JLS Paeds Flashcards
What is the medical term for croup?
Laryngotracheobronchitis
What is the typical presentation and clinical course of croup?
1 - 2 days of coryza. On the 2nd or 3rd night / early morning, awake with a barking cough. Stridor might develop after that. Barking cough / stridor only lasts 2-3 days. Viral symptoms last 7 days
What is the typical microorganism which causes croup?
Parainfluenza virus
What is the management of croup?
- Basics - minimal handling. Supplemental oxygen or respiratory support if required in severe cases. 2. Place and person - admit to hospital if worried about increased WOB or hypoxia. 3. Investigations and definitive diagnosis - clinical diagnosis 4. Management - oral prednisolone (1mg/kg), oral dexamethasone (0.15 - 0.6 mg/kg), IV dexamethasone (0.2mg/kg), nebulised adrenaline (1:1000), ETT 5. Long term
What are the two main types of croup?
Acute viral croup or recurrent spasmodic croup
What are the symptoms of epiglottis?
The four Ds Dysphagia Dyphonia Drooling Dyspnoea
What is the most common microorganism which causes epiglottis?
H. influenzae B
What is the most common microorganism which causes bacterial tracheitis?
Staphylococcus aureus (now more common than epilglottitis due to Hib vaccine)
what is the dosage of ipatropium bromide given in moderate / severe acute exacerbations of asthma?
6 yo give 8 puffs with salbutamol burst therapy (every 20 minutes for one hour)
What are the signs of respiratory distress in a child?
(Hint there are 7)
7 SIGNS OF INCREASED WOB IN KIDS
(general inspection -> obs -> hands -> face -> neck -> chest)
Cyanosis
Tachypnoea
Head bobbing (younger kids)
Grunting
Nasal flare
Tracheal tug
Intercostal and subcostal recession
What is the pathophysiology of bronciolitis?
Inflammation of the bronchioles
Often caused by infections with RSV
What is the usual causative microorganism of brinchiolitis?
RSV
In what age group is bronchiolitis most common?
What does RSV tend to cause?
Bronchiolitis
What does parainfluenza virus usually cause?
croup
What is the typical presentation of Bronchiolitis?
Child
URTI + asthma like symptoms [cough, dyspnoea, wheeze]
(remember, can’t diagnose asthma
What would you consider for “Place and Person” in a child with bronchiolitis, when deciding whether or not to admit them?
- Oxygen requirement - if requiring oxygen to maintain SpO2 > 93% admit
- Apnoeic episodes - marker of severity
- Behaviour - poor feeding, lethargy and irritability are signs of severity
- Work of breathing
What is the management of bronchiolitis?
Basics
- DRABC
- Vital Signs
Place and Person
- Assess severity
- If increased WOB, requiring O2 to maintain SpO2 > 93%, apnoeas or lethargy/poor feeding/irritabilty –> ADMIT [if RURAL - if parents are anxious / nervous / “irresponsible” or if live far away]
Ix and confirm diagnosis
- Usually aclinical diagnosis
- If diagnostic uncertainty, can do CXR
Definitive Management
- Supportive management
- Minimal handling and frequent feeds’
- Oxygen via NP / HFNP
- NGT / IV fluids if poor feeding
- Can be discharged once maintaining adequate oxygenation and adequate feeding
- Can triabl salbutamol if 2 years old to see if salbutamol responsive
Follow Up
- Follow up with GP
- Educate RE signs to return (apnoeic, lethargic, poor feeding, wheeze, increased WOB)
Braking cough = ?
Croup
Laryngotracheobronchitis
What are the causative microorganisms of croup?
95% is Parainfluenza
Can be bacterial (H. influenzae, S. aureus) = bacterial tracheitis
BONUS WOMENS QUESTION
What are the causes of menorrhagia?
Bleeding disorder
Iatrogenic (IUDs and drugs)
Thyroid dysfunction (especially hypo)
Cancer (Endometrial, cervical)
Hyperplasia of the endometrium
Fibroids (leiomyomata) and polyps
Adenomyosis and endometriosis
Chlamydia, gonorrhea and STIs
Ectopics, miscarriage, pregnancy
At what age do you get croup?
6 months - 6 years
What are the typical symptoms/ signs of croup?
What is added to make this bacterial tracheitis?
URTI followed by barking cough, hoarse voice, wheeze [even though LRTI], increased WOB
If there is also high fever + toxic looking child –> consider BACTERIAL TRACHEITIS [OR EPIGLOTTITIS FOR THAT MATTER?!]
What is the management of croup?
Basics
- DRABC
- Vitals
Place and Person
- Do they need to be admitted?
- Stridor at rest
- Requiring O2 - VERY LATE SIGN
- Increased lethargy/irritability
- Poor feeding
- Live far away [rural]
- Parents don’t seem “sensible” [rural]
Ix and Confirm Diagnosis
- Want to avoid over-investigating because can worsen
- CXR if uncertainty: steeple sign if severe
Definitive management
- Mild: D/C home and supportive care. Freqeunt small feeds and minimal handling
- Moderate:
- Oral corticosteroids:
- 1mg/kg prednisolone
- 0.15mg/kg dexamethasone
- Oral corticosteroids:
- Severe:
- Nebulised adrenaline
- plus oral steroids as above
Follow Up
- DC once no stridor at rest
- Follow up with GP a few days later
- Educate RE signs to come back in
What are the markers of severity for croup?
Stridor at rest
Poor feeding
Lethargy / irritability
Increased WOB
Reduced SpO2 is a very late sign
What is the aetiology of epiglottitis?
Haemophillus infleunzae
Or, if immunised, more likelt to be
Beta haemolytic strep
Moraxella catarrhalis
Strep pneumoniae
What are the causes of epiglottitis in an immunised child?
Group A Strep
Moraxella Catarrhalis
Streptococcus Pneumoniae
How do you differentiate between croup and epiglottitis?
Croup
- sickness comes on over a few days
- Preceeding URTI symptoms
- Not usually with high fever
- Miserable
- Loud, barking, brassy cough
- Loud, harsh stridor
- Hoarse voice
- Able to drink, not drooling
Epiglottitis
- Comes on suddenly
- No preceeding URTI symptoms
- High fever
- Flat / flopppy
- Soft, muffled cough
- Soft stridor
- Quiet voice, reluctant to speak / dysarthria
- Dysphagia and drooling
What is the management of epiglottits!
Straight to ED
Secure the airway (be prepared to perform a crycothyroidectomy)
Take bloods once intubated
Empiral antibiotics (Ceftriaxone)
Treat contacts with Rifampicin prophylactically
What is the aetiology of cystic fibrosis?
autosomal recessive mutation on chromosome 7
inteferes with CFTR gene which cuases altered ion transportation across epithelial cells
What are the clinical features of CF?
Respiratory
- Thickened secretions
- Recurrent infections
- Bronchiectasis
- Recurrent pneumothroacies
- ABPA
- Nasal polyps
- Chronic sinusitis
Pancreas
- Exocrine insufficiency (which then blocks the endocrine ducts)
- Malabsorption
- Steatorrhea
- Failure to thrive
- Recurrent pancreatitis
- T1DM
Hepatobiliary System
- Prolonged neonatal jaundice
- Hepatic cirrhosis
- Portal HT
- Fat soluble vitamin deficiency (vitamin ADEK)
- Recurrent cholecystitis
GIT
- Meconium ileus
- DIOS
Reproductive system
- Absence of vas deferens
- Delayed puberty due to malnutrition
- Infertility
What is involved in testing for CF using the Gutehrie Test?
- First Test for IRT (immunorecative trypsinogen level)
- If this is high - then test for CFTR
What is the screening test for CF?
What is the diagnostic test?
Screening test = Gutherie Heel Prick (IRT & CFTR)
Diagnostic Test = Sweat Test
If you had a child with symptoms of CF, what FIRST investigation would you order?
Sweat Test
(Sweat chloride levels >60mmol/L = diagnostic of CF)
NOT the heel prick test, this is a screening test
What is the overall management of CF?
Basics
- Explain there is NO CURE - only manage potential complications
Place and Person
- Referral to paediatrician, respiratory physician, allied health including physiotherapists and dieticians
Ix and CD
- Sweat Test if not already done
Definitive Management:
Think of each system
- Respiratory
- physiotherapy
- aerolysed mucolytics
- ABx if infection, also given resuce antibiotics
- Lung transplant (last line)
- GIT & Pancreas
- High calorie diet
- Pancreatic enzyme replacement (Creon)
- Fat solumble vitamin replacement (A,D,E,K)
- Salt replacement occasionally
- Insulin later in life
Prevntative / Ongoing
- Flu vaccine
- Pneumococcal vaccine
- NO SMOKING
- Avoid sick people
- Regular follow up
- Yearly mucous cultures taken (and at every exacerbation). Eventually get infected with pseudomonas.
- DEXA scan at puberty
*
How do you classify asthma in cenhildr?
Infreuent intermittent
- Attacks less often than every 6 weekly
- No interval symptoms
Frequent intermittent
- Attacks more often than every 6 weekly
- No interval symptoms
Persistent
- Attacks more often than every 6 weekly
- Mild: Interval symptoms fewer than 1 x per week
- Moderate: interval symptoms 1 x per week
- Severe: interval symptoms >1 x per week
How do you classify infrequent intermittent asthma?
Attacks less often than every 6 weeks
No interval symptoms
How do you classify frequent intermittent asthma?
Attacks more often than every 6 weeks
No interval symptoms
How do you classify mild persistent asthma?
attacks more frequent than every 6 weeks
interval symptoms less than once per week
How do you classify severe persistent asthma?
Attacks more frequently than every 6 weeks
Interval symptoms more than once per week
How do you classify moderate persistent asthma?
Attacks more frequently than every six weeks
Interval symptoms 1 x per week
What are interval symptoms?
