some methods of increasing caloric intake in infants with FTT
Dietary advice and monitoring
Breast-fed infant:
Supplementing breastfeeds with EBM or formula afterwards
Formula-fed infant:
- Increase forumla concentration or add glucose polymer (extra calories) to bottle
- introduce solids or add calories to solids
Indications for an epipen
- anaphylaxis
- also has asthma as well as allergy
- geographical distance from emergency medical services
Indications for Food challenge
- uncertain HX
- borderline skin prick testing (~3mm)
What organism causes meningococcaemia?
What is different about managing this condition as a cause for sepsis and/or meningitis?
Neisseria Meningiditis
Notifiable disease!
- patient req isolation until 12hours IV antis
- notify the Department of Human Services
- Rifampicin prophylaxis to all close contacts (household, day-care, intimate relations in pst 7 days)
Emergency management of severe anaphylaxis
Adrenaline - 0.5mc Adrenaline IM, give every 5 min if not responding
Airway - intubation + neb adrenaline if required
+/- oral corticosteroids and nebulised salbut for bronchospasm
B - high flow O2
C - circulation (supine w legs elevated to prevent collapse)
Exposure - H2 antagonists for skin involvement
DX and MX of eosinophilic esophagitis
DX: gastroscopy and biopsy histology
MX: food avoidance (dairy, wheat, egg, soy triggers), swallowed aerosolised CS
Emergency fluid rhesus in shocked patients
Give boluses of 10-20ml/kg of 0.9% sodium chloride (normal saline), which may be repeated once (Give second 20ml/kg bolus if required to a total vol of 40ml/kg)
® If persisting hypotenseion after second bolus, give inotropes (Adren/NA in 500ml 0.9% normal saline)
Prophylactic antibiotics for sepsis
<1mo: benpen and cefotaxime
>1mo: flucloxacillin and ceftriaxone
What is HSP and how does it typically present?
Most common vasculitis of childhood
Purpura + abdo pain + arthralgia +/- renal involvement (haematuria/proteinuria/hypertension)
Often preceded by viral URTI
Dx and Mx of HSp
Dx: urine test
Mx: supportive (paracetamol +/- NSAIDs, oral or IV corticosteroids relieve joint and abdo pain)
features of colic
Completely benign, normal part of development
Peaks at 2 months (Begins: 2 weeks of age and continues until about 3-4 months of age). Unexpected Resists soothing (INCONSOLABLE crying) Pain-like face Long-lasting (up to 5 hours of crying) Evening
Newborn that appears normal but has resp distress when NOT crying. Pink when crying but makes vigorous resp efforts and becomes dusky when stops crying.
What is the likely explanation and how would you diagnose this?
Choanal atresia. Infants are obligate nose breathers until 4 months of age - choanal atresia occurs when an infant has a structurally non-patent nose.
DX by inability to pass a feeding tube through nostril or clouding of cold metal under infant’s nose?
Contraindications to vaccines
Known allergy to ingredient
Previous anaphylaxis
Immunocompromised
