Paeds Flashcards
Sore throat - management and Ix in aboriginal peoples
Testing for GAS is recommended in children with pharyngitis who do not have symptoms of viral illness.
Initial evaluation is typically with rapid antigen detection testing (RADT), which is quick and highly specific but has limited sensitivity.
Because the risk of acute rheumatic fever is much higher in high risk group such as Aboriginal and Torres Strait Islander people, a negative RADT in a child should be confirmed with a throat culture, which has greater sensitivity.
Start antibiotics if GAS suspected in high risk groups. Stop if culture is negative.
Phenoxymethylpenicillin Oral
15 mg/kg (max 500 mg) two times daily for
10 days
Amoxicillin Oral 50 mg/kg (max 1 g) once daily for 10 days
Antistreptolysin O antibodies peak approximately a month after streptococcal infection and are not helpful in diagnosing acute pharyngitis.
Main cause of bacterial meningitis in the neonate? Dx?
After first 7 days, is most commonly caused by in developed countries.
Group B Streptococcus (GBS), Escherichia coli, and other gram-negative bacilli are most common <7 days.
In the neonate, a cerebrospinal fluid white cell count of more than 20 to 30 cells/microL is consistent with meningeal inflammation, and bacterial meningitis should be a consideration.
A cerebrospinal fluid glucose concentration (less than 1.7 mmol/L) in a term infant is consistent with bacterial meningitis in the neonate.
Gram stain may be negative in up to 60% of cases of bacterial meningitis even without prior antibiotics. Neither a normal gram stain nor a lymphocytosis excludes bacterial meningitis
Baby gags, gasps, turn blue and stops breathing for few seconds. There is no vomiting after these episodes. He is up to date on his vaccines. What’s the most likely diagnosis? How to find out?
Whooping cough - Nasopharyngeal swab PCR
Don’t dismiss the Dx because coughing paroxysms, post-tussive whoop or post-tussive vomiting are often absent.
Nephrotic syndrome in children - overview, most common cause, main cause of death
Classically characterised by four clinical features, but the first 2 are used diagnostically because the last 2 may not be seen in all patients:
1-Nephrotic range proteinuria-urinary protein excretion greater than 50 mg/kg per day.
2-Hypoalbuminemia-serum albumin concentration less than 30 g/L.
3-Edema
4-Hyperlipidemia.
Most common cause: minimal change disease
It has generally good prognosis and the majority of children with the idiopathic nephrotic syndrome are steroid-responsive.
Children with the idiopathic nephrotic syndrome are at increased risk of developing a serious bacterial infection, especially with encapsulated bacteria.
Sepsis remains one of the main causes of death in children with NS.
Streptococcus pneumoniae is known to be the most important organism in primary peritonitis. However, other organisms such as β-hemolytic streptococci, Haemophilus and Gram-negative bacteria are also frequently found.
Autism - indacated pharmacoterapy and clinical features in adolescence
Aggression and irritability can be a feature of autism, especially during adolescence.
Atypical antipsychotics have been seen to improve behavioural symptoms such as repetitive behaviour, hyperactivity, irritability and aggression.
Risperidone, an atypical antipsychotic is the drug of choice for management of anger outbursts in children with autism in Australia and is (PBS)
Bronchodilators are effective in any age in Asthma?
Bronchodilators inhaled or oral; both are ineffective under 12 months.
Use a spacer with a face mask in children age between 1-2 years for adequate delivery of medication.
Isolated thrombocytopenia in an otherwise healthy child following an URTI is highly suggestive of?
Immune (idiopathic) thrombocytopenic purpura (ITP).
Immune (idiopathic) thrombocytopenic purpura (ITP) - Overview
TP in children is a benign disease of unknown aetiology.
ITP is an autoimmune bleeding disorder characterised by all three of:
- Isolated thrombocytopenia (platelet count of <100 x109/L, often <20 x109/L)
- Well child with no concerning features on clinical history or examination
- Otherwise normal FBE and film
ITP is the most common cause of symptomatic thrombocytopenia in children.
It is a diagnosis of exclusion as there is no specific laboratory test to confirm the diagnosis.
Newly diagnosed ITP is within 3 months of diagnosis. ITP often resolves within 3 months, and resolves in 75% of children by 6 months. Chronic ITP is longer than 12 months.
The decision to treat a child should be based on the clinical symptoms and not the platelet count. Treatment decisions also need to take into consideration the presence of active bleeding, the risk of future bleeding (eg impending surgery) and psychosocial factors.
Intravenous immunoglobulin (IVIG) is not routinely used and is reserved for patients with severe, life threatening hemorrhage
Immune thrombocytopenic purpura (ITP) - Risk classification and management
Low Risk of bleeding:
Many petechiae or large bruises
Painless oral/palatal petechiae or purpura
Blood crusting in nares
Treatment:
Outpatient without medical treatment (unless significant psychosocial or safety concerns)
Repeat FBE and review in 1 week
Moderate: Often require hospital admission
Epistaxis >5 mins
Haematuria
Haematochezia
Painful oral purpura
Significant menorrhagia
Treatment: Film must be reviewed by a haematologist prior to starting treatment
Increase platelet count to stop bleeding (not to normal level)
First line: oral prednisolone 2 mg/kg (max 60 mg) for 4–7 days
Second line if poor response or rapid platelet rise is required (eg prior to surgery): IVIG 0.8–1 g/kg (discuss with haematology team)
Additional treatments:
epistaxis: oral tranexamic acid 25 mg/kg (max 1.5 g), may need ENT intervention
heavy menstrual bleeding
!!!!!tranexamic acid must not be used if haematuria present
> Severe
Suspected internal haemorrhage (brain, lung, muscle, joint, etc) OR mucosal bleeding that requires immediate intervention
Urgent consultation with haematology team
Ttx: Combination IVIG 0.8–1 g/kg and pulse IV methylprednisolone 15–30 mg/kg (max 1 g) daily for 3 days
Platelet transfusion 20 mL/kg, continuous if required
IV tranexamic acid 15 mg/kg
Urgent surgical intervention or referral depending on site of bleeding
Life-threatening: Documented intracranial haemorrhage or life-threatening bleeding at any site
Ttx:
Urgent surgical intervention or referral depending on site of bleeding
Hives/Generalized urticaria - overview and management
If isolated, without other symptoms envolvement:
Oral antihistamines (e.g. promethazine) are mainstay of therapy in most cases.
EV route is used when the urticaria is severe or eyelids are involved.
If there is no response to antihistamines,oral corticosteroids are considered.
Croup (laryngotracheobronchitis) - overview (cause, epidemiology, symptoms)
The croup is a viral illness and is caused by
Parainfluenza viruses are the most common cause of croup
Occurs generally between the ages of 6 months and 6 years
Symptoms:
– Barking cough
– Inspiratory stridor
– Widespread wheeze
– Work of breathing is increased
– Fever with no signs of toxicity
- Often worse at night
Epidemiology:
It is most common in 1 to 3-year-old children and has the duration of 2 to 5 days
Croup (laryngotracheobronchitis) - severity classification and management
The severity of croup is assessed by key features:
1-Mild airway obstruction: mild chest wall retractions and tachycardia, but no stridor at rest.
2-Moderate airway obstruction: stridor at rest, chest wall retractions, use of accessory respiratory muscles (TWO MUSCLES) and tachycardia.
3-Severe airway obstruction: persistent stridor at rest, irritable or drowzy, increasing fatigue, markedly decreased air entry, marked tachycardia, USE OF THREE ACESSORY MUSCLES
Mild and Moderate = steroids alone
- Dexamethasone 0.15mg/kg orally OR
- Prednisolone 1mg/kg orally with repeated dose the next evening.
- Budesonide 2mg by nebulizer if oral route not tolerated
! Discarge if stridor free at rest!!! - Severe:
Nebulised adrenaline 5ml of undilluted 1:1000 OR 0,5ml of 1% respirator solution (10mg/ml) dilluted to 4ml AND Dexamethasone 0,6mg/kg (IV, IM, PO)
!! Discharge after 4h if no stridor at rest or repeat dose if deterioration
Supplemental oxygen is not often required, except in children with severely obstructed airway. Even so, nebulized adrenaline takes precedence to provide a patent airway for oxygen supplementation.
7yo with fever, ataxia, weakness, headache, and emesis and tonic-clonic seizures - what dx to think?
Acute disseminated encephalomyelitis
Acute disseminated encephalomyelitis - overview, cause, dx, symytoms, ttx
It is an autoimmune-demyelinating disease seen in children less than 10 years of age.
Presents with fever, ataxia, weakness, headache, and emesis and tonic-clonic seizures
It may follow many different types of infections, including upper respiratory tract infections, varicella, mycoplasma, herpes simplex virus, rubella, rubeola, and mumps; it may also follow immunizations.
The history and physical examination is similar to multiple sclerosis; differences include age of onset (ADEM is usually seen in < 10-year olds), the presence of systemic findings like fever and emesis, and the lack of progression in the lesions once identified.
MRI of the brain shows disseminated multifocal white matter lesions that enhance with contrast
Mortality is high, with 10% to 30% of affected patients dying.
Treatment is high-dose corticosteroids.
Coin sitting sagittal or sideways - aspiration or ingestion?
Aspiration is likely
When it is localized in the trachea it is seen in the sagittal plane because the cartilaginous tracheal rings in children are incomplete and remain open posteriorly, causing the coin to sit sagittal or sideways.