What else can you ask to grade the severity of asthma?
Interval Symptoms
Night cough / wheeze
Morning cough / wheeze
Exercise tolerance
Days of school missed?
Youcan also ask
- When was the last time / has he ever / how often does he require steroids for his asthma?
- Has he been to ED / wards / ICU with his asthma?
What is the defnitive management of infrequent intermittent asthma?
SABA prn
What is the defitive management of frequent intermittent asthma?
SABA prn
+
low dose/higher dose ICS
AND/OR
LTRA
AND/OR
cromone
What is the definitive management of persistent asthma?
SABA prn
+
low dose/higher dose ICS
AND/OR
LTRA
AND/OR
cromone
+
LABA
oral CS
Name two generic types of SABA and some brand name?
Salbutamol (Vontolin)
Terbutaline (Bricanyl)
Name two different types of ICS and their brand names?
Fluticasone (Flixotide)
Budenoside (Pulicort)
Name two different types of combined ICS / LABA?
Fluticasone + Salmetorol = Seretide
Budenoside + efometerol = Symbicort
Name two types of LABA and their brand names?
Efometerol = Foradile
Salmeterol = Serevent
(usually see this combined with an ICS)
Name one generic type of LTRA and it’s brand name
Monteleukast (Singulair)
Name one type of cromone and their brand name
Cromoglycate (intal)
How do you diagnose asthma in a child?
Trial of salbutamol
(not with lung function tests or PEF until over 7-8)
In what age group would you use LABAs?
No evidence for children
What is the emergency management of asthma, to instruct parents of a child >6 years old, to do at home?
> 6 y.o. = maximum 12 puffs of ventolin
‘4,4,4’ rule
- 4 puffs (4 breaths per puff)
- wait 4 minutes
- 4 puffs (4 breaths per puff)
- wait 4 minutes
- 4 puffs (4 breaths per puff)
- wait 4 minutes
Then if not better, call an ambulance
/ bring in to hospital.
Can bring straight in to hospital if:
- If you are worried – call an ambulance straight away even before administering ventolin
- If are requiring ventolin more frequently than every 3-4h
- If wheezing lasts >24h and is not getting better
- If you get little or no relief from ventolin
What is the home emergency management of asthma of a child
‘2,2,2 rule’
2 puffs (3-4 breaths)
- wait two minutes
puffs (3-4 breaths)
- wait two minutes
2 puffs (3-4 breaths)
- wait two minutes
if not better call ambulance / bring in to hospital
other reasons to call an ambulance / seek medical attention
- If you are worried – call an ambulance straight away even before administering ventolin
- If are requiring ventolin more frequently than every 3-4h
- If wheezing lasts >24h and is not getting better
- If you get little or no relief from ventolin
What are the causes of cyanotic congenital heart disease?
12345T
- Truncus arteriosus
- Transposition of the Great Arteries
- Tricuspid / Pulmonary Atresia
- Tetralogy of Fallot
- Total anomolous pulmonary venous return
What are the two classes of acyanotic congenital heart disease?
Obstructive and L-R shunt
What are the causes of obstructive heart disease?
- Hypoplastic L heart syndrome
- AS
- Coarctation of the aorta
- Interruption of the aortic arch
As a general rule, which group of congenital heart defects are ALWAYS duct dependent? How is this treated in the early stages?
Obstructive congenital heart defects (hypoplastic L heart syndrome, AS, interruption of the aortic arch and aortic coarctation). They are treated by PGE1 in the short term, to keep the duct open
As a general rule, which group of congenital heart defects are USUALLY duct dependent? Is it harmful to treat with PGE1, while still in the diagnostic process?
R–>L shunts (1T2T3T4T5T) but this time you depend on the duct being open for blood to flow into the PULMONARY circulation
How and when do obstructive congenital heart defects present?
A shocked neonate. Often on D2 of life when PDA closes. Present as a dusky / grey coloured neonate with weak / absent pulses and a low BP, with a metabolic acidosis.
What are the defects of tetralogy of fallot?
- PULMONARY STENOSIS 2. RVH 3. VSD 4. Overriding aortic arch
When does tetralogy of fallot tend to present and how?
6-12 months of life. “Tet spells” or “hypoxic spells” - cyanosis or LOC / going floppy on feeding, crying or exertion
What is the surgical correction of transposition of the great arteries?
balloon atrial septotomy
What is the surgical correction of hypoplastic L heart syndrome?
Norwood operation
Which two congenital heart defects are associated with DiGeorge syndrome? Which chromosomal abnormality is this and what are the other associated features?
TOF and transpos are both associated with microdeletion of the long arm of chromosome 22. The other associated features are ‘CATCH 22’ Cardiac (trasnpos, TOF) Abnormal (long) facies Thymic hypoplasia Cleft palate Hypocalcaemia / hypoparathyroidism
With which CHD is Turner’s syndrome associated?
Aortic coarctation
Compare the timing of onset of transposition of the great arteries and TOF?
Transpos always presents as cyanosis in the newborn period. TOF presents 6-12 months of life as cyanosis.
What is the most common cause of ACQUIRED heart disease in paediatrics?
Kawasaki disease
What are the diagnostic features of Kawasaki disease?
Fever persisting 5 days or more (usually high, >39 degrees)
AND
4 of the following 5 features
Important note: you can also diagnose Kawasakis with only 3 of the 5 features if you get a positive echo.
- bilateral nonpurulent conjunctivitis
* ie. redness without exudate
- red fissured lips, strawberry tongue, erythema of oropharynx (without tonsillitis or evidence of URTI)
- changes of the peripheral extremities
- acute phase: erythema, edema of hands and feet, groin peeling. May manifest as refusal to weight bear.
- subacute phase: peeling from tips of fingers and toes
- polymorphous rash
- usually begins in the nappy area (where there may be desquamation early in the disease) and spreads to involve the trunk, extremities and face.
- Rash may be maculopapular, annular or scarlatiniform.
- cervical lymphadenopathy > 1.5 cm in diameter
What is the treatment of Kawasaki disease
- Intravenous immunoglobulin (2 g/kg over 10 hours; preferably within the first 10 days of the illness.)
- Aspirin 3 - 5 mg/kg once a day for at least 6 to 8 weeks
What should be organised before a patient treated for Kawasaki disease is discharged?
Follow-up echocardiogram in 6-8 weeks
Kawasaki disease is primarily a clincial diagnosis, but what Ix would you perform (and what might you expect to see)?
Bedside tests ECG - check for ischaemia / infarction Urine dipstick - negative Laboratory Tests FBE - neutrophilia, anaemia, thrombocytosis ESR/CRP - markedly raised LFTs - ALT raised Imaging Echocardiogram
What are the clinical features of a Patent ductus arteriosus?
- Patients with a small PDA are usually asymptomatic
-
Murmur
- Continuous murmur audible at the upper left sternal border or left infraclavicular area – called a machinery murmur
- May disappear during diastole and be mistaken for a systolic murmur, especially if the duct is large and there is associated pulmonary hypertension.
- Radiates along the pulmonary arteries, and often well heard over the left side of the back
- With a large duct, the large left-to-right shunt causes left heart dilation
- Can cause symptoms such as failure to thrive, dyspnea and recurrent chest infections.
- Bounding pulses
- Low diastolic BP
- Apex may be displaced and forceful, and an apical mid-diastolic murmur may be heard due to increased flow through the mitral valve
- A thrill may be palpable
What is the management of a patent ductus arteriosus in preterm infants?
IV indomethacin
IV ibuprofen can be used in infants of larger weight
What is the management of PDA in term infants?
Percutaneous catheter closure
What is Eisenmenger syndrome?
Intracardiac communication with severe pulmonary vascular disease which is inoperable
What is the most common congenital heart defect?
Ventricular septal defect
What are the clinic presentation of VSDs?
- Small VSDs with little shunt are often asymptomatic but have a loud murmur
- Loud, harsh, high pitched pansystolic murmur usually heard best at the lower left sternal border
- There may be a thrill
- Large VSDs - pulmonary overcirculation and heart failure
- Increase flow across the mitral valve causing a mid-diastolic murmur
- Parasternal heave
- Difficulty feeding due to tachypnea
- Hepatomegaly
- Splitting of S2 and intensity of P2 – depending on the pulmonary artery pressure
Eisenmenger syndrome
- At rest patients may be asymptomatic, but experience exertional dyspnea, cyanosis, chest pain, syncope and hemoptysis with exercise
What are the four structural defects of Tertalogy of Fallot?
Ventricular septal defect
Pulmonary stenosis
Overriding aorta
Right ventricular hypertrophy
At what age would you expect to see cyanosis in children with tertaology of fallot?
6 to 12 months
How do you treat a hypercynanotic spell or tet spell?
Treatment of hypercyanotic spells
Basics
ABC, oxygen, sedation and pain relief (morphine)
Place and person
Hospital, ICU
Investigate and confirm diagnosis
Text
Non-invasive management
Keep the child calm – stress will exacerbate
Definitive management
IV propranolol
- Works as a peripheral vasoconstrictor and by relieving the subpulmonary muscular obstruction that is the cause of reduced pulmonary blood flow
IV volume administration
Bicarbonate to correct acidosis
Muslce paralysis and artificial venticlation in order to reduce metabolic oxygen demand
At what age does transposition of the great arteries usually become apparent?
- Presentation is usually on day 2 of life when ductal closure leads to a marked reduction in mixing of the desaturated and saturated blood.
Physical signs
- Cyanosis is always present
- Quiet tachypnea
- The second heart sound is often loud and single
- Usually no murmur, but may be a systolic murmur from increased flow or stenosis within the left ventricular outflow tract
- Metabolic acidosis may develop because of tissue hypoxia.
What are the signs of heart failure in a child?