Undescendent testes - overview, normal range
Testes which are undescended at birth may well descend into the scrotum during the first TWO WEEKS of life;
> The descent is UNLIKELY AFTER 1 YEAR
A testis which was palpable in the scrotum in infancy may ascend and become impalpable due to the failure of the spermatic cord to elongate at the same rate as body growth.
Orchidopexy is best performed by 12-18 months of age as spermatogenesis in the undescended testis is impaired if surgery is done after the age of two years.
The undescended testis is at 5-10 times greater risk of developing a malignancy.
Postpartum clavicular fractures - manegement
Conservador - reassurance and guidance
Birth weight >4 kg, shoulder dystocia, and vacuum delivery are risk factors
Infantile hemangiomas - overview
Most common benign vascular tumour of childhood, and they affect up to 10% of infants.
Arise in the first few weeks-to-months of life
Risk factors include female sex, breech delivery, amniocentesis, Caucasian ethnicity, premature birth, low birthweight and advanced maternal age.
Differentials for IHs include congenital haemangiomas, which are present at birth; pyogenic granulomas; tufted angiomas; and vascular malformations that do not show any signs of regression and grow in proportion with the child.
Most IHs are usually small superficial lesions that spontaneously resolve and parents require only reassurance and education.
Some of these lesions are high risk, and up to 10% can cause complications including ulceration, airway obstruction, functional impairment or disfigurement.
In this situation, treatment is initiated with oral or topical β-blockers, most commonly oral propranolol, and monitored closely.
Primary survey of a sick child - PALS ASSESSMENT
Airway
Breathing
Circulation
Disability (neurological assessment)
Exposure
Fluids: in and out
Glucose
How to check neurological response in children?
A is Alert, or
V responds to Voice, or
P responds to Pain by localizing appropriately, flexing limbs or extending limbs to pain, or
U is Unresponsive.
Acute management of anaphylaxis
Oxygen 6-8 L by mask
Adrenaline IM (.01ml/kg 1:1000 dilution)
Nebulised salbutamol
IV crystalloid or colloid
> > Intubate, admit, OBSERVE FOR AT LEAST
12 HOURS
Long Term management of anaphylaxis
Anaphylaxis action plan
Prescribe Epipen
Medicalert bracelet
Referral to paediatric allergy specialist
Treatment of acute Urticaria (< 6 weeks):
Remove identifiable cause if any
If symptomatic:
Cool Compresses
Avoid aggravating factors such as excessive heat or spicy foods
Aspirin and other NSAIDs should also be avoided as they often make symptoms worse
Anti-histamines to alleviate itching. A non-sedating antihistamine is preferred
> > Cetirizine (Zyrtec) 0.25mg/kg/dose 12-24H oral. Can give up to 4 times the recommended dose to a maximum total daily dose of 40mg. Can be used in children from 6 months of age
Steroid creams do not work.
> > For severe cases, not responding to increased doses of non-sedating antihistamines, a single dose of oral prednisolone may be considered
Croup - other name and causative organism
Laryngotracheobronchitis
Parainfluenza virus
How to differ Croup from Epiglotitis?
Croup has URI signs preceding the acute laryngeal obstruction.
- harsh, barking cough in a febrile, miserable, but otherwise well child
Epiglotitis presents WITHOUT COUGH and with low pitched expiratory stridor and drooling
Assessment of severity of croup and management
MILD - barking cough + stridor only when active or upset
> Symptomatic management at home
+
Prednisolone if stridor present
MODERATE - Some irritability + stridor at rest (during activity) + Increased Resp rate, Tracheal Tug, Nasal Flaring + none or minimal accessory muscle use
> Prednisolone 1mg/kg AND prescribe second dose for the next evening.
Observe 30 minutes post steroid administration.
Discharge once stridor-free at rest.
SEVERE - Increasing irritability and/or lethargy + Stridor present at rest + high RR, use of accs. mm, hypoxemia
> Nebulised adrenaline, IM/IV dexamethasone, Observe for 4 hours post adrenaline, Consider discharge once stridor free at rest.
Epiglottitis - overview
HiB is the usual causative organism
Life threatening emergency, toxic febrile illness
Signs: fever, soft voice, soft stridor, sitting quietly (child sits with limited head movements to protect compromised airway), toxic look (lethargic, pale, drooling)
DO NOT EXAMINE THE THROAT. Initial diagnosis made on history and appearance.
Management: keep child calm, transport to hospital via ambulance, give oxygen, may need emergency cricothyroidotomy, intubation in hospital & IV antibiotics
> > cefotaxime 50 mg/kg up to 1 g IV 8 hourly for 5 days or ceftriaxone 50 mg/kg to max 1 g/day IV daily for 5 days)
When X-rays are recommended under suspicion of nasal foreign body?
When there is possibility of button battery or paired magnets which cannot be directly visualised.
When to give ipratropium during asthma crisis?
Severe and Critical presentations
Severe:
1 dose - 3 times in 1st hr only (20 minutely)
(250microgram)
Critical:
Nebulised 3 times in 1hr
www.rch.org.au/clinicalguide/guideline_index/Asthma_acute/
Indication of corticosteroid in Asthma
From moderate-on presentations
(limited ability to talk, work of breathing slightly increased)
Moderate-severe
Oral prednisolone 1mg/kg/dose OD for up to 3 days
Critical
IV Methylprednisolone on day 1 only
Asthma classification per symptoms and treatment
Infrequent episodic => SABA
Duration between attacks = 6-8w;
mild symptomatic and WITHOUT interval symptoms
Frequent episodic => SABA + ICS (or Montelukast for 4-6w - if no symptom improvemente -> ICS)
DBA < 6 w
Moderate symptomatic and WITH interval symptoms
Persistent => SABA + ICS + LABA
DBA < 6 w
Severe
Severe pneumonia in children - Treatment
Ceftriaxone 50mg/kg (max 1g) IV dailly
PLUS
Flucloxacilin 50mg/kg (max 2g) IV 6-hourly
Consider addition:
- Vancomycin IF MRSA SEPSIS SUSPECTED
- Azithromycin 10mg/kg (max 500mg) IV Daily IF PNEUMONIA PROGRESSING DESPITE ANTIMICROBIAL THERAPY
- Oseltamivir for Influenza
Pneumonia in children - Treatment
Amoxicillin 30mg/kg (max 1G) orally TDS for 3-5 Days
If admitted and unable to tolerate oral intake or vomiting:
- Consider benzylpenicilin 60mg/kg (max 1.2g) IV 6-hourly
Bronchiolitis - overview
Commonest acute LRTI in infants - caused by SRV
2 weeks to 12 months (after 1 year, consider overlap with asthma)
Prodromal symptoms for 48 hrs, 3-5 days of severe symptoms
Wheezy breathing, often distressed, nasal flaring, tachypnoea, hyperinflated chest, bilateral crepitations
Severe bronchiolitis is associated with respiratory failure
Infants < 6weeks are at risk of apnoea
Self limiting disease in 7 to 10 days
CXR findings in bronchiolitis
Chest Xray not routinely recommended but when performed show hyperinflated lungs and perihilar or bronchial markings.
Bronchiolitis classification, management and treatment
(see table)
MILD
O2 sat > 93%
> Improve fluid intake at home
Red flags
MODERATE
Tachypnea; Tracheal tug/nasal flaring
Sat 90-93%
> O2 for 1-2 hrs NG or I/V fluids 2/3rd maintenance
SEVERE
Lack of apetite, fatigues, hypoactive,
SO2 < 90%
> O2, IVF, CPAP, ICU
Meningococcemia - overview and management
Rapid onset of symptoms, may appear shocked, petechial rash on limbs & trunk, may deteriorate rapidly
Investigations: LP (in stable child), CT scan, Blood culture & CSF MCS/ PCR
Acute Management:
Antibiotics IV ceftriaxone/cefotaxime (50mg/kg) or benzylpenicillin for 7 days
Fluids if shocked give 20ml/kg Normal saline
Steroids IV dexamethasone (0.15mg/kg IV)(for >2mo)
Isolate till >12 hr of antibiotics
Notify DHS
Meningococcemia - chemoprophylaxis (general and pregnancy)
Chemoprophylaxis with Rifampicin FOR TWO DAYS for all household, day care or intimate contacts within 7 days of onset.
If pregnant or BF women are contacts then ceftriaxone IM as single dose
Assessment of degree of dehydration
Bare child weight estimation & comparison with premorbid weight is more accurate
Assessing with clinical signs (sunken eyes, lethargy, dry mucous membranes) is less reliable
Mild Dehydration <4% body weight loss
may have increased thirst, no clinical signs, manage with Oral Resuscitation
Moderate Dehydration 4-6% body weight loss
- Delayed CRT > 2 secs, high respiratory rate, mildly decreased tissue turgor, manage with NG resuscitation
Severe Dehydration >/=7% body weight loss
- Very delayed CRT > 3 secs, mottled skin, other signs of shock (tachycardia, irritable or reduced consciousness, hypotension), deep, acidotic breathing, decreased tissue turgor, manage with IV resuscitation
Dehydration - management
Urgent component: Boluses of 10-20ml/kg of normal (0.9%) saline, which may be repeated.
Do not include this fluid volume in any subsequent calculations of hydration
Slow Component: Maintenance Fluid
- For child’s 1st 10 kg -> 100ml/kg/24hrs
- 2nd 10 kg -> 50ml/kg/24hrs
- Remaining kgs -> 25ml/kg/24hrs
(max is 2400ml in 24 hrs or 100mls/hr)
Deficit = (weight x body weight loss x 10 )
Assessment and management of head injury
Minor:
No LOC, Stable, alert conscious state, may have scalp bruising or laceration, normal examination otherwise
Discharge home with analgesia and warn of red flags
Moderate:
Brief LOC at time of injury, may be drowsy, two or more episodes of vomiting, persistent headache
May have a large scalp bruise, haematoma or laceration, normal examination otherwise
Observe in ED for 4 hours, anti-emetics, analgesia, discuss with senior, discharge if improving
Severe:
Decreased conscious state – responsive to pain only or unresponsive
Localising neurological signs (unequal pupils, lateralising motor weakness)
Signs of raised ICP, penetrating head injury, CSF leak from nose or ears
Maintain oxygenation, ventilation and circulation, avoid rises in ICP.
Urgent CT of head and c-spine. Ensure early neurosurgical and ICU intervention.
Hypoglicaemia in children - definition and management
Hypoglycaemia is defined as a blood glucose level of <2.6 mmol/L.
The most appropriate treatment of severe hypoglycemia when the patient is unconscious and unable to take oral glucose is with a bolus of intravenous dextrose 10%, 2.5 to 5 ml/Kg followed by 0.03 to 0.05 ml/Kg/minute until the patient is stable.
In adults with hypoglycemia, 50% glucose solution is used for treatment of severe hypoglycemia. This solution is not recommended for children because it can result in serum hyperosmolarity and death.
In a conscious and cooperative child, oral route is preferred.
What’s the most common prenatal viral infection
CMV
The most common cause of noisy breathing in infancy.
Laryngomalacia
Laryngomalacia - overview
Laryngomalacia is congenital softening of the tissues of the larynx above the vocal cords. This is the most common cause of noisy breathing in infancy. The laryngeal structure is malformed and floppy, causing the tissues to fall over the airway opening and partially block it.
Laryngomalacia symptoms are usually present at birth, and can become more obvious within the first few weeks of life.
Most children outgrow laryngomalacia by 18 to 20 months of age.
Symptoms of laryngomalacia include:
Noisy breathing – an audible wheeze when a baby inhale. It is of ten worse when the baby is agitated, feeding, crying or sleeping on his back
High pitched sound
Difficulty feeding (in severe cases)
Poor weight gain (in severe cases)
Choking while feeding (in severe cases)
Measles - transmission
Patients with established measles should be excluded until 4 days after the onset of rash.
Guillain-Barre syndrome - Presentation
The initial diagnosis of GBS is based on the clinical presentation.
The cardinal clinical features of GBS are progressive, mostly symmetric muscle weakness and absent or depressed deep tendon reflexes.
The weakness can vary from mild difficulty walking to nearly complete paralysis of all extremities, facial, respiratory, and bulbar muscles
Guillain-Barre syndrome - Diagnostic tests
The diagnosis of Guillain-Barre syndrome (GBS) is confirmed if cerebrospinal fluid (CSF) and clinical neurophysiology studies show the typical abnormalities.
Therefore, lumbar puncture and clinical neurophysiology studies are performed in all patients with suspected GBS.
Of these two however, nerve conduction studies (NC) and needle electromyography (EMG) are more accurate.
They are used not only for confirmation of diagnosis. but also for providing information regarding prognosis.
Performance of a detailed neurophysiologic study enables diagnosis of pediatric GBS in as many as 90 percent of cases during the first week of symptoms
The typical CSF finding, known as albuminocytologic dissociation, starts approximately 48 hours after symptoms onset and is present in 50-66% o f the patients in the first week and over 75% in the third week.
Nerve conduction studies show a typical demyelinating pattern . NCV changes often slower than those of CSF.
Guillain-Barre syndrome - How to monitor?
Patients with GBS should always be managed in an inpatient setting.
Vital capacity should be monitored 4- hourly, using forced vital capacity (FVC), and if it falls to less than 20ml/kg or is declining rapidly, the patient should be transferred to an intensive care unit.
FVC monitoring is not diagnostic though.
Cardiac monitoring is also recommended for such patients due to significant risk of cardiac arrhythmia.
What’s the most common congenital cardiovascular diseases?
The congenital heart disease is very common, and it is reported to affect 1 in 100 Australian infants
1 - Ventricular septal defects.
2- atrial septal defects
3 - patent ductus arteriosus
4- pulmonary stenosis.
Febrile convulsions - presentation and types
Simple febrile convulsions are generalized, have duration of less than 15 minutes and do not occur more than once in 24 hours.
Complex seizures are focal in onset, may last for longer than 15 minutes and recur in the course of 24 hours.
Terminal haematuria in early adolescents without other findings
benign condition associated with hormonal changes leading to engorged vessels
Ventricular septal defect - overview (presentation, dx, ttx)
Ventricular septal defect is the most common congenital heart lesion.
The defect connects the two ventricles with the left to right shunt. The child may present with following clinical features:
-The breathlessness of crying and feeding.
-Recurrent chest infections.
-Failure to thrive.
-Congested heart failure.
The cardiac examination is remarkable with a palpable thrill at the left sternal edge and a pansystolic murmur at the right sternal edge.
If a child with a ventricular septal defect, develop heart failure symptoms, consider surgical closure by six months of age or at any age when the child is diagnosed with the condition.
Risk Factors for Cerebral Herniation in Patients Undergoing Lumbar Puncture
Altered mental status
Focal neurologic deficit
History of central nervous system disease
Hypertension with bradycardia
Immunosuppression
Papilledema
Respiratory abnormalities
Seizure (in the previous 30 minutes to one week)
thyroglossalduct cyst - REVIEW
TDCis the most common type of developmental cyst encountered in the neck region, and is a condition that results from the failure of obliteration of the thyroglossal duct that results in the formation of a bridge between the base of the tongueand the thyroid gland.
A TDC usually presents with a palpable asymptomatic midline neck mass usually at or below the level of the hyold bone, above the thyroid cartilage. The mass is most often in the midline, although it can present slightly off the midline to one side or the other. A TDC may present in childhood (less than 50%) or later in life, usually as a young adult below the age of 20 years.
Characteristically on examination, a TDC moves up when the tongue is protruded, and moves up and down upon swallowing reflecting the attachment of these cysts to the base of the tongue by the thyroglossal tract. Some patients have neck or throat pain, or dysphagia, but usually most patients are just concerned by the lump itself.
A TDC may become complicated. Complications of TDCs include:
Infection.
Malignancy
Overgrowth and pressure of the underlying structures.
Rupture and fistula formation.
Of these, Infection Is the most common complication. An Infected TDC usually presents with redness and swelling.
Malignancy is the second most common complication of TDCs. It can complicate the cyst in approximately 1% of patients. Papillary carcinoma is the most common malignancy arising from a TDC. Follicular, papillary and Squamous cell carcinoma follow in order of commonality.
Cyst enlargement and compression or the underlying structures is another complication of TDCs. Obsrtuction of the airway is of significance importance. However, compared to infection and malignancy, this complication is less common.
Categories and Risk factors for neonatal sepsis
Neonatal sepsis is categorized as either early onset defined as up to 48 hours after birth and late onset sepsis if it happens after 48 hours of birth.
Risk factors for early onset sepsis include:
– Maternal group B streptococcus colonization in current pregnancy.
– A previous baby with GBS infection.
Risk factors for late-onset sepsis:
– Artificial ventilation with an endotracheal tube.
– Extreme prematurity.
– Total parenteral nutrition.
jaundiced within 24 hrs after delivery - Diganosis? Investigations?
Haemolysis **
Neonatal Hepatitis (rare and due to high conjugated bilirubin)
Sepsis
Investigations:
SBR (split unconj&conj)
Maternal & neonatal blood group
**Direct Coomb’s Test (Antibodies on baby’s cells)
FBE/film/reticulocyte, CRP,
Blood cultures ( septic screen if required)
Causes of severe haemolysis
ABO incompatibility
Rh iso-immunisation
Sepsis
Other rare causes:
red cell enzyme defects such as G6PD deficiency (x-linked)
red cell membrane defects, for example, hereditary spherocytosis( AD)-abnormal shapes in blood film (spherocytes-can also be seen in ABO incomp.)
Prolonged Jaundice
(Jaundice persisting > 2 weeks in term baby, > 3 weeks in preterm).
Can be unconjugated:
breast milk jaundice, hypothyroidism etc.
OR
conjugated:
Galactosemia etc.
Exclude important causes but breast milk jaundice is very common.
Always investigate!
Rarely requires treatment.
Breast milk jaundice:
Cause is not known but unsaturated fatty acids or a lipase, which inhibits glucuronyl transferase have been suspected.
Common, Jaundice may continue for many weeks
Cessation of breast feeding is NOT indicated
Transient tachypnea of the newborn - overview (risk factors, clinical features, cause)
TTN
Term or late preterm (≥34 weeks-36 GA).
C/S delivery, maternal diabetes and asthma.
Inadequate clearance of fetal lung fluid at birth.
Signs of increased work of breathing:
Tachypnoea: RR>60/min, intercostal, subcostal recessions, nasal flaring, cyanosis, expiratory grunting.