Recurrent chest infections
FTT
Difficulty feeding
Hepatomegaly
Tachycardia
Respiratory distress
Profuse sweating when feeding
What is Eisenmenger’s Syndrome?
Eisenmenger syndrome refers to any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, reversal of flow, and cyanosis. The previous left-to-right shunt is converted into a right-to-left shunt secondary to elevated pulmonary artery pressures and associated pulmonary vascular disease.
What are the common and less common presentations of HSP?
Common - purpuric rash over legs and buttocks - migrating arthlagia and swelling - abdominal pain Less common - HSP nephritis (HT, proteinuria, haematuria) - intussuception - malaena and haematemesis - scrotal swelling
Describe the management of HSP
Basics - analgaesia for joint pain (paracetamol not NSAIDs) - analgaesia for abdo pain (steroids have evidence) Place & Person - Referral to outpatient paeditrician for ongoing observation Definitive management - Education & supportive care Prevention - continue to review for 6 months (including BP and urine dipstick) - steroids are NOT indicated for nephritis prophylaxis
What are the DDx for brusing in children?
‘SHIELD’ Sepsis (meningoccoal) HSP / HUS / Haemophilia ITP Events (Trauma or non-accidental injury) Leukaemia DIC (usually in the setting of severe illness)
How do you diagnose ITP?
An isolated thrombocytpoaenia (platelet count of
What is the management of ITP?
Basics - stop any active bleeding Place and Person - refer to paediatric haematology Investigations and confirm diagnosis - FBE and blood film to confirm isolated thrombocytopaenia - BMAT if unsure / need to rule out leuakaemia Conservative Management - avoid contact sports / high-risk activities - monitor menstural bleeding if post-pubertal female - avoid NSAIDs and 5-ASA - ongoing follow up and FBE Definitive Management’ - steroids (low or high dose) - IVIg
What is the most dangerous complication of ITP?
Intra-cranial haemorrhage Although the risk if
What are the causes of Fe deficiency anaemia in a child?
Poor stores
- Maternal iron defficiency
- Prematurity / low birth weight
Reduced intake
- Haven’t switched to solids at 6 months
- Vegeterian (adolescents)
Reduced Absorption
- Coeliac disease
Increased Loss
- Meckel’s diverticulum
- Cows milk in the first 12 months (causes micro GI bleeds)
- Menstural loss (adolescents)
What are the “next step” investigations for anaemia?
microcytic –> ferritin + Hb electrophoresis
normocytic –> reticulocyte count
macrocytic –> vit B12 / folate
What are the causes of anaemia in a child?
Microcytic
- Fe defficicency
- Thalasseaemia
Normocytic
- With increased retics
- Haemolysis
- Blood loss
- With decreased retics
- transient erythroblastaemia of childhood (caused by parvovirus B19)
- leukaemia
Macrocytic
- B12 / folate defficiency - rare
What questions should you ask in history when presented with a child with anaemia?
Microcytic
- Fe defficicency
- “Diet, on solids, bleeding from anywhere, drinking cows milk before 12 months, abdmonial pain and bloating, prematurity, low birth weight”
- Thalasseaemia
- “FHx of thalassaemia”
Normocytic
- With increased retics
- Haemolysis
- Jaundiced at birth?
- Blood group? Child and maternal?
- Blood loss
- Bleeding from anywhere?
- Haemolysis
With decreased retics
- transient erythroblastaemia of childhood (caused by parvovirus B19)
- unwell with viral ilness?
- Slapped cheeks?
- leukaemia
- Brusing?
- Severe unusally persistent recurring infections?
Macrocytic
- B12 / folate defficiency - rare
What initial investigations should you order for a child with suspected anaemia?
FBE
Ferritin
Blood Film
Reticulocyte count
What is the management of iron defficiency anaemia in the paediatric population?
- Treat underlying cause
- Diet
- Foods rich in iron
- Avoid cows milk until after 6 months
- Encourage orange juice and vitamin C
- Avoid coffee and tea
- Supplementation
- Oral (tablet or drops) or infusion
- Oral will make stools turn very dark, and cause constipation or diarrhoea
- Beware of iron overdose! Keep in locked cupbpard
What would the coagulations studies of someone with ITP show?
The coags would be normal. This is a disorder fo platelets.
What are the different types of ITP?
Acute
- ITP
- Occurs in children 2-5 years old
Chronic
- ITP >12 months
- Occurs in children older than 7 and in adults
- Females > males
Recurrent ITP
- Rare
What is the management of ITP
Conservative - watch and wait
Low dose steroids
High dose steroids
IVIg
Splenectomy is a very last line option
What advice would you give to a parent who has a child with ITP?
- Management options
- Conservative - watch and wait
- 75% of children will recover within 4-6%
- No side effects
- Steroids
- Side effects of steroids
- Quicker recovery
- IVIg
- Quicker recovery
- Would have to stay in hospital
- Conservative - watch and wait
- Risk of IVH
- Risk is
- Precaitions
- Avoid contact sports
- Take to hospital if suffers trauma, especially to the head, or if symptoms of drowisness, dysarthria, dysphagia
- AVOID ASPRIN AND NSAIDs
30% of patients with haemophilia will have “inhibitors”.
Explain what this means and how the lab tells?
A raised APTT may suggest
- factor defficiency [what you typically think of in haemophilia]
OR
- factor inhibitor [an antibody made against a factor, such as lupus anticoagulant or antibodies formed by haemophilia patients receiving recombinant factors]
How can the lab tell the difference? Mixing studies
What is the treatment of haemophilia?
Haemophilia A
Mild - Moderate
- DDAVP after Challenge Test
- Tranexamic acid
Severe
- Recombinant factor VIII infusions
Haemophilia B
Mild - Moderate
- Tranexamic acid
Severe
- Recombinant factor IX infusions
In what conditions can DDAVP be used? What needs to be done before it’s use?
VWF Type 1 and Factor VIII defficiency (Haemophilia A)
A challenege test (give DDAVP and monitor factor VIII / VWF levels. Also watch for hyponatraemia / BP)
What is the most common malignany of childhood?
And of this, what is the most common type?
Leukaemia
ALL is the most common (80%)
AML is the next common (20%)
What are the symptoms of Leukaemia?
With which symptoms do acute leukaemis tend to present with, and which do chronic leukaemias tend to present with?
Constitutional symptoms
(B symptoms)
- Fever
- Nigh sweats
- LOW
Symptoms of bone marrow infiltration - ACUTE LEUK
- symptoms of anaemia
- severe, persistent, unusual or recurrent infections
- bruising
Symptoms of other ogran infiltration - CHRONI LEUK
- lymphadenopathy
- splenomegaly
- hepatomegaly
What are the causes of bruising in a child?
Sepsis (meningococcal)
HSP / HUS / Haemophilia
ITP
Events (non accidental injury or trauma)
Leukaemia
DIC (usually in the context of severe illness)
What are the typical features of HSP?
HSP typically presents with the triad of:
- Purpuric rash (non-blanching rash usually over lower limbs and buttocks, may be over posterior aspect of elbows)
- Joint pain / swelling (migratory in nature)
- Abdominal pain
May also consist of
- Renal disease: A nephritic syndrome - haematuria, proteinuria, isolated hypertension, renal insufficiency and renal failure (
- Subcutaenous oedema of the scrotum, hands, feet and sacrum
- Abdominal - intussusception, malaena, haematemasis, spontaneous bowel perforation or pancreatitis
What basic Ix should you perform for HSP?
Bedside Test
- Urine dipstick
- BP
Labratory Tests
- UEC
- Urine MC&S
What is the management of HSP?
Basics
- Paracetamol for pain relief
Place & Person
- Admit for observations and investigations
- Can usually be managed as an out-patient
Ix and confirm diagnosis
- BP
- urine dipstick
- urine MC&S
- UEC
Defitive management
- Supportive care and frequent monitoring (including BP and urine dipstick)
- HSP nephritis (IgA nephropathy) can occur at the time of HSP, or 6 weeks – 6 months later. Continue to screen for this time.
Prognosis
- The use of prednisolone has not been shown to make clinically important improvements in the rate of long-term renal complications – this was recently removed from the RCH guidelines!
What type of renal syndrome can occur in HSP?
Nephritic syndrome
What are the common childhood malignancies?
When does neuroblastoma tend to present in children?
When does a retinoblastoma tend to present in children?
What is the most common type of SOLID tumor in paeds?
brain tumours!
What are the two types of neurfibromatosis and what are they associated with?
- Neurofibromatosis type I, in which the nerve tissue grows tumors (neurofibromas) that may be benign and may cause serious damage by compressing nerves and other tissues.
- Neurofibromatosis type II, in which bilateral acoustic neuromas (tumors of the vestibulocochlear nerve or cranial nerve 8 (CN VIII) also known as schwannoma) develop, often leading to hearing loss.
What are the top two causes of abdominal mass in a child (for Monash exams)?
Neuroblastoma
Wilm’s Tumour (Nephroblastoma)
What is a neuroblastoma?
A cancer which arises from the neural crest cells that precede the sympathetic ANS & can occur in adrenal medulla (most commonly) or abdominal, thoracic and pelvic ganglia.
in what age group does a neuroblastoma occur?
How does it present?
The most common cance of infancy
Arises in children
Fatigue, loss of apetite, loss of weight, night sweats
mass in the abdominal cavity
sometimes causing constipation
hypertension (from catecholamine secretion or comression of renal artery)
tacchycardia
May have interesting paraneoplastic effects:
- Opsomyoclonus (dancing eyes, dancing feet syndrome)
- Excessive catecholamines: flushing, tachycardia, HTN
- VIP secretion – severe refractory diarrhea with FTT and low K+
Does neurofibromatosis cause an increased risk of neuroblastoma?
NO
The two are unrelated.
Neurofibromatosis is a SYNDROME characterised by skin lesions, and patients have an increased risk of BRAIN TUMOURS.