Mostly starts at 2 hours after birth and resolves at 24 hours. If persists exclude Pneumonia and other DDX.
Supportive Mx: Fluid restriction, nutrition support, oxygen supply
Start AB if tachypnoea persists beyond 6 hours or there is other risk factors.
Physiological VS Pathological neonatal jaundice - aspects
Physiological
Day 2-14
Mild jaundice
Common & harmless
Dx of exclusion
Self resolves in 2 weeks in term infants (in 3 weeks for preterm)
Unconjugated hyperbilirubinemia
Pathological
> > > > Too early (< 24 hours of age)
> > > > Too high ( SBR >200-250 umol/L, 24 hours -10 days of age)
> > > Too Long (> 10 days of age, especially > 2 weeks)
> > > Conjugated hyperbilirubinemia
Congenital Diaphragmatic Hernia - overview (clinical features, cause, dx)
Failure of fusion of the components of the diaphragm (posterolateral).
Some abdominal contents (bowel, liver, spleen and stomach) herniate into the thoracic cavity through a congenital defect.
Causes pulmonary hypoplasia and severe respiratory distress at birth.
Mostly left-sided (so called Bochdalek- type hernia).
- Signs and Symptoms:
»» Triad of respiratory distress, scaphoid abdomen and barrel chest.
Respiratory distress SOON AFTER BIRTH and CYANOSIS occurs.
Decreased air entry on the left side.
Displaced heart sounds to the right.
Diagnosis:
Chest X-ray: loops of bowel within the thoracic cavity
Barium studies, routine blood tests.
Congenital Diaphragmatic Hernia - Management
Stabilise infant with ventilatory and circulatory support if needed
Optimise serum glucose and calcium levels
Ventilatory support
Insert NG tube with gentle suction to keep bowel decompressed.
High frequency oscillatory ventilation with nitric oxide is often used
Avoid bag mask/intubation
Immediate transfer to tertiary paediatric
hospital for surgery
Morbidity and mortality due to pulmonary hypoplasia/hypertension.
Post surgery complications: chronic lung disease, gastro-oesophageal reflux and growth/developmental delay.
Overall survival rates of infants with CDH vary between 40-90%.
Cyanotic Congenital Heart Diseases
Tetralogy of Fallot (TOF)
Tricuspid atresia (TA)
Total anomalous pulmonary venous return (TAPVR)
Truncus arteriosus
Transposition of the great vessels (TGV)
Hypoplastic left heart syndrome (HLH) - cyanosis late due to PDA
Pulmonary atresia (PA) / critical PS
Duct-dependent systemic circulation (critically obstructed systemic circulation)
Coarctation of the aorta (if critical duct-dependent)-causes differential cyanosis.
Hypoplastic left heart syndrome
Critical aortic stenosis (if critical duct-dependent)-
Presenting with:
cardiac failure with systemic hypoperfusion
poor or absent peripheral pulses
increasing metabolic acidosis
cyanosis may not develop until the latter stages of the clinical course.
Congenital Heart Diseases - Murmur present
T4F
PDA
TGA
VSD (ventricular septal defect)
Speech delay - Causes, screening
Causes:
Maturational language delay* (constitutional language delay)
Hearing impairment
Prematurity and/or low birth weight
Infectious diseases (COM etc.)
Neurologic conditions (CP etc.)
Metabolic/toxicological conditions
Genetic conditions/ Family history
Lack of language stimulation, parent-child dysfunction, or disruption in parenting
Significant hearing loss occurs in 1 to 3/ 1000 live births.
> > > > Routine screening in Australia à Automated auditory brainstem responses (AABR)& otoacoustic emissions (OAE) AT 6 WEEKS!!!
Any child with parental concern of hearing loss or language delay and risk factors for acquired hearing loss (e.g., kernicterus) should be assessed with formal audiological evaluation.
Frequently asked Milestones - Complete
Gross Motor:
Lifts head à 4 months
Rolls supine-prone à 5 months
Sits with support à 6 months
Sits without support à 8 months
Walks alone à maximum 18 months
Rides tricycle à 3 years
Fine Motor
Thumb finger grasp à 9 months
Pointing à 12 months
Tower of 2 cubes à 16 months
Tower of 4 cubes à 26 months
Cognitive:
Plays peekabooà 8 months
Waves goodbye à 8 - 12 months
Pretend play à 18 - 24 months
Social:
Social smile à 6 weeks
Stranger anxiety à 9 months
Buttons à 4 years
Dress without supervision à 5 years
Separation anxiety à 6 - 18 months peaks, decreases preschool.
Language
Coos à 3 months
Babbles à 6 months
Single word à by 16 months
Two-word phrase à by 24 months
50 words-à 2 years
Frequently asked Milestones - MUST KNOW!!!!
Social smile = 6w
Buttons = 4 y
Dressing = 5 y
Pointing (fine motor) = 12 m
Sitting with support = 6 m
Walk alone = 18 m
Down Syndrome - Clinical features, incidence, prevalence
Most common cause of intellectual disability all over the world
Typical facies (flat facies, slanting eyes, prominent epicanthic folds, small ears)+ hypotonia + single palmar crease
95% have extra chromosome of maternal origin(trisomy 21).
Prevalence 1 in 1100 live births in Australia
Down Syndrome - Associated disorders and management
Associated Disorders:
Seizures (usually later onset)
Impaired hearing
Leukaemia
Hypothyroidism
Congenital anomalies (e.g. heart (septal defects most common), duodenal atresia, Hirschsprung, TOF)
Alzheimer-like dementia (fourth–fifth decade)
Atlantoaxial instability
Coeliac disease, Diabetes
Management: Refer for hearing, vision, developmental disability unit for assessment! MDT.
Genetic counselling for parents.
Down Syndrome - Screening
Prenatal screening available (combined first trimester screening, 11 - 13 weeks, risk assessment based on maternal age + USG nuchal translucency thickness + maternal serum analytes – free beta HCG and pregnancy-associated plasma protein A)
Duodenal atresia - overview
Rare disorder of unknown cause,
May be inherited (autosomal recessive) or associated with Down’s syndrome (25%)
Risks: hypoglycaemia, electrolyte imbalance, aspiration
Immediate transfer to tertiary care centre for urgent surgery (duodenoduodenostomy)
Congenital hypothyroidism - dx, clinical features and epidemiology
Mostly detected on the Newborn Screening (elevated TSH!).
1:2000 to 1:4000 newborns and is one of the most common preventable causes of intellectual disability!
Clinical features may include:
dry skin
hoarse cry
constipation
puffy face, prominent tongue, enlarged fontanelle
listless
umbilical hernia
Hypothermia, bradycardia
failure to thrive
Neonates may also present with jaundice due to an unconjugated hyperbilirubinaemia
Causes of large fontanelles & delayed closure + normal age of closure
Achondroplasia,
Congenital hypothyroidism
Down syndrome,
Rickets,
Increased intracranial pressure
Head circumference
Posterior Fontanelle - no larger than 1 - 1.5 cm in diameter, closes at 2m
Anterior Fontanelle - 6 cm in diameter through the first 6 months of life, closes between 10 and 24 months of age.
Toddler’s diarrhea - Overview (clinical fx, management)
Very common around the age of 2-5 years.
Chronic diarrhoea with undigested food particles, may be foul smelling
Not associated with Failure to thrive or anaemia.
Rx: normalization of four F’s in child’s diet
Limit fruit juice
Avoid excessive fluid intake and “grazing” with bottles or sipper cups
Increase the amount of fat in your child’s diet with whole milk, butter and olive oil
Increase the amount of fibre in your child’s diet with fresh fruit, bread, cereal and beans
Chronic diarrhoea - overview of causes and risk
Chronic diarrhoea: increased stool frequency or loose stools, lasting > 2 weeks
Risks: poor growth or FTT, anaemia, nutritional deficiencies
Causes:
- Non Bloody Diarrhoea
Toddler’s diarrhoea
Overflow constipation
Giardiasis
Celiac disease
Pseudomembranous colitis
Irritable Bowel Syndrome rarely
- Bloody diarrhoea
Inflamatory Bowel Disease
Infectious colitis
Cow’s milk protein colitis
Infantile colic - clinical fx, management
Usually between 2-16 weeks old
Prolong crying at least 3hrs/day, 3 times/ week
Crying in late afternoon & early evening
Flexing legs, clenching fists appears in pain
No vomiting (apart from post-feed small posit), no diarrhea with excoriation, no eczema, no fever, not acute onset!
Other wise well & thriving
No workup required if clinically normal.
Acute crying and vomiting -> Urine MCS.
Abates by 4 months in 90% of infants
Mx:
After excluding organic causes,
REASSURANCE AND SLEEP/CYCLE DIARY
Assess mother`s mental condition. Never stop breastfeeding if no indication.