Neuroblastoma is a cancer arising from the sympathetic peripheral nervous system, and often presents as a mass in the abdominal cavity
Is a neuroblastoma symptomatic at diagnosis?
yes, it often is.
Moreover, at diagnosis 75% of patients with neuroblastoma have metastases
What is the other name for a Wilm’s tumour?
Nephroblastoma
Is a Wilm’s tumor normally symptomatic?
No
What are the symptoms of a Wilm’s tumour?
- Often asymptomatic mass
- May rupture, bleed and cause pain (20%)
- Haematuria and HTN occur in some patients. Can cause an aquired vWD.
What are the features of Tetralogy of Fallot? What are the features of Pentology of Fallot?
- pulmonary stenosis
- RVH
- VSD
- over-arching aorta
(5. ASD)
When and how does TOF tend to present?
When the child is >3 months of age
Presents as failure to thrive, reduced exercise tolerance, clubbing of fingers and tet spells.
They are not cyanosed at birth - may be cyanosed after 6-12 weeks
What is a Tet spell?
The classic story is severe, painful cyanosis on exertion/stress (feeding or crying).
Older children will classically squat in order to increase systemic resistance and reduce R–>L shunting
What is the management of Tet spells?
Basics
Comfort the child in a position with their hips and knees flexed to increase systemic resistance and thereby R–>L shunt.
Oxygen
IV fluids
B blockers
IM morphine
Place and Person
Refer to paediatric cardiac surgery
Ix and confirm diagnosis
With echocardiogram
Definitive management
Surgical
Long Term
Ongoing paediatric review
What chromosomal abnormality is TOF related to?
What else is related to this abnormality?
Deletion of the long arm of choromosome 22
What else is related? Think CATCH 22
Cardiac (TOD, TGA)
Abnormal facies
Thymic hypolasia (T cell deficiency)
Cleft palate
Hypocalcaemia/hypoparathyroidism
What is the most common cyanotic congenital heart disease?
TOF
What are the murmurs / added heart sounds of a large and small VSD?
small VSD: loud pansystolic murmur
large VSD: softer pansystolic murmur + loud P2 (due to pulmonary hypertension)
When does TOF normally present?
6-12 weeks of life (Tom)
3-6 months of life (BMJ)
Lis the age-specific causes of a limp in a child.
List the general causes.
0-4 years: DDH & Toddler’s #
4-10 years: Perthes
10 + years: SUFE, stress fracture, overuse injury
General (non-age specific causes)
MINIVAN
Malignancy - leukaemia, solid tumour infiltration and osteosarcoma
Infection - transient synovitis, septic arthritis, osteomyelitis
Non-accidental injury / other trauma
Ingionoscrotal (testicular torsion)
Vasculitis (HSP) and other rheumatological conditions (JIA) or rheumatic fever
Appendicitis with psoas involvement / other abdominal pathology
Neuromuscular disease (CP and DMD)
How does transient synovitis of the hip usually present, and how long does it take to improve naturally?
Often a viral ilness is preceding it.
It should improve in two days and resolve in 3 weeks.
what pain relief is recommended for children?
simple analgaesia
- paracetamol: 15mg / kg four hourle (never exceed 1g / dose)
- NSAIDs - care in asthma
Do NOT give asprin (Reye’s syndrome; asprin + viral ilness)
DEscribe the movements involved in Barlow’s and Ortolani’s Test
Barlow:
Flexion + adduction/IR + compression along the line of the femur
Ortolani:
Flexion + abduction/ER
When should the Ortolani’s and Barlow’s Test be performed?
at birth
within the first 48 hours
6 weeks
3 months
6 months
1 year
what are the risk factors for DDH?
“Packaging Problems”
- Macrosomia
- Oligohydramnios
- Breach position
- Multiple gestation?
Also..
- Female
- First born
- FHx
What are the appropriate investigations for DDH?
After 6/52 - can use ultrasound
After 6/12 - can use xray
If a neonate has risk factors for DDH, but has a negative Ortolani and Barlow’s test immediately after birth and after 48 hours, what investigations should be performed?
They should still receive a 6/52 ultrasound
What is Perthes?
Who is most likely to get it?
AVN of the femoral head
Boys
4-8 years old
Who gets SUFE?
How is it diagnosed?
Overweight children
Late childhood / adolescence
Plain xray
“Frog leg” position
If the line of the femoral neck does not intersect with the head –> Dx SUFE
What is the Rx of DDH / Perthes?
Young - Pavlik Harness
Older - Broomstick cast
Both are to increased apposition between the femroal head and the acetabulum
What is Still’s Disease?
The systemic sub-type of JIA
What are the main subtypes of JIA?
- Oligoarthritis - 4 or fewer joints affected in the first 6 months of the disease
- Polyarthritis - more than four joints affected in the first 6 months. This can be further classified into Rh + or Rh -
- Systemic
What investigations should you perform if suspecting JIA?
Bedside Tests
- Temperature
Lab Tests
- FBE (May be a microcytic anaemia of CD)
- CRR, ESR
- ANA (carries risk of anterior uveitis)
- Rh Factor
- HLAB27 genotyping
Imaging
- Plan xray may reveal eroded joints, but not diagnosic
What are the diagnostic crietria of kawaski disease?
A temperature of >39 for >5 days + 4/5 of the following criteria
- Lymphadenopathy >1.5cm
- Red mouth and lips “Strawberry tongue”
- Desquamation of the extermities
- Bi-lateral non-purulent conjunctivitis
- Rash
But if have abnormal echocardiogram, can have
How to remember?
FLAMER
Fever
Lymphadenopathy
Atypical - Arteries
Mouth & Lips
Extremities & Eyes
Rash
CRASH and Burn
Conjunctivities
Rash
Adenopathy
Strawberry tongue
Hand and feet
Burn = Fever
What is the management of Kawasaki Disease?
Basics
- Analagaesia for pain relief
- Encourage fluids / NGT if dehydrated or poor feeding
Place and Person
- Contact paediatrics rheumatology
- Admit
Investigate and Confirm Diagnosis
- Bedside tests
- ECG
- Urinalysis
- Labratory Tests
- ASOT/Anti DNase B (to exclude strep throat, scarlett fever)
- FBE
- CRP/ESR
- LFT
- Imaging
- Echocardiogram
Definitive Management
- IV Ig (10 days)
- Asprin (6-8 weeks)
Ongoing Management / Follow-Up
- Repeat echo at 6/52
what are the major crieria for rheumatic fever?
what is the required criteria?
how do you diagnose ARF?
Required criteria - evidence of antecedent strep infection (ASO or anti DNA-se B, strep grown from NPA, previous scarlett fever)
Major criteria - JONES
Joint
O - Carditis
Nodules
Erythema marginatum
Sydenham’s chorea
Diagnose with required criteria + 2 major criteria
OR
required criteria + 1 major + 2 minor
OR sydenham’s chorea alone
What is the management of ARF?
Basics
- Analgaesia for arthlagia
- Fluids / NGT if dehydrated
Place and Person
- Contact paediatrics
- May need to admit if CHF
Investogate & Confirm Diagnosis
- Bedside Tests
- ECG
- Labratory Tests
- FBE
- Blood cultures
- NP swab
- ESR / CRP
- ASOT / Anti-DNAse B
- Imaging
- Echo
- Xray of painful joints
Definitive Management
- Benzathine Penicillin IM
- 10 day course of phenoxymethylpenicillin V
Follow Up
How do you conceptualise paediatric heart defects?
- Cyanotic Heart Defects
- R–>L shunt
- Acyanotic Heart Defects
- L–>R shunt
- Obstructive heart defects
What are the obstructive heart lesions?
hypoplastic L heart syndrome
aortic stenosis
coarctation of the aorta
interrupted aortic arch
Which group of congenital heart defects are always duct dependent?
Which group of congeintal heart defects are sometimes duct dependent?
Which group of congenital heart defects are never duct dependent?
always - obstructive
sometimes - cyanotic / R –> L shunt
never - ASD, VSD, PDA
how do obstructive cardiac defects normally present?
“shocked neonate” – dusky colour, weak or absent pulses, low BP, reduced UO, metabolic acidosis
Often present on day two of life when ductus arteriosus closes
What is the general management of all obstructive heart defects?
DRABC
PGE1
Urgent surgical referral
Which congenital heart defect is associated with Turner’s syndrome?
Aortic coarctation
What are some causes of neonatal cyanosis?
“CRI”
(Think: “cry”)
Cardiac
- R –> L shunts
Pulmonary
- RDS
- PPHN
- Mecosium aspiration
Infection
- GBS
- E coli
- Listeria
When should Apgars me performed?
At 1 and 5 minutes after both (if low at 5 minutes, might be done again at 10)
What are the components of Apgar?
Appearance (blue, partly blue, pink)
Pulse (absent, under 100, over 100)
Grimace (no response to stimulation, some response to stimulation, cry to stimulation)
Activity (Flat, Some flexion, some flexion which resists extension)
Respiratory effort (None, some, good cry)
What is the murmur which can be heard in TOF?
ES murmur in the pulmonary area
Loud, single S2
what might severe TOF look like on CXR
boot shaped heart
what might TGA look like on CXR?
heart looks like ‘egg on its side’
When does TGA usually present?
When does TOF usually present?
TGA - in neonatal period. Often after day 2-3 when ductus has closed.
TOF - in infancy, as cyanotic / tet spells when crying or exerting oneself + failure to thrive + recurrent respiratory infections
what is heard on ausculatation with an ASD?
wide fixed splitting of S2
What is heard on auscultation of a PDA?
What is felt on palpation of the pulses?
Machinery murmur with bounding pulses
Such murmurs may be present throughout the cardiac cycle (‘machinery murmur’), but may disappear during diastole and be mistaken for a systolic murmur, especially if the duct is large and there is associated pulmonary hypertension.