In very severe cases can trial CMP elimination diet or hydrolyzed formula
Short stature - rule based on parental height
Rough rule for expected adult height based on parental height:
Boys—mean of parents’ heights + 5 cm
Girls—mean - 5 cm
Short stature - causes
- Constitutional Delay
Common normal variant. Delay in maturation
Bone Age < Chronological Age
- Familial Short Stature
Familial trend. Determine parental height
Bone Age = Chronological Age
- Organic Causes
Coeliac Disease, Crohn Disease, Chronic Kidney Disease, Hypopituitarism, GH deficiency, Genetic syndromes(Turner/Noonan), Hypothyroidism, Skeletal Dysplasia, Cushing Syndrome, Precocious puberty. Malnurition, Glucocorticoid therapy, Eating Disorders
Puberty - Females
First sign is breast budding between 8 - 13 years! (Average age 10.5)
<8y precocious, >13y delayed
*Pubertal Changes,Tanner`s Staging ->
Breast bud enlargement (Thelarche)
Growth spurt
Pubic hair growth (Pubarche)
Menstrual flow (Menarche), on average, 2-2.5 years after the onset of puberty .
Amenorrhea - primary X secondary
(see the fluxogram for management)
Primary amenorrhoea :
Lack of menses by 15 (<16) and breast development is present or
Lack of menses by 13 and no breast development (pubertal delay)
The major pathological causes are genetic or anatomical problems.
Secondary amenorrhoe:
Absence of menses for >6 months after initial onset of the periods. First exclude Pregnancy!
Refer to endocrinologist for unsolved cases or for further Ix and Mx, according to the underlying cause
Mucocutaneous lymph node syndrome - other name?
Kawasaki disease
Kawasaki disease - overview (dx, clinal features, age of onset)
Systemic vasculitis that predominantly affects children <5yo
Diagnostic criteria:
Fever for 5 days or more plus
4/5 following features:
Bilateral Conjunctivitis (Red but non purulent)
Polymorphous Rash.
Peripheral changes; e.g. Erythema, oedema & desquamation of the palms or soles
Cervical Adenopathy(>1.5cm, unilateral, non-purulent, not painful!)
Mucous membrane changes; e.g. red/dry/cracked lips, strawberry tongue or a diffuse redness of oral mucosa
Scarlet fever - clinical features, rash features, cause
Group A Strep pyogenes, erythrogenic toxin.
Prodrome: 2 days of malaise, sore throat, fever & vomiting.
Features of the rash
Appears on 2nd day of illness
First appears on neck à Rapidly generalises
Blanches on pressure
Feels like fine sandpaper
Prominent on neck, in axillae, cubital fossa (Pastia lines), groin, skinfolds
Absent or sparse on face, palms and soles
Lasts about 5 days
Fine desquamation
Scarlet fever - investigations and management, school exlusion
Investigations: A throat swab should be taken, ASOT
Treatment: Phenoxymethylpenicillin 10 days
School exclusion à Children can return to school 24 hours after taking antibiotics.
Influenza - overview (clinical fx, diagnosis, ttx, complications, control of case, prevention)
measured temperature >38.5C
OR
significant history of fever (with rigors, sweating chills)
plus 2 or more of:
cough,
sore throat,
body aches,
fatigue/tiredness
shortness of breath.
But excluding patients with acute wheezing illnesses (asthma, bronchiolitis, virus associated wheezing)
The incubation period is 1 to 4 days.
Complications:
bacterial superinfection with pneumonia, otitis media or sinusitis;
neurological: encephalitis, meningitis, encephalopathy;
myositis and cardiomyopathy.
Diagnosis: No need for viral studies unless admitted.
Control of case:
Exclude from school until resolution of symptoms.
Treatment:
Not recommended for immunocompetent patients
Neuraminidase inhibitors (zanamavir, oseltamivir) indicated within 48hrs for immunocompromised pts or with chronic medical illnesses)
Recommend oseltamivir (prophylaxis) for family members if they:
have risk factors for more serious disease, or
attend/work in ‘vulnerable settings’.
Prevention: Annual vaccination to prevent influenza in children (<6 months-9 years 2 doses, >9 years 1 dose)
Chicken pox - clinical features and complications
Incubation period à 10-21days
Infectious period à 1–2 days before onset of rash until rash is fully crusted.
Exclusion from School period à Until the blisters dried (Usually 5-7 days in unimmunized children, less in immune children).
C/F: No prodrome in children, mild 2-3 days of:
Fever, irritability, anorexia and lymphadenopathy in adults.
Pruritic rash(pleomorphic) maculopapular,vesicular, crusting by 5–10 days.
Lesions appear in crops with a central distribution. Affects scalp, face, trunk, mouth, conjunctivae & extremities.
Complications:
Secondary bacterial infection of skin lesions, most common complication (Give Flucloxacilin).
bacterial pneumonia
neurological (cerebellitis, transverse myelitis, GBS)
Herpes zoster ‘shingles’
Chicken pox - Ttx and contact prophilaxy
Treatment:
Acyclovir iv for patients with impaired immunity, neonates, complications such as pneumonia, cerebellitis-admit!
Adolescents >12 years, presenting in < 24 hours- Oral Aciclovir.
Antibiotics for secondary bacterial skin infection
Antiviral Tx treatment is not for immunocompetent child.
Aspirin is contraindicated because of the association with Reye’s syndrome.
- Contacts:
** ZIG within 96 h of exposure to Immunocompromised children + Newborn infants (no symptoms) whose mums have varicella onset from within 7 days before delivery to 4 weeks after delivery.
Varicella vaccine for adults or children >12 years after contact in 3 days to prevent infection.
Give ZIG for newborn <7 days for postnatal contact and mother is seronegative or unknown status.
Prevention: MMRV at 18 months.
Chicken pox - Congenital Varicella Syndrome, period of highest risk for infection during pregnancy
Varicella in pregnancy, highest risk at 2nd trimester.
Skin scarring, limb defects, ocular anomalies and neurological malformations.
Hand, Foot and Mouth Disease - transmission, incubation, CF, Dx,
Cause: Enterovirus (usually Coxsackie A16)
Transmission: direct contact/droplet, orofecal.
Incubation period à3–6 days.
Infectious period -> until blisters have dried
Clinical features:
Mouth or throat pain or refusal to eat,
Low grade fever.
Vesicles on cheeks, gums, sides of the tongue;
Papulovesicular lesions of palms, fingers, toes, soles, buttocks, genitals, limbs
Non-pruritic, non-tender, bilateral
Vesicles lead to shallow ulcers on buccal mucosa, gums and tongue
Diagnosis > Clinical
Exclusion > until blisters have dried.
Hand, Foot and Mouth Disease - Ttx and complications
Treatment > Symptomatic.
Complications > Uncommon
Decreased oral intake, dehydration and may necessitate hospitalization for parenteral fluid therapy
Rhombencephalitis (brainstem encephalitis)
Acute flaccid paralysis
Aseptic meningitis
Myocarditis
No Jab, No Pay Policy
Only parents of children who are fully immunised or are on a recognised catch-up schedule can receive the Child Care Benefit, the Child Care Rebate and the Family Tax Benefit Part A end of year supplement
Children with medical contraindications or natural immunity for certain diseases will continue to be exempt from the requirements.
Conscientious objection and vaccination objection on non-medical grounds will no longer be a valid exemption from immunisation requirements.
Immunisations: Contraindications
All vaccines
**Acute febrile illness (if fever > 38.5°C, postpone vaccination)
**Previous anaphylaxis contraindicates further dosage of same vaccine
DTPa
Encephalopathy within 7 days of previous
DTP vaccination
Live vaccines (e.g. MMR, MMRV, varicella, zoster, BCG, OPV, Oral Rotavirus vaccine, Yellow fever) :
Contraindicated in immunosuppressed children and pregnant ladies (avoid [pregnancy within 28 days of live vaccines)
Persons living with someone with lowered immunization should be vaccinated including live vaccines.
Other vaccines
Severe adverse reactions (extremely rare)
Immunisations: False contraindications
Cold, or low-grade fever (<38.5°C).
Family Hx of any reactions to vaccination
Past Hx of convulsions
Hx of pertussis-like illness, measles, rubella or mumps
Premature (vaccination should not be postponed)
Stable neurological condition such as CP or Down Syndrome
On antibiotics.
On locally acting steroids (inhaled/topical)
Recent or imminent surgery.
Low weight but otherwise healthy.
OPV vs IPV
OPV is no longer available in Australia.
However both OPV & IPV are interchangeable.
OPV is a live vaccine so it can not be given to immunocompromised children.
Recommended doses are at 2,4,6 months & 4yrs.
If no previous polio vaccination à Give 3 doses of IPV 4 weeks apart.
Hialine membrane lung disease- Risk factors, dx
Premature Newborn - 32-36 W
Symptoms begin within 6 hours of life, gradually worsens in 48h.
Triad of tachypnoea, grunting and retractions.
On CRX - Can’t see the “edges” of the lungs, air bronchograms, ground glass opacity in final stages.
Prevention by antenatal corticosteroids
Ttx with surfactant therapy
Haematological exams alterations in Haemophilia A (factor VIII deficiency) and von Willebrand disease and disseminated intravacular coagulation
Fator VIII Def - PLT normal; aPTT LONG
von Willebrand - PLT normal or long; APTT LONG
DIC - PLT low; PT, aPTT, TT long; Fib LOW
Aplastic Anaemia (AA) - clinical fx, Dx,
AA is characterized by diminished or absent hematopoietic precursors in the bone marrow, most often due to injury to the pluripotent stem cell
Acquired (%70) or inherited (Fanconi aplastic anaemia).
Acquired causes are mostly idiopathic or secondary to cytotoxic drugs, radiation, drug reactions or viral infections.
Clinical signs of bone marrow failure and pancytopenia.
Anaemia: Fatigue, pallor, CVS complaints.