What is the general definitive management in INFANTS with heart failure?
Medical
Diuretics - frusemide or spironolactone
ACEi
Oxygen
Consider inotropic support if necessary
High caloric diet
Urgent surgical referral
When does ductus arteriosus close in a term child?
In a preterm child?
Usually after 2 days
May take one month in a term child
May take 2 years in a preterm child
what is used to close a symptomatic PDA?
INDOMETHACIN OR IBUPROFEN
CAN BE SLOSED SURGICALLY IF REQUIRED
What are the GI causes of vomitting in a child?
FAMINE HIP GAIT
Food allergy
Atresia (oesophageal or duodenal)
Meconium ileus
Intussception
Necrotising enterocolitis
Eosinophillic oesophagitis
Hirschbrungs
Intestinal malrotation
Pyloric stenosis
GOR / GORD
Appendicitis & strangulated inguinal hernia
Imperforate anus
Trahceo-oesophageal fistula
What are the causes of vomiting in a child?
GI
- FAMINE HIP GAIT
Infectious
- Meningitis
- Gastroenteritis
- Pertusis
Neuroligcal
- Increased ICP
Endocrinological
- DKA
- Errors of inbron metabolism
Other
- over-feeding in infants
- bulaemia in adolescents
- pregnancy in adolescents
At what age does intussusception present?
How common is it?
How does it present?
The most common cause of bowel obstruction between 6 months and 2 years of age.
Presnts as:
- Intermittent episodes of crying + knee flexion (intermittent episodes of pain)
- Turn white during this period (as opposed to red)
- Bilious vomiting
- Recurrent jelly stools
- Sausage shaped mass palpable in RUQ
What is seen on abdominal xray of intussusception?
Target sign
Cresent sign
What is the management of intussusception?
Basics
- DRABC if shocked
- Analgaesia
- NGT / IV fluids if dehydrated
Place and Person
- Admit and contact paeds surgical team
Ix and confirm diagnosis
- FBE & group and hold prior to surgery
- UEC if dehrydrated
- AXR
- US
Management
- IV antis prior to enema? discuss with surgical team
- Air enema
- Surgical reduction if this is unsuccessful (25% are unsuccessful)
Follow Up
- Follow up with paeds surg post op
What are two mimickers of appendicitis?
Meckel’s diverticulum
Mesenteric lymphadenopathy
Ovarian pathology in an older female
Constupation
What is bilious vomiting in the first week of life, until proven otherwise?
Intestinal malrotation
If a neonate has bilious vomiting in the first week of life, and their mother had polyhydramnios, what is the cause?
duodenal atresia
what is the gold standard investigation of malrotation, and what is the sign seen?
Barium meal
Corkscrew sign
What is the management of intestinal malrotation?
Basics
- Analgaesia
- NBM
- NGT
- IV fluids to replace deficit and for maintenance
Place and Person
- Admit
- Contact paeds surg / NETS if in rural setting
Ix and Confirm Diagnosis
- FBE
- Group and hold
- AXR
- Barium meal - look for corkscrew sign
Definitive management
- Ladd procedure
Follow-Up
- Organise follow up with paeds gastro / general paediatrician - ensure adequate growth and weight gain
Explain the pathophysiology of Malrotation
Embryologically, the bowel should rotate 270 degrees (in three stages, each 90 degrees).
The last 90 degrees fails to take place.
This means the colon is in the wrong position and the mesentery has a narrow base, the small bowel can therefore twist on itself –> ischaemia –> necrosis
Is it really the malrotation which is dangerous?
No, it is malrotation + VOLVULOUS
How do meconium ileus and hirschprungs present similarly?
How do they present differently?
Both present with progressive abdominal distension and failure to pass meconium. Vomiting is a later sign and is bilious / faeculent.
The difference is:
Meconium ileus has an empty rectum on PR examintaion
Hirschprungs has an explosive rectum on PR examination
When should meconium be passed?
99% passed in 24 hours
Abnormal if not passed after 3 days
How do you investigate for Hirschprungs?
Suction rectal biopsy
What is the carrier rate of the CF gene in the caucasian population?
what is the incidence of CF?
1 in 25
1 in 2500
polyhydramnios + bilious vomits = ?
polyhydraminios + respiratory disress = ?
polyhydramnios + macrosomic baby = ?
duodenal atresia
TOF (tracheooesophageal fistula)
GDM
What is the feature of duodenal atresia on AXR?
double bubble sign
When monash sates that liqor is “apparnetly” meconium stained?
this could be bilious vomiting
What is the management of duodenal atresia?
Basics
- NBM
- ‘Drip and Suck’
- IV fluids
- NGT
Place and Person
- Paediatric Surg / NETS
Ix and Confirm Diagnosis
- AXR - look for double bubble sign
- Barium meal
Defiitive management
- Surgical - anastomsis of the duodenum
Follow-up
- Small feeds regularly
- Follow up with paediatrician / GP to ensure weight gain
- Consider important associations eg. Trisomy 21, cardiac defects
What is the electrolye and pH disurbance seen in pyloric stenosis?
hypocholaraemic, hyponatraemic, hypokalaemic metabolic alkalsosis
- hypocholaramiec and hyponatraemic from vomiting
- acidotic from vomiting
- hypokalaemic because the nephron swaps H+ for K+ to compensate for alkalosis
What features of PS would you ascertain on history?
Projectile, non-bilious vomiting
Weight loss
Feeding immediately after meals
Male
First born
Caucasian
FHx PS
What might you see on examination of an infant with pyloric stenosis?
The three Ps
palpable olive in the RUQ
visible peristalsis
projectile vomiting
+
signs of dehydration
What is the management of pyloric stenosis?
Basics
- NBM
- NGT
- IV fluids to replace deficit and for maintenance prior to surgery
Place and Person
- Paeds gastro / NETS
Ix and Confirm Diagnosis
- Measure weight
- Blood Group and Cross Match prior to surgery
- UEC
- ABG
- Ultrasound
Definitive Management
- Correct electrolyte / acid-base derrangement
- Ramstedt operation: pyloromyotomy
Follow Up
- Organise follow up to ensure weight gain and meting normal growth parameters
What are the signs of dehydration?
- General appearance
- Flat / floppy OR miserable OR well
- Not cyring tears
- Thirsty
- Vitals
- Loss of weight
- Tacchypnoeic (early sign)
- Tacchcardic (later sign)
- Hypotensive (very late sign)
- Hands
- Cold peripheries
- Mottled skin
- Head / Face
- sunken fontenelles
- suken eyes
- dry mucous membranes
- Chest
- Central capillary refill
- Reduced skin turgor
- Other
- crying tears?
- wet nappies?
What are the components of fluid one needs to replace (in terms of IV rehydration) according to the RCH?
- Bolus fluid (if if hypovolaemic shock)
- Replace deficit (according to degree of dehydration)
- Maintenance fluid (according to body weight)
(+ replace ongoing losses if vomiting whlist in hospital)
What fluid should be given first if a cihld is in hypovolaemic shock? How much and at what rate?
How do you then calculate further fluid requirements?
Bolus of 10-20mL per kilogram of 0.9% NS
keep on giving until signs of shock improve
As quick as possible
Don’t include this fluid in further calculations for fluid requirements.
How do you decide how much fluid deficit there is?
What fluid do you give? How much? How quickly?
Assess clinical picture of dehydration
Mild dehydration
Moderate 4-6%
Severe >7%
Should use 0.9% NS
The amount of fluid is this % of the childs body weight (eg. a 10kg child who is 5% dehydrated should receive 500mL)
The rate of rehydration should be adjusted with ongoing assessment of the child.
what does mild dehyradtion mean according to the RCH guidelines (both clinically and in terms of deficit)?
moderate?
severe?
Mild - (0.4%)
- no clinic signs, maybe thirsy
Moderature - (4-6%)
- essentially signs other than shock
- Delayed CRT > 2 secs
- Increased respiratory rate
- Mild decreased tissue turgor
Severe (>7%)
- shocked
- Very delayed CRT > 3 secs, mottled skin
- Other signs of shock (tachycardia, irritable or reduced conscious level, hypotension)
- Deep, acidotic breathing
- Decreased tissue turgor
what methods of rehydration should you try to employ?
- oral (eg. gastrolyte icypole)
- NGT
- IV
what type of fluid should you use for a bolus?
what type of fluid should you use for replacement of deficit?
what type of fluid should you use for maintenance?
bolus = 0.9% NS
replacement of deficit = 0.9% NS
maintenance = 0.9% NS + 5% glucose / 0.45% NS + 5% glucose
(Premade solutions with potassium chloride 20mmol/L are available and should be used unless the serum potassium is elevated, there is anuria or renal failure.)
how do you calculate maintenance fluid?
how much fluid would a 30kg child receive as maintenance?
What would this fluid be?
4,2,1 rule
4mL/kg/hour for the first 10kg
2mL/kg/hour for the next 10kg
1ml/kg/hour for every kg after that
A 30kg child would receive 70mL/hour
NS+5% glucose or 1/2 NS + 5% glucose
what is the difference between GOR and GORD?
GOR - physiological vomiting due to reduced tone of oesophageal sphincter. Baby is meeting all centiles for height and weight.
GORD - GOR + complications (FTT, oesophagitis, respiratory symptoms)
What is the management of GOR / GORD?
Basics
- Weight child, and plot
- Measure height and HC
Place and Person
Investigate and confirm Dx
- Clinical diagnosis - but screen in history for any complications (haematemesis, respiratory issues, FTT) to see if GORD vs GOR
Management
- Non-Pharmacoloigical
- Can add thickener to formula or to EBM
- Prop upright / at angle after feeding
- Pharmacological (if severe or if GORD)
- H2 receptor antagonists
- PPI
Follow Up
- Continue to check weight and other measurements
When does PS present?
When does intussusception typically present?
PS: 2-6 weeks
Intussusception: 6 months - 2 years
What are the DDx for abdominal pain?
MIDGUT MISHAP
Migraines - abdominal
Intussception
DKA
Gastroenteritis
UTI
Testiicular Torsion
Malignancy (Wilm’s, Leukaemia, Neuroblastoma)
Inguinal hernia - stranulated
Stuck poo (constipation)
HSP
Appendix + mimickers (mesenteric adenopathy / Meckel’s diverticulum)
Pregnancy / ectopics / gynae
what is the Dx of a child who has had gastroenteritis, and no longer had any abdominal pain, vomiting or abdominal distension but has ongoing diarrhoea for two weeks?
(common Monash EMQ)
post gastro-enteritis lactase deficiency
A kid with wasted buttocks, abdominal distension and FTT?
(Common Monash EMQ)
Coeliac Disease
What is the clinical picture of coeliac disease?
Chronic diarrhoea / steatorrhea
FTT
Abdmonial pain / bloating
Wasted buttocks
*consider iron deficiency as a complication
What investigations are required to diagnose coeliac disease?
Bedside Tests
- random BGL
Labratory Tests
- Coeliac serology (anti-TTG, anti-gliadin & IGA)
- FBE (to see if anaemic)
- TFTs (because associated with CD!)
- HBA1c (because associated with CD!)
Invasive
- SOMETIMES an intestinal biopsy is performed
What is the management of coeliac disease?
Basics
- Ensure adequate hydration
Investigations and Confirm Diagnosis
- Coeliac serology
- FBE
- TFTs
- HBA1c
- BGL
Definitive Management
- Gluten Free Diet (avoid Barkey, Rye, Oats and Wheat)
Ongoing Management
- Screen for and treat throid dysfunction
- Screen for and treat T1DM
- Iron supplementation / increase iron in diet / monitor iron levels
- Vit D / Calcium supplementation / increase in diet / monitor levels
- Monitor folate levels / increased folate in diet / folate supplementation
What are the possible complications of coeliac disease?
FTT / short stature / delayed puberty
Increased risk of malignancy (reduced if controlled)
Iron deficieny anaemia
Ostoepenia
Dental enamel hypoplasia
what is the difference between an inguinal hernia and a hydrocele, anatomically?
both involve a patent processus vaginalis
in an inguinal hernia, the processus vaginalis is big enough to allow a part of the small bowel thorugh
in a hydrocele, it is patent but only big enough to let water thorugh
how does an inguinal hernia normally present?
how should you treat it?
swelling in the groin
if reducible - likely to be intermittent, painless swelling
if irreducible / strangulated - painful abdomen
Basics
- NBM
- IV maintenance fluids
- analgaesia
Place and Person
- Urgent surgical referral (state whether it is reducble or irreducible)
Investigate
- may perform U/S
Definitive management
- Surgery
Differientiate between undescended testes and retractile testes.
What are the clinical classifications of undescended testes in a newborn?
Undescended testes - the scortal sac is empty. The testes can be palpable or non-palpable.
Retractile testes - normal. Testes are still in the scrotal sac, but are lifted up into the abdominal cavity, for example, when the boy is cold.
What is the management of undescended testes diagnosed in a newborn?
Palpable - wait 3 months. Then if not descended –> surgical referral. Surgery at 6-9 months.
Non-palpable - surgical referral now
What are the complications of CF?
MR PANCREAS
Meconium Ileus / Distal Intestinal Obstruction
Recurrent infections
Pancreatic failure (exocrine and endocrine)
Allergic Bronchopulmonary Aspergilliosis
Nasal polyps and sinusutus
Cirrhosis of the liver
Restricted growth
Emotions
Airway leaks (males)
Sterility in males
What is the initial investigate performed in newborn screening for CF?
Levels of immunoreactive tripsin are tested for on the Gutherie Card (with the blood collected via heel prick test).
If IRT is high when testing for CF, what tests are performed next?
CFTR gene mutations screened for on Gutherie Card
(most common is delta F507)
+/-
Sweat Test
What is the incidence of CF?
What inheritence pattern is it?
What is the most common genetic mutation causing CF?
1:2500
autosomal recessive
Delta F507 (Long arm of Chromosome 7)
What is tested for on newborn screening?
Congenital hypothyroidism
CF
Metabolic disorders eg. PKU
What is the DDx of a wheeze?
Concerning Airway Wall
- Constrction*
- Asthma
- Compression*
- Mediastinal mass
- Congenial heart disease eg. causing L-R shunt and causing engorgment of the pulmonary vasculature
Structure
- Bronchomalacia
- Tracheomalacia
- Bronchopulmonary Dysplasia
Concerning Airway Lumen
Pus / Infection
- Bronchiolitis
- Viral Induced Wheeze / Asthma
- Pneumonia
- Petussis
- Croup (even though an URTI)
- Gunk*
- CF
- Other*
- FB
What are the causes of stridor?
With Fever
- Abcess (peritonsillar - qunsiy, or retrophrayngeal)
- Big tonsils / bacterial tonsillitis
- Croup
- Diptheria
- Epiglottitis
Without Fever
- Floppy airways (tracheomalacia, laryngomalacia)
- Gagging on a foreign body
- Hypersensitivity / haemangioma
How do you classify asthma in children?
Infrequent Intermittent
Frequent Intermittent
Persistent
- Mild
- Moderate
- Severe
How do you classify asthma as infrequent intermittent?
Attacks are >6 weeks apart
No interval symptoms (morning cough / wheeze, night cough / wheeze, exercise tolerance, days at school missed)
How do you classify Frequent intermittent asthma?
Attacks are
No interval symptoms (morning cough / wheeze, night cough / wheeze, exercise tolerance, number of days missed at school)
How do you classify persitent asthma?
How do you further classify it?
Attacks
Mild = interval symptoms are less than 1 x per week
Moderate = 1 x per week
Severe = >1 x per week
What questions ascertain whether or not a person has interval symptoms?
Morning cough / wheeze?
Night cough / wheeze?
Reduced exercise tolerance? (Able to keep up with kids in sport / at school)
Missed days at school because of asthma?
What questions in the HOPC should you ask to classify a child’s asthma?
Q - how often do you have attacks?
Q - when you do have attacks, do you have to
- miss school
- go to ED
- be admitted to the ward
- be admitted to ICU
- take prednisolone (how many times have you used prednisolone in the last 12 months)
A - what triggers your asthma?
A - which medications allieviate it? Have you had to take prednisolone in the last 12 months? How often do you have to use your reliever?
What should be used in the treatment of infrequent intermittent asthma?
SABA prn
What treatment should be used for frequent intermittent asthma?
SABA prn
+preventor (ICS or chromone or LTRA or combination)
what treatment should be used for frequent presistent asthma?
SABA prn
Symptoms controller: ICS + or minus LTRA / cromone
LABA
oral corticosteroid
What would you look for on examination to ascertain the severity of a respiratory illness, such as asthma?
Primary Features
- WOB
- Neurological Status
Secondary Features
- SPO2
- HR
- Ability to talk
What are the signs of increased WOB?
- Increased RR
- Cyanosis
- Grunting
- Nasal flare
- Intercostal / Subcostal recession
- Head bobbing
What is the mnemonic to remember the management of asthma?
OASIS
Oxygen
And (Amyophilline / MGSO4 if severe, in ICU)
Salbutamol
Ipatropium Bromide
Steroids
Describe the management of a mild exacerbation of asthma
Basics
- make comfortable and reassure
- paracetamol for comfort if febrile due to viral induced
- assess hydration status: oral, NG or IV fluids if dehydrated (but avoid IV, procedure will make breathing more difficult)
Place and Person
- Contact Paeds resp team, likely to be monitored in ED
Ix and Confirm Diagnosis
- SpO2
Definitive Management
O - no oxygen unless SpO2 is
A
Salbutamol - 6 puffs if 6
I
Steroids - 1mg/kg of prednisolone for 3 days
Plan / Follow Up
Medication review
Education RE asthma delivery devices
Describe the management of a moderate exacerbation of asthma?
Basics
- Make the child comfortable
- Paracetamol for comfort if febrile (viral-induced exacerbation)
- Assess hydration status - encourage oral fluids, consider NGT or IV fluids if necessary, but try to avoid procedures as this may further upset patient
Place and Person
- Contact paediatric team
Ix and confirm Dx
- SpO2
Definitive Management
- Oxygen via NP
- A
- Salbutamol - burst therapy:
- Six puffs every 20 minutes x 3 if
- 12 puffs every 20 mins x 3 if >6yo
- Iprtropium bromide - not in moderate asthma in victoria
- Steroids: 1mg/kg for 5 days
Follow Up
- Medication review
- Ensure correct use of asthma delivery devices
What is salbutamol burst therapy?
When should you give it?
6 puffs of salbutamol every 20 minutes x 3 if
12 puffs of salbutamol every 20 minutes x 3 if >6yo
In moderate or severe exacerbations of asthma
What is the trade name for ipratropium bromide?
Atrovent
When should you give ipratropium bromide?
(ie. in what severity of acute asthma)
how much should you give?
in severe exacerbations of asthma
4 puffs every 20 mins if
8 puffs every 20 minutes if >6 years old (with salbutamol)
What is the management of a severe exacerbation of asthma?