Thrombocytopenia: Haemorrhage
Neutropenia: Fever, mucosal infections and bacterial infections.
> > > > > No splenomegaly!
Diagnosis: Bone marrow aspiration and biopsy.
Aplastic Anaemia (AA) - findings on blood smear for suspicion
Peripheral blood smear:
Normocytic or macrocytic red cells with a marked reduction in polychromatophilia (reticulocytes).
Neutrophils and platelets are decreased in number. No blasts.
Aplastic Anaemia (AA) - Treatment
Treatment:
Withdraw offending agents, supportive treatment.
Blood and platelet transfusions .
Antibiotics
Hematopoietic cell transplantation and immun-suppresive therapy.
Slipped capital femoral epiphysis - overview, cf, age of onset
SCFE is more commonly seen in adolescents of 10 to 15 years of age. The classic case would be an oversized prepubertal boy. The condition is bilateral in 20% of cases.
CSFE presents with the following:
Limp and irritability of hip on movement
Knee pain – referred from the affected hip
On flexion of the hip. it rotates externally. Hip is often in external rotation on walking.
Most movements restricted, especially internal rotation.
The first symptom is hip stiffness that abates with rest. Later on, limping and hip pain radiating down the anteromedial thigh to knee follows. Early hip examination neither detects pain nor movement limitation. In more advanced stages. hip movements become painful and there is decreased flexion, abduction and internal rotation.The affected leg is externally rotated on walking.
The most significant aspect of the SCFE is the great number of patients who develop avascular necrosis of the femoral head despite expert treatment. Therefore, diagnosis of the condition before major slipping occurs is important. This necessitates early investigation and referra
Slipped capital femoral epiphysis - management, ix
Any adolescent with a limp or knee pain should have X-rays (AP and frog view) of both hips. Otherwise, this important condition will be overlooked.
The most important management principles include:
Cease weight-bearing and refer urgently
If acute slip,gentle reduction via traction is better than manipulation for prevention of later avascular necrosis.
Once reduced, pinning is performed
Legg-Calve-Perthes - overview, cf, age of onset
This disease, also called Pethes disease, is a temporary condition in the hip joint characterized by decreased blood supply to the femoral head and consequent avascular necrosis. As a result. femoral head collapses and the area becomes inflamed and irritated.
Legg-Calve-Perthes disease causes the hip joint to become painful and stiff.
Affected children are usually between 4 and 10 years old. physically active and small for their age.
Osgood-Schlatter disease - overview, cf, age of onset
Is seen in preadolescent children and is characterized by pain localized to the tibial tubercle and occasionally the patellar tendon.
The pathophysiology of the disease is by repetitive traction effect of patellar tendon on an immature tibial tubercle.
There is often tenderness over the tibial tubercle on examination. Hip movements are not painful or restricted.
Supratentorial brain tumors - age of onset, cf
Supratentorial tumors predominate in the first year of life (including choroid plexus tumors and teratomas).
After 10 years of age, supratentorial tumors (eg, diffuse astrocytoma) are again more common.
Infratentorial brain tumors - age of onset, cf
Brain tumors in children 1 to 10 years old are more frequently infratentorial (posterior fossa) and include cerebellar and brainstem tumors such as medulloblastoma or cerebellar astrocytoma.
Most patients with posterior fossa brain tumor have evidence of increased intracranial pressure due to obstructive hydrocephalus. As a result, headache, nausea and vomiting, ataxia, vertigo, and papilledema are common at presentation. Cranial nerve palsies are also common, especially involving cranial nerves VI to X. Brainstem invasion may occur.
Typhoid fever - cf
Travellers to developing countries are at risk of infection. This risk varies from 1:30 000 for prolonged stays in endemic regions to 1:3000 in high endemicity areas such as the Indian subcontinent, where risk is highest. The mainstay of prevention is hygiene and food and water precautions. This child has a history of making a trip to India and now presenting with fever and gastroenteritis symptoms. The stool culture grew positive for Salmonella Typhi. This child had develop typhoid fever and he should receive oral or intravenous azithromycin. The usual incubation period is 7–14 days with a range of 3–60 days.
Typical symptoms include:
* fever, which increases with disease progression
* dull frontal headache
* malaise
* myalgia
* anorexia, and
* dry cough.
Constipation (or less commonly diarrhoea, which occurs more often in young children), abdominal pain and tenderness, relative bradycardia, splenomegaly and rash (‘rose spots’) may also occur. Complications, which include gastrointestinal bleeding, intestinal (usually ileal) perforation and typhoid encephalopathy tend to occur after 14 or more days of illness in 10–15% of patients.
Typhoid fever - Treatment
Australian guidelines recommend:
azithromycin 1 g (child: 20 mg/kg up to 1 g) orally or intravenous (iV) until oral azithromycin can be tolerated, daily for 10 days
OR (if not acquired in the indian subcontinent and southeast Asia)
ciprofloxacin 500 mg (child: 15 mg/kg up to 500 mg) orally, 12 hourly for 7–10 days, or ciprofloxacin 400 mg (child: 10 mg/kg up to 400 mg) iV, 12 hourly until oral ciprofloxacin can be tolerated
As an alternative regimen for initial iV therapy, or if the clinical response is delayed (eg. fever longer than 7 days) use
ceftriaxone 2 g (child: 50 mg/kg up to 2 g) IV,daily
fluoroquinolones still remain superior for preventing clinical relapse and are still recommended for empirical therapy in adults
approach to a child with an abdominal mass - what two possibilities should always be considered
1) Wilms tumor (nephroblastoma) and
2) neuroblastoma.
Wilms tumor - overview
Wilms tumor is the most common intra-abdominal malignant tumor of childhood that often presents with a smooth firm abdominal mass that usually do not cross the midline. Abdominal pain either constant and vague or intermittent is another finding.
Hematuria and hypertension are other possible manifestations. The median age of diagnosis is 3.5 years. Although not impossible, it is less likely to present within the first year of life.
Wilms tumor
calcification uncommon: 10-15% (10% rule of Wilm’s tumor)
displaces adjacent structures without insinuating between them
slightly older age group: peak 3-4 years of age
well circumscribed
claw sign with the kidney
extension into IVC/renal vein.
bony metastasis are rare, rather lung metastasis are common.
extension into spinal canal never seen.
retroperitoneal lymphadenopathy is uncommon.
Neuroblastoma - overview
Neuroblastoma is the most common extracranial malignant tumor of childhood with the initial presentation most commonly being within the first 2 years of life. The tumor is intraabdominal in two-thirds of cases, of these two-thirds originating from adrenal glands. It can also present with a palpable abdominal mass that is non tender.
Neuroblastoma
calcification very common: 90%
encases vascular structures but does not invade them
younger age group (<2 years of age)
poorly marginated
elevates the aorta away from the vertebral column
more commonly crosses the midline, especially behind the aorta
more common to have extension into the chest
bony metastasis are common (Hutchinson syndrome)
extension into spinal canal can be seen.
retroperitoneal lymph nodes are more often seen.
When to check serum MG levels or to administrate it in children?
Serum magnesium level is required if:
(a)an infant is suffering from the seizure of unknown aetiology (in the presence of normal or replaced serum calcium).
(b) in a hypotonic infant born to a mother who received magnesium sulphate therapy before delivery.
Giving magnesium sulphate without checking serum magnesium level is not recommended as it can lead to hypermagnesemia and cause respiratory muscle paralysis.
Marfan’s syndrome - cf and genetics
Marfan syndrome is a genetic disorder transmitted as an autosomal dominant trait with variable expression. People with this disorder typically have tall stature, arachnodactyly, subluxation of the lens, dilatation of the aorta, and dissecting aneurysm. Mental retardation is not a part of this syndrome. Vascular complications can be serious if not identified early; aortic dissection can lead to sudden death.
Atrial septal defects - types, cf, dx
Atrial septal defects connect two atria and are of two main types:
-Ostium Secundum-it is the most common type of atrial septal defects, and the hole is higher in the septum. It is not a serious condition, and symptoms are very uncommon in infancy.
-Ostium Primum-it is the most dangerous type of atrial septal defects which can lead to pulmonary hypertension and heart failure.
Prophylactic antibiotics are recommended for patients with ostium primum due to increased risk of respiratory tract infections.
Signs of atrial septal defects include a mid-systolic murmur at the pulmonary area, a split second heart sound and a loud P2. An echocardiogram is usually diagnostic, and MRI is not usually required.
precocious puberty - definition
defined as the appearance of pubertal signs before age 8 in girls and before age 9 in boys.
Contraindication to HPV vaccine
anaphylaxis to yeast
acute rheumatic fever - Standard ttx and alergy alternative
The most appropriate treatment is bed rest, benzathine penicillin intramuscular injection once only followed by oral phenoxymethyl penicillin for 10 days.
If a patient is allergic to penicillin, consider Roxithromycin as an alternative.
This patient also needs treatment for arthritis and non-steroidal anti-inflammatory drugs would be a good choice.
choanal atresia - cf, dx, ttx
Choanal atresia is a congenital abnormality in which there is failure of canalization of the bucconasal membrane. This can be either unilateral or bilateral and is usually due to a combination of bone and soft tissue anomalies.
Unilateral atresia is more common, with a predilection for females. CHARGE Syndrome ( coloboma, heart defect,.atresia choanae, retarded growth and development, genital abnormality and.ear abnormality) or other congenital abnormalities are present in 50% of patients with bilateral choanal atresia.