Basics
- Comfort child (but the child is usually flat)
- Paracetamol for comfort if febrile
- Oral, NG or IV fluids if dehydrated
Place and Person
- Contact paeds resp / paeds ICU
- Contact PIPER if rurally
Investigate and confirm Dx
- SpO2
- ABG (if doesn’t further upset child)
Definitive management:
- Oxygen - via HFNP or CPAP or consider intubation
- Salbtamol Burst therapy - MDI or nebulised
- Ipretropium bromide
- 4 puffs every 20 minutes if
- 8 puffs every 20 minutes if >6yo, x 3
- Steroids - IV methylprednisolone
- MgSO4 or amiophilline in ICU
Follow Up
- Medication review
- Ensure correct understanding and usage of asthma delivery devices
Compare the rash in measels (rubeola) to the rash in roseola infantum (exanthem subitum)
Measels - the rash starts around hairline and spreads cephalocaudadly over 3 days
Roseola infantum - the rash starts on the trunk after a fever
How does the rash in rubella (German measels) present?
Begins of face and spreads cephalocaudadly
What are the different types of PCKD?
When does each present?
How common and severe is each one?
Autosomal Dominant PCKD presents later in life, is not as dangerous. Is more common.
Autosomal Recessive PCKD presents in infancy, is more dangerous. Is rare.
How do you differentiate MCKD with PCKD?
PCKD involved both kidneys
A 3-year-old boy with a large unilateral palpable mass found on examination, carried out because of his intermittent abdominal pain and recent onset of haematuria.
This is HSP
According to RH, what does a big spleen favour and what does lymphadenopathy favour?
A big spleen favours leukaemia, while
lymphadenopathy favours lymphoma
Chest X-ray – lungs have a ground glass appearance with air bronchograms
= ?
Hyaline Membrane Disease
What is SMA?
How does type 1 typically present?
Autosomal recessive degeneration of the anterior horn cells
SMA Type 1 presents at birth (if not as reduced FM beforehand). Typical signs include:
- Tongue fasciulations
- Lack of antigravity power in hip flexors / loss of tone
- Absent deep tendon reflexes
- IC recession
These babies will never sit and will die at 12 months due to respiratory failure.
Type 2 will sit but never walk.
Type 3 will walk
What is Friedrich’s Ataxia?
What is it’s clinical picture?
Autosomal recessive disorder causing degeneration of peripheral and spinal nerves.
It presents as:
- Progressive ataxia
- Optic atrophy
- Kyphoscoliosis
- Cardiomyopathy
What is ataxia telangiectasia?
What is it’s clinical presentation?
Autosomal recessive condition
A disorder of DNA repair
Increased suscetibility to infection
Cerebellar signs / ataxia
Increased risk of ALL
Broadly speaking, what is the definition of the neurocutaenous syndromes?
What are the major types?
The skin and the nervous system are derived from the same embryological tissue.
Embryological distruption causes syndromes involving abnormalities to both systems. These are called the neurocutaenous syndromes.
Types include NF Type 1 and 2 as well as Tuberose Sclerosis and Sturge-Weber Syndrome
What is NF and how does it present?
A neurocutaneous syndrome.
Neurofibromata appear along the course of a peripheral nerve, including CNs. They may cause neuro signs if they are at a point at which the nerve passes through a bony foramen.
Cafe au lait spots and axillary freckling are common
What is Tuberous sclerosis?
How does it present?
An autosomal dominant neurocutaneous syndrome.
Cutaneous features include:
- depigmented ash leaf patch
- Roughened patches of skin (Shagreen patches) usually over the lumbar spine
- Adenoma sebaceum (angiofibromatoma) in a butterfly distribution over the nose
Neurological features:
- Infantile spasms
- Epilepsy
- ID
- Develpomental delay
What is Sturge Weber Syndrome?
Port Wine stain over the distribution of the trigeminal nerve which is associated with a similar intracranial lesion.
In the most severe form this presents as eplispesy, ID and hemiplegia.
how do you differentiate between a conjugated and unconjugated hyperbilirubinaemia?
If conjugated is >15% = conjugated
If unconjugated is >85% = unconjugated
A full term infant is noted to be jaundiced at birth. His bilirubin is elevated at 205 umol/L (normal range;
Diagnosis?
Congenital CMV
What is alagille syndrome associated with?
Traingular facies
peripheral pulmonary stenosis / pulmonary valve stenosis
intra-hepatic biliary hypoplasia
eye defects
butterfly vertebrae
what is associated with a bounding peripheral pulse?
PDA
What is Dravet Syndrome?
Really a type of epilepsy
Dravet syndrome appears during the first year of life, often beginning around six months of age with frequent febrile seizures (fever-related seizures).
Can present as different types of seizures
Persist into later life, cause significant developmental delay
How migh rhabdomyosarcome present?
Head and neck are the most common sites of the tumor causes proptosis, nasal obstruction or blood stained nasal discharge
what is the treatment of Giardiasis?
oral metronidazole
A 2-week-old male infant presents with failure to thrive and recurrent vomiting.
He has a metabolic acidosis, high K, and low Na and Cl?
CAH
Congenital lack of mineralocorticoids and glucocorticoids gives rise to salt wasting and sometimes ambiguous genitalia because of increased androgens.
what do you use as ABx prophylaxis post splenectomy?
oral penicillin
What is Sandifer’s syndrome?
Although not common Sandifer syndrome is seen in some babies with GORD and is not epilepsy.
A 7 month old girl with severe gastro-oesophageal reflux is staying with her grand parents. She has not been receiving her normal reflux medication. She is now having episodes of back arching and posturing of the head.
Sandifer’s Syndrome
‘fixed split of S2’ = ?
ASD
what is the most common congenitall heart defect in Trisomy 21?
AVSD
How do you diagnose Hirschprung’s?
Suction Rectal Biopsy
What is the significance of a recent infection in the context of intussception?
Looking for a pathological lead point
Peyers patches are often a lead point
(HSP can give a lead point as well)
What is another name of an undescended testis?
Cryptorchidism
At what age do you consider surgical referral in cryptorchidism?
What is the surgical procedure called and at what age is it performed?
If the testis hasn’t descended by 3 months conisder surgical referral.
Orchidopexy is the name of the procedure, it is best done at 6-12 months of age
what are the risks of cryptorchidism?
are these risks reduced with orchidopexy?
What are the benefits of orchidopexy?
infertility and malignancy
these risks are not reduced with orchidopexy
improves the endocrine function of the testis and facilitates testicular self-examination, also reduces the risk of torsion and direct trauma.
What are the findings on blood film for G6PDD?
Heinz bodies
You are called urgently to see a 6 hour baby who is jaundiced. Upon history, you find that the ethnic origin of the baby is Anglo-Saxon and that there is some history of ‘blood problems’ in the family. You are told by the consultant that a blood film will confirm the diagnosis.
What is this and what owuld you find on blood film?
Spherocytosis is more common in white ethnic groups and the classic blood film picture is of round spherical red blood cells.
On a routine GP checkup, the doctor notes that a 3 week old baby is jaundiced. The mother complains that his urine constantly stains his clothes a dark colour and that his stools are an unusual colour and has a strong odour. A liver biopsy is needed to confirm the diagnosis.
What is this?
Biliary atresia is a potentially fatal condition if not picked up early. It presents with conjugated jaundice after day 14 of life and requires a liver biopsy before urgent surgery (where a final diagnosis is made based on intraoperative cholangiography). Choledochal cysts can usually be diagnosed on ultrasound and do not require a liver biopsy.
A 15 year old girl complains of severe throat pain and lethargy. On examination, you find petechiae on her palate and cervical lymphadenopathy.
What does this girl have?
EBV
Apparently petichae are a classical finding
An 11 year old boy suffers from disabling runny noses during springtime and the summer.
What should you give him?
What shouldn’t you give him?
Intranasal corticosteroids are first-line for allergic rhinitis.
INCS have been shown to be superior to antihistamines in controlling nasal symptoms of AR.
Nasal decongestant sprays are not recommended due to the potential long-term effect of rhinitis medicamentosa.
Other effective therapies also need to be used with care. In cases of severe nasal blockage, intranasal decongestants can be used for 2–3 days to improve access to the nasal mucosa for INCS, but overuse of these can result in rhinitis medicamentosa.
A one-year old boy is brought to ED after experiencing a seizure at home. On examination, he has a temperature of 40oC. He is admitted to hospital, where the team note that he develops a maculopapular rash on his neck as his fever subsides.
Roseola infantum
“Fever subsides –> rash”
A very common cause of fever
Strep agelcactiae = what on microscopy?
Neisseria meningidites = what on microscopy?
Gram +ve cocci
Gram -ve diplococci
What virus causes hand, foot and mouth disease?
Cocksakie A
A fifteen-year-old boy is brought to the GP, complaining of sudden onset of fever and headache. He is crying, complaining of severe pain in his muscles and joints, as well as behind his eye. He recently returned from a family holiday to Cambodia and Laos. His FBE shows a leukopenia and thrombocytopenia.
What is this?
Dengue fever – also known as ‘breakbone’ fever – usually presents with sudden onset fever, headache, retro-orbital pain, arthralgias and myalgias. Leukopenia and thrombocytopenia are common findings on FBE. It is reported to be excruciatingly painful.
Describe the classification of burns according to the RCH?
Surface:
Superficial – dry, minor blisters, erythema
Superficial dermal – moist, reddened with broken blisters
Deep dermal – moist white slough, red mottled
Full thickness – dry, charred whitish
CRT:
Superficial, superficial dermal – brisk
Deep dermal – sluggish
Full thickness – absent
Pain:
Superficial, superficial dermal – painful
Deep dermal, full thickness – painless
What is the most important component of neonatal resus?
Opposite to adult resuscitation: ventilation is more important than chest compressions, but both may need to be performed.
What is the name for the onset of female breast development?
Thelarche
What is the name for the onset of androgen-dependent body changes such as growth of axillary and pubic hair, body odor, and acne
adrenarche
What is adrenarche?
the onset of androgen-dependent body changes such as growth of axillary and pubic hair, body odor, and acne
What is thelarche?
The onset of female breast development
What is a posterior urethral valve?
How common is it?
Why is it a problem?
What is it?
An abnormal leaflet of tissue exists in the urethra, causing an obstruction to urine flow. It is a developmental anomaly, present before birth and only affects boys.
How common?
PUV is rare, occurring in 1 in 4000-6000 boys
Why is it a problem?
Urethral blockage near the bladder makes it hard for the bladder to expel urine, so the bladder has to push harder to try to empty. This increases pressure in the urinary tract. The pressure may push the urine back through the ureters to the kidney and cause the ureters, kidneys and bladder to dilate (expand).
What are the investigations, management and prognosis of posterior urethral valves?
Investigations…
- UEC
- Ultrasound (antenatally or posnatally)
- Micturating cystourethogram (MCU)
- This is the definitive test for PUV. It is performed with a catheter placed through the urethra into the bladder. Contrast material is injected through the catheter to outline the bladder. An X-ray is taken which will show the shape of the bladder, whether there is any back flow up the ureters (reflux). Xrays are taken to identify the contrast outlining the urethra and any internal obstruction (valve).
- Cystoscopy
- This is both a confirmatory and therapeutic intervention. It is a surgical procedure, performed under anaesthesia. A small telescope is placed inside the urethra to identify the obstruction. Treatment of the valves can be performed at the same time. Other tests may be needed to check the function of the kidneys, the drainage, and to monitor treatment
Management
Catheter insertion then ablation via cystoscopy
Prognosis
About one third will develop kidney failure at some stage, requiring dialysis or renal transplant.
About one third of patients will have a degree of renal impairment, managed with medication and diet.
About one third of patients will have normal kidney function, but may have ongoing issues with urinary tract drainage, infection and bladder function.
What is the rule about brain tumors in children?
What is the most common type of brain tumor in a kid?
Almost always are primary
60% are infratentorial (most are supratentorial in adults)
Most common type = (cerebellar) astrocytoma
What is the keyhole sign?
An ultrasonographic sign showing PUV
When do you measure APGARs?
1 minute
5 minutes
(Maybe again at 10 minutes and five minutely intervals after that)
How do you grade VUR?
Grade 1: reflux limited to ureter
Grade 2: reflux up to the renal pelvis
Grade 3: mild dilatation of ureter and pelvicalyceal system
Grade 4: tortuous ureter with moderate dilatation, blunting of fornices but preserved papillary impressions
Grade 5: Tortuous ureter with severe dilatation of ureter and pelvicalyceal system, loss of fornices and papillary impressions
What is the eponymous name of an innocent murmur?
What is the main DDx?
What should you do if you are a GP and you note an innocent murmur when a child is sick?
Soft
Systolic
Short
Sounds (S1 & S2) normal - THIS IS THE MAIN DDX FROM ASD
Symptomless
Special tests normal (X-ray, ECG)
Standing/ Sitting (vary with position)
The main DDX is ASD
Get the child to come back when they’re well, and make sure the murmur is not still there
When is posterior urethral valve usually diagnosed and what is the clinical presentation?
Clinical presentation depends on the severity of obstruction.
Severe obstruction
- diagnosis is usually made antenatally
- Potters Sequence
- Oligohydramnios
Less severe cases
- the diagnosis is often not apparent until early infancy
- Weak flow / stream
- Recurrent UTIs
What is a MCUG?
How is it performed?
When should you do it?
What can it help you DDx?
Micturating Cysto Urethro Gram
Inject contrast into bladder through the urethra.
In those who can’t urinate on demand. Also note that it is invase and unpleasant, and gives a high dose of radiation.
Can visualise bladder and urethral anatomy. Can diagnose Vesicouretertic reflux, Posterior urtheral valve and obstruction (pelviureteric junction obstrutcion, vesicoureteric junction obstruction)
What ultrasonographic sign is pathagnomonic of PUV?
Keyhole sign
What do you use to identify VUR?
If can urinate on demand: MAG 3 renogram (put radioisotope in blood)
If can’t urinate on demand: MCUG (put contrast into bladder through urethra)
what infection acquired in NVD can cause neonatal conjunctivitis & pneumonia?
Chlamydia
Which infection only causes vaginal discharge and is not routinely screened for but increases the risk of miscarriage and preterm labour?
Bacterial vaginosis
What is the management of HSP?
Basics
Joint pain / abdominal pain – paracetamol and bed rest (not NSAIDs due to renal risk).
- NB. There is some evidence that steroids may improve abdominal pain.
Place and person
Refer for surgical review if possible surgical requirement – intussusception, testicular torsion, bowel perfiration
Investigate and confirm diagnosis
Monitor BP
Monitor urine dipstick and urine microscopy
Monitor UEC?
Non-invasive management
Rest (joint pain)
Definitive management
Supportive care and frequent monitoring (including BP and urine dipstick)
- HSP nephritis (IgA nephropathy) can occur at the time of HSP, or 6 weeks – 6 months later. Continue to screen for this time.
Long term
The use of prednisolone has not been shown to make clinically important improvements in the rate of long-term renal complications – this was recently removed from the RCH guidelines!
Tongue atrophy and fasciculations
Paradoxical breathing pattern
Severe proximal muscle weakness
Absent tendon reflexes
Diagnosis?
Spinal Muscular Atrophy Type 1
Ataxia
Weakened Immune System
Increased risk of cancer
= diagnosis?
ataxia telangiectasia
What are the features of ataxia telangiectasia?
Ataxia
Weakened immune system
Increased risk of cancer
What are the features of spinal muscle atrophy type one?
Tongue fasciculations
Absent deep tendon reflexes
Severe proximal muscle weakness
paradoxical breathing pattern
What is involved in an anti body screen in a new diagnosis of T1DM?
islet cell antibodies
insulin antibodies
GAD (confirm T1DM)
IgA level
antiendomyseal
anti-gliadin
tissue transglutaminase antibodies
TFTs
How does the newborn hearing screen work?
Ears are covered, connected to the earphones, emit a series of soft ‘clicking’ sounds.
There are 3 sensor tabs that are placed on the baby’s neck, shoulder and forehead that measure auditory nerve (8th nerve) activity in response to the sound played.
What are the three possible results of a newborn hearing screen?
*Pass
*Repeat – there was not a clear response to sound on the first screen. Another hearing screen will be arranged.
*Refer – a clear response to sound was not recorded during two hearing screens. Further hearing testing is recommended.
What further hearing testing can be organised?
Behavioural Tests
- Behavioural observation audiometry (BOA)
- Visual reinforcement orientation audiometry (VROA)
- Play audiometry
Electro-physiological Tests
- Oto-acoustic emission testing (OAE)
- Brainstem evoked response audiometry (BERA)
- Electro-cochleography (EcoG)
- Tympanometry and acoustic reflex
Jenny is 5 years old. She has started school this year. Her teacher has expressed concern to her parents about her hearing, as she doesn’t seem to be listening at school.
What are your DDx?
Hearing
Behavioural
Oppositional defiant disorder
Conduct disorder
ADHD
Autism Spectrum Disorder
Intellectual Disability
How do you tell the difference between sensorineural and conductive hearing loss on an audiometry curve?
Same curve for bone and air conduction = Sensorineural hearing loss
Different curve = conductive hearing loss
What is the difference between conduct disorder and oppositional defiant disorder?
Unlike children with conduct disorder, children with oppositional defiant disorder are not aggressive towards people or animals, do not destroy property, and do not show a pattern of theft or deceit
What is normal hearing as represented on an audiogram?
Hearing at 0-20dB at all frequencies for both bone and air conduction
Describe how right, left, bone and air conuction are represented on an audiogram?
Right = Red = Circle
Left = Blue = Cross
What are the systems questions used in DKA?
Causes
- Recent infection / stress / adherence to insulin
Symptoms
Think: DKA
- D - polyuria, polydipsia, eneuresis, LOW
- K - abdominal pain & nausea
- A - increased respiratory rate
Complications
- Recurrent infections
- Recurrent hypos
- Neurological status
What are trhe investigations required in DKA?
Bedside Tests
- Insert urinary catheter to monitor urine output
- Glucose / ketones finger prick
- Urine disptick if suspect infection
Labratory Tests
- Serum gluocse and ketones?
- UEC
- VBG - especially potassium
- Urine MC&S if suspect infection
Secondary Investigations
- Septic screen if suspect infection
- C peptide if overweight and suspect T2DM
- If first presentation - insulin antibodies, GAD antibodies, coeliac screen, TFTs
What is the management of DKA?
- Resuss
- intubate if GCS
- bolus fluid (NaCl) if severe dehydration
- Fluids
- 0.9% NaCl
- 5% dextrose when BGL drops below 12 - 15
- K+ when drops below 5.5
- Insulin
- 50U act rapid
How do you classify the severity of an asthma attack?
WOB
Mental status
HR
Ability to talk in sentences
what is the name of the rash affecting children in the first 3 months of life causing a thick, scaly, yellow rash on their scalp?
seborrheic dermatitis
which rash comes on usually after a viral illness, and is in a christmas-tree distribution on the trunk?
pityriasis rosea
How would you typically compare the clinical presentation of factor defficiency / dysfunction versus platelet deficiency / dysfunction?
Factor Dysfunction
- Bleeding at surgery
- Spontaneous bleeding
- Bleeding into muscle and joints
- Purpura and ecchymosis
Platelet Dysfunction
- Bleeding at surgery
- Worsened normal bleeding (epistaxis, menorrhagia, cuts)
- Mucous membranes, skin
- Petechiae
What would you find on Hb electrophoresis for Thal major, intermedia, minor?
In essence, beta thalassaemia leads to upregulation of HbA2 and HbF because these are beta chain independent.
How does Roseola Infantum / Subitum clasically present?
And in what age group?
High fever
Sudden onset of rash on trunk which then extends down the limbs
Classically presents after 6 months and before 4 years
It is the most common viral exanthem under the age of 2