Bilateral choanal atresia is a relatively rare anomaly of the upper airway. As neonates are obligatory nasal breathers, presentation may be with life-threatening respiratory distress, retractions and paradoxical cyanotic episodes which are relieved by crying as the infant begins to mouth breath. Unilateral choanal atresia does not usually produce severe symptoms.
When choanal atresia is suspected the diagnosis can be confirmed with trying to pass a nasogastric tube. It is not possible to pass a nasogastric tube through the nares and choanae if there is choanal atresia.
Other measures to consider as parts of management plan includes:
Oxygen
Oropharyngeal airway
Intubation and ventilation if there is life-threatening hypoxaemia
CT scan
ENT consultation and referral for surgical treatment
indications for hospitalization/pediatric consultation in Whooping cough
indications for hospitalization/pediatric consultation include the following:
Infants less than 6 months of age
Any child who has had apnea, cyanosis, pneumonia, or encephalopathy as a complication of
With cyanosis following the attacks of cough, this child needs to be admitted to the hospital.
Antibiotics should be considered if:
The patient is diagnosed in catarrhal or early paroxysmal phase (may reduce severity)
Cough for less than 14 days (may reduce spread; reduces school exclusion period)
Admitted to hospital
There are complications (pneumonia, cyanosis, apnoea)
Antibiotics of choice are azithromycin or clarythromycin. They can be used after the child is admitted to the hospital
What is the recommended evaluation approach for UTIs in children younger than 3 years of age with the first episode of UTI?
In children younger than 3 years of age (2-36 months), in addition to antibiotic treatment, an ultrasound scan of the kidney, ureter, and bladder should be considered for the first episode of UTI. 🩺👶
For children less than 1 year old, an ultrasound should be the initial investigation. If normal, a voiding cystoureterogram (VCU) may follow to detect urologic structural abnormalities and vesicoureteric reflux.
What are the characteristics of innocent murmurs, often referred to as the “7 ‘S’s”?
Innocent murmurs are characterized by the “7 ‘S’s”:
Sensitive (change with child’s position or respiration) 🔄
Short duration (not holosystolic) ⏲️
Single (no associated clicks or gallops) 🙅
Small (limited to a small area and non-radiating) 🎈
Soft (low amplitude, up to 2/6 or very rarely 3/6) 🤫
Sweet (not harsh sounding, no thrills) 🍬
Systolic (limited to systole) ❤️
What factors indicate that a murmur is pathological?
A murmur should be considered pathological if it has any of the following features:
Grade 3/6 or higher intensity 🔊
Harsh quality 😠
Abnormal S2 🚫
Presence of a systolic click 🖱️
Symptoms related to cardiac conditions (e.g., shortness of breath, chest pain, poor feeding, failure to thrive) 😓🍼
Increased intensity when venous return decreases (e.g., when the patient stands) 🚶♀️
What additional factors should lead to considering a murmur as pathological?
Every murmur should be considered pathological until proven otherwise if any of the following are present:
Family history of sudden cardiac death or congenital heart disease 👨👩👧👦
In utero exposure to certain medications or alcohol 🤰🍷
Maternal diabetes mellitus 🤰🩺
History of rheumatic fever 🩺
History of Kawasaki disease 🩺
When should antibiotic prophylaxis be considered for infants and children with UTIs and VUR?
Antibiotic prophylaxis should be considered for infants and children with recurrent UTIs or vesicoureteric reflux (grades III to V). 🔍
Prophylaxis is not routinely recommended following the first episode of UTI due to the risk of multidrug-resistant infections. 🚫
What are the recommended antibiotics for UTI prophylaxis in children?
Recommended antibiotics for prophylaxis include:
Trimethoprim+sulfamethoxazole (child 1 month or older) 2+10 mg/kg up to 80+400 mg orally, at night 💊
Trimethoprim (if a suitable formulation is available) 2 mg/kg up to 150 mg orally, at night 💊
Cefalexin 12.5 mg/kg up to 250 mg orally, at night 💊
Nitrofurantoin (child 1 month or older) 1 mg/kg up to 50 mg orally, at night 💊
When should the index case of pertussis be excluded, and for how long?
The index case should be excluded until:
5 days after starting appropriate antibiotic treatment, or
For 21 days from the onset of any cough (catarrhal phase), or
14 days after the onset of paroxysmal cough if the date is known. 🤒💊
: How should unimmunized household and close childcare contacts less than 7 years of age be excluded due to pertussis exposure?
Unimmunized (< 3 doses) household and close childcare contacts less than 7 years of age must be excluded for:
14 days from the last exposure to infection OR
Until they have taken 5 days of effective antibiotics for prophylaxis. 🏡👶📆💊
What are the recommended approaches for managing pediatric neck masses?
Management of pediatric neck masses often relies on clinical judgment and surveillance for red flags.
Common approaches include:
Watchful waiting for up to six weeks in patients with suspected reactive lymphadenitis, especially evident by bilateral lymphadenopathy without red flag features for malignancy or deep cervical abscess. 👀🕒
Empirical antibiotics may be used in cases of suspected suppurative lymphadenitis, particularly when marked erythema, tenderness, asymmetric lymphadenopathy, and systemic symptoms are present. 🦠💊
If symptoms persist or do not improve with antibiotics, further investigation with ultrasound and serological screens for atypical infections, including mycobacteria, is warranted. 🩺🧪
Routine full blood count (FBC) may be considered if systemic disease is suspected or the diagnosis of infection is uncertain. FBC and blood film can help identify pancytopenia and atypical cells suggestive of hematological malignancy or indicate viral or bacterial pathology. 🩸🔬
What defines nephrotic syndrome in children?
Nephrotic syndrome in children is defined by the presence of:
Generalized edema
Heavy proteinuria (+++ or ++++ on dipstick)
Hypoalbuminemia
Hypercholesterolemia 🏥🔬
What are the common causes of nephrotic syndrome in children? (renal histologic features)
Common causes of nephrotic syndrome in children include:
Minimal change disease (80%)
Focal segmental glomerulosclerosis (5–10%)
Occasional microscopic hematuria may be seen (15–30%) 📊🔬
What is transient proteinuria, and when does it occur in children?
Transient proteinuria is seen in as many as 30–50% of children and often resolves over 1–2 weeks. It can occur during febrile illnesses, strenuous exercise, emotional stress, and following seizures or abdominal surgery. 📈💧
What is the recommended approach to evaluating proteinuria in children?
Evaluation of proteinuria should start with:
A careful history and thorough physical examination
Urine microscopic examination
Determination of protein excretion rate (PER)
Protein-to-creatinine ratio (PCR) on a spot urine specimen is a reliable alternative to 24-hour urine collections. It correlates with 24-hour PCR and is not influenced by urine dilution or concentration. 🩺🔬
Children with Port-wine stain develops seizure, most likely dx?
Sturge - weber - syndrome
capillary malformation along the trigeminal nerve distribution
also assocx with glaucoma
Most common brain tumor in children
Low grade astrocytomas
High grade astrocytomas, like glioblastomas, are malignant and much less common
What is congenital umbilical hernia in newborns, and how is it managed?
👶 Congenital Umbilical Hernia in Newborns
Definition: Results from incomplete closure of abdominal muscles around the umbilical ring at birth. Can be associated with hypothyroidism, syndromes (Ehlers-Danlos, Beckwith-Wiedemann, Down), or occur in healthy newborns.
Clinical Presentation: Soft, nontender bulge protruding with abdominal pressure (crying, straining). May contain omentum or small intestine.
Spontaneous Closure: Small hernias often close as muscles fuse, less likely in large hernias or with underlying issues.
Surgical Intervention: Recommended around age 5 for persistent hernias or earlier if complications (incarceration, strangulation) occur. 🩹
What is Duchenne Muscular Dystrophy (DMD), and how is it clinically diagnosed?
Duchenne Muscular Dystrophy (DMD) is a genetic disorder characterized by a deficiency or absence of dystrophin in muscle fibers, leading to severe, progressive muscle weakness. [Description, Dystrophin deficiency, Muscle weakness 💪]
DMD typically presents in toddlers with gross motor delay but normal fine motor and language skills. They often don’t walk independently until after 18 months and experience difficulty running, jumping, and climbing stairs. Frequent falls and activity-related fatigue are common. [Clinical presentation, Gross motor delay, Walking delay, Difficulty with physical activities, Frequent falls, Fatigue 😓]
The Gower sign, in which patients use their hands to assist in standing, is an early sign due to proximal lower extremity muscle weakness and atrophy. Calf enlargement (pseudohypertrophy) develops by early childhood, and progressive muscle weakness leads to joint contractures. Most patients become wheelchair-dependent by adolescence. [Gower sign, Proximal muscle weakness, Calf enlargement, Joint contractures, Wheelchair-dependent ♿]
The initial screening tool to assess myopathy in DMD is a markedly elevated creatine kinase level. As the disease progresses and more muscle is replaced by fat and fibrosis, creatine kinase levels decrease. A definitive diagnosis is made through genetic analysis, which identifies dystrophin gene mutations. [Diagnosis, Elevated creatine kinase, Muscle replacement, Genetic analysis, Dystrophin gene mutation 🧬]
What is the etiology of otosclerosis, and how does it present clinically?
Autosomal dominant inheritance pattern with incomplete penetrance 👪
Imbalance of bone resorption and deposition leading to ossicular chain stiffening 🦴
Primarily affects the stapes in the ossicular chain 🦻
Results in conductive hearing loss (CHL) 🙉
Paracusis of Willis: Paradoxical improvement of speech understanding in noisy environments due to CHL damping background noise 🗣️🔇
Clinical findings and Management options for otosclerosis.
Generally unremarkable ear examination 🩸
Excessive bony resorption may expose blood vessels behind the tympanic membrane, leading to a reddish hue 🩺🔴
Significance: Exposed blood vessels can indicate underlying otosclerosis 🚨
Hearing amplification 📢
Surgical reconstruction of the stapes (stapedectomy) 🪒
Management aimed at improving hearing and alleviating conductive hearing loss 🛠️👂
Individualized treatment plans based on patient preferences and severity of the condition
What are the key characteristics of Tuberous Sclerosis Complex, and what are some associated tumors?
Autosomal dominant disorder 🧬
- TSC (Tuberous Sclerosis Complex): Most commonly associated neurocutaneous disorder with infantile spasms 🧬
- Look for characteristic dermatologic manifestations (e.g., ash-leaf spots) or a family history of similar findings to consider TSC 🌱🔍
Characterized by benign tumors in multiple organs, including the brain, heart, and kidney 🧠❤️🏥
Classic CNS lesion in TSC: Subependymal giant cell tumor 🧠
May cause obstructive hydrocephalus (e.g., headache, vomiting, focal neurologic deficits) 🚧🤕
Other tumors associated with TSC: cardiac rhabdomyomas, renal angiomyolipomas, retinal hamartomas 🩺💔👁️
What is galactosemia, and what is its primary cause?
Galactosemia is a autossomal recessive metabolic disorder most commonly caused by galactose-1-phosphate uridylyltransferase (GALT) deficiency. 🧪
In affected newborns, galactose cannot be reduced to glucose, leading to elevated serum galactose-1-phosphate, galactose accumulation in tissues, and hypoglycemia. 🩸👉🍼
How does galactosemia typically present in affected newborns, and what are the common signs and symptoms?
Galactosemia usually presents in the first few days of life after ingesting galactose or lactose. 📅🍼
Clinical signs and symptoms include jaundice, conjugated hyperbilirubinemia, unconjugated hyperbilirubinemia, seizures (due to severe hypoglycemia), vomiting, failure to gain weight, hepatomegaly, lethargy, and hypotonia. 🩺💡
How is galactosemia diagnosed, and what is the treatment approach?
Galactosemia can be identified on routine newborn screening, although these results are often not available in the first week of life. 🩺📅
Supportive laboratory findings on presentation include nonglucose urine reducing substances suggestive of galactosuria, and absent GALT activity in red blood cells confirms the diagnosis. 🩸🩺📊
Treatment involves dietary elimination of galactose through the use of soy-based formula, which typically resolves end-organ dysfunction and results in a good prognosis. 🍼👩⚕️📈
What are the management strategies for neonatal hyperbilirubinemia based on its severity?
Mild neonatal hyperbilirubinemia is managed by maximizing feeding (e.g., every 2-3 hours). 🍼👶
Moderate hyperbilirubinemia is treated with phototherapy and may involve hydration (e.g., formula supplementation in breastfed infants, intravenous fluids) if the infant is dehydrated or has excessive weight loss. 🌞💧
Severe hyperbilirubinemia (bilirubin >20-25 mg/dL) necessitates exchange transfusion, which involves removing bilirubin and circulating antibodies and replacing most of the infant’s red blood cells with donor red blood cells. 🩸🩸
Indications for exchange transfusion include severe hyperbilirubinemia (>425 umol/L), rapid bilirubin rise despite phototherapy, anemia with a hemoglobin level below 10 g/dL, cardiac failure, hydrops, symptomatic bilirubin-induced neurologic dysfunction (BIND), or suspected kernicterus (e.g., lethargy, change in tone). 🩸🩸💉🏥🧠
What are common presenting features of Hirschsprung’s Disease?
Common presenting features of Hirschsprung’s Disease include:
Delayed passage of meconium (more than 48 hours in healthy term neonates)
Neonatal bowel obstruction (distended abdomen, bilious vomiting, fever, etc.)
Neonatal bowel perforation (features of perforative peritonitis)
Neonatal enterocolitis (sudden onset of diarrhea with foul-smelling stools, abdominal distension, fever, etc.)
Constipation in older infants and children, often refractory to treatment. 🩺👶🍼💩
What are the presenting features of neonatal bowel obstruction due to Hirschsprung’s Disease?
Neonatal bowel obstruction in Hirschsprung’s Disease presents with a distended abdomen, bilious vomiting, fever, dehydration, lethargy, failure to pass meconium, and occasionally visible dilated peristaltic loops upon abdominal examination in neonates with a normal anus. 🩺👶🤢🌡️🍼
How does neonatal bowel perforation relate to Hirschsprung’s Disease?
About 5% of children with Hirschsprung’s Disease experience bowel perforation, often presenting with features of perforative peritonitis. Diagnosis can be challenging, requiring colon examination and seromuscular biopsies during exploration to confirm HD. 🩺👶🤕💉
What is neonatal enterocolitis, and how does it relate to Hirschsprung’s Disease?
Approximately 30% of neonates with Hirschsprung’s Disease develop enterocolitis, which presents with sudden-onset diarrhea, foul-smelling stools, abdominal distension, fever, lethargy, dehydration, and potential sepsis. Early diagnosis and treatment are crucial to avoid toxic megacolon and life-threatening complications. 🩺👶💩🤢🌡️
How should newborns be managed when exposed to maternal chickenpox 7 days before to 2 days after birth?
Newborns should receive Varicella-Zoster Immune Globulin (VZIG) 200 IU intramuscularly (IM) immediately after birth, preferably within the first 24 hours but up to 72 hours.
Discharge term neonates as soon as possible.
No isolation is required.
Encourage breastfeeding. 🩺👶💉🌡️🤱
How should neonates be managed when exposed to maternal chickenpox more than 2 to 28 days after birth?
If neonate is < 28 weeks gestation or < 1000 g birth weight, administer VZIG, preferably within 96 hours but it can be given up to 10 days post-maternal rash.
Due to increased risk in newborns of seronegative women, provide VZIG to neonates exposed to varicella between 2 to 28 days of age.
Discharge term neonates as soon as possible.
No isolation is required.
Encourage breastfeeding. 🩺👶💉🌡️🤱
Abdominal mass causing recurrent pain, tenderness on palpation - dx
ureteropelvic junction (UPJ) obstruction
Tumours are non tender
What is Marfan Syndrome, and what are its cardinal manifestations?
Marfan Syndrome (MFS) is an autosomal dominant connective tissue disorder. 🧬
It affects the cardiovascular, skeletal, ocular, skin, lung, and dura systems. 💔💀👀🦴👁
Cardinal manifestations of MFS include aortic aneurysm and dissection, ocular lens dislocation, and long bone overgrowth. 🫁🦴👁
Why is cardiac disease significant in MFS, and what is the initial diagnostic step for cardiac evaluation?
Cardiac disease is the leading cause of morbidity and mortality in MFS. 💔
An echocardiogram (cardiac ultrasound scan) is the most appropriate initial step for cardiac evaluation in suspected MFS. 🫁🔍
Echocardiography helps assess aortic root dilation (the most important) and mitral valve prolapse, common in MFS. Aortic root dilation is clinically more significant. 🩺🔍
What is the recommended approach for managing aortic dilatation in MFS, including treatment options?
Serial echocardiographic surveillance is indicated for all affected individuals. The frequency should be tailored to each person by their cardiologist. 🩺📈
Beta blockers are the first-line treatment for aortic dilatation in MFS unless contraindicated (e.g., in asthmatic patients). 🚑
If beta blockers are ineffective or contraindicated, second-line treatment options include verapamil or ACE inhibitors. 🩺💊
What should be the next step in the management of children presenting with vertigo?
Exlude epilepsy and CNS tumours
EEG and CT
What is Food Protein–Induced Allergic Proctocolitis (FPIAP), and what are its characteristics?
FPIAP is a non–IgE-mediated reaction typically triggered by proteins in cow’s milk, including casein and whey, found in standard formula. It can also occur in breastfed infants as breast milk contains maternal diet-derived proteins. 🍼🐄
Disease onset is insidious, with symptoms often appearing weeks (commonly at age 1-4 weeks) to months (up to age 6 months) after first exposure to the food allergen. 🗓️
A typical presentation involves well-appearing infants with painless bloody stools that may also be loose and mucus streaked. 💩
Symptoms that may indicate a different diagnosis include failure to thrive, profuse diarrhea, and forceful vomiting. This patient’s spit-up is likely due to physiologic gastroesophageal reflux. 🤢
How is FPIAP diagnosed, and how is the diagnosis confirmed?
FPIAP is primarily a clinical diagnosis based on the characteristic presentation and history of exposure to specific food proteins. 🏥
The diagnosis is confirmed when bleeding ceases after removing the trigger protein from the infant’s diet. 🚼
This confirmation supports the diagnosis of FPIAP, and the prognosis is generally excellent. 📈
Patients usually become tolerant of products containing the offending protein (e.g., milk, yogurt) by around age 1. 🥛🍦
