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Chapter: Medicine Study Notes : Paediatrics

Respiratory Tract Infections in Children

Common: During the first 3 years of life, a child may have up to 6 episodes of otitis media, 2 episodes of gastro-enteritis and 6 respiratory infections per year. 10 – 15% have 12 colds per year.

Respiratory Tract Infections in Children


·        Epidemiology: 

o  Common: During the first 3 years of life, a child may have up to 6 episodes of otitis media, 2 episodes of gastro-enteritis and 6 respiratory infections per year. 10 – 15% have 12 colds per year.

o  Other risk factors:

§  Breast feeding is protective

§  Passive smoking

§  Exposure to infection: older siblings, day care, etc

§  Socio-economic status (multifactorial)

o  95% of respiratory infections involve the upper respiratory tract and 90% are viral

o  But antibiotics prescribed in 70% of cases.  Leads to:

§  Unnecessary adverse effects: rashes, diarrhoea, thrush, plus more serious ADRs 

§  ­Cost

§  Antibiotic resistance ® major increases in cost.  Especially S pneumoniae and S. aureus 

§  Reduce unnecessary prescribing by developing guidelines, practitioner education, public relations and ¯OTC antibiotic sales (eg mupirocin) 

·        Pathogenesis: 60% due to rhinoviruses and coronaviruses, then RSV, parainfluenza viruses, influenza and adenovirus


Common cold


·        Starts with nasal congestion, throat irritation ® sneezing, watery nasal discharge

·        Low grade fever, malaise, cough, headache 

·        After 1 – 3 days nasal discharge becomes thicker and mucopurulent. This is part of the natural history of URTI and does not indicate a bacterial super-infection 

·        Generally improved by day 10, although cough (in 30%) and nasal discharge (in 40%) may persist for > 2 weeks

·        Numerous RCTs have consistently failed to show that antibiotics alter the course of the common cold


 Acute Otitis Media


·        = Infection of the middle ear cleft

·        Presentation: 

o  Eardrum opaque (not semitransparent), red, normal landmarks lost, bulging. But if kid is screaming, ear will be red regardless

o  Otalgia, otorrhoea, hearing loss

o  Systemic signs: fever, irritability 

o  If it ruptures, child will be instantly better (but parents will panic!). Acutely ruptured eardrum will heal in 24 hours 

·        Pathogens:

o  S pneumoniae (30 – 50%)

o   Non-typeable strains of H influenzae (20 – 30%)

o   M Catarrhalis (10 – 20%)

o   Viral (10 – 20%) especially RSV

o   Mixed bacterial/viral infections account for 50% of antibiotic failures

·        Treatment:

o   Without treatment, 70 –90% of infections resolve spontaneously

o   Those least likely to respond are:

§  Aged < 2 years

§  Those with constitutional disturbance (eg > 39 C)

§  Where S pneumoniae is the pathogen

·        Antibiotics: 

o   Should be directed against S pneumoniae: it is the most common pathogen, the least likely to resolve spontaneously, and the most commonly associated with mastoiditis. Amoxycillin for 7 – 10 days (?5 days just as good) is the treatment of choice, even when there are non-susceptible S pneumoniae isolates. Good penetration of middle ear. Erythromycin/cotrimoxazole if allergic. Main reason for antibiotics is to prevent rare complications 

o   For the 90 – 95% of otitis media that responds to antibiotics, 90% are due to spontaneous resolution

o   If < 2 years, constitutional disturbance and persistent symptoms > 48 hours:

§  Amoxycillin 15 – 30 mg/kg TID for 10 days (ie high dose).

§  If no improvement after 48 – 72 hours try Augmentin (cover H influenzae and Moraxella)

§  Main aim is to reduce the very small chance of suppurative complications

o   Treatment for Acute Otitis Media in children (NZ Guideline for Acute Otitis Media):

§  Main benefit from antibiotics is less pain on the 2nd or 3rd day in 1 in 17 kids, and failure to spread to other side in 1 in 17. No effect on pain on first day, prevention of recurrence or build up of middle ear fluid 

§  Side effects of skin rash, vomiting or diarrhoea are as common as benefits 

§  Recommendation: use Paracetamol, return to doctor if symptoms persist beyond 48 hours, and have ears checked in a month for persisting fluid (common in first several weeks) – this occurs in about 1 in 10 

o   Oral cephalosporins and 2nd generation macrolides don‟t penetrate the middle ear and/or have poor activity against S pneumoniae

·        Complications:

o   Mastoiditis in 0.1%.  Incidence is not increased by delayed treatment

o   Little evidence to suggest that untreated otitis media causes mastoiditis

o   Very rare: petrositis, labyrinthitis, facial palsy, subdural/epidural/brain abscess


Recurrent Acute Otitis Media


·        Risk factors for recurrent acute otitis media: childcare centres, passive smoking, family history, reflux

·        Management:

o   Ensure correct diagnosis

o   Reassure: spontaneous improvement in many after age 2 – 3 years and during summer

o   Limit passive smoking, discourage pacifier use

o   Encourage breast feeding in infancy

o   Antibiotic prophylaxis generally ineffective 

o   Avoid unproven therapies: antihistamines, decongestants, chiropractic, homeopathy and naturopathy 

·        Refer to paediatrician/ENT surgeon if febrile seizures, antibiotic intolerance, hearing loss/speech problems, underlying facio-cranial abnormalities

·        In the future, conjugate pneumococcal vaccines are likely to play an important role


Chronic Otitis Media with Effusion


·        = Presence of sterile or infected fluid in middle ear 

·        Chronic OME (=Glue Ear) if > 3 months. If it hasn‟t cleared by then, less likely to clear spontaneously.

·        Common up to age 5 or 6

·        Symptoms:

·        Incidental finding in asymptomatic child

o  Hearing loss and its effects: speech delay, slurred speech, failing at school, irritable, poor balance, falling over. But delayed language and cognitive problems related more to genetic and SES than previous otitis media 

·        Pathogenesis: eustachian tube dysfunction (not just blockage)

·        Sequalae of otitis media: Middle ear effusion:

o  In 70% after 2 weeks

o  In 50% after 1 month

o  In 20% at 2 months

o  In 5 – 10% after 3 months

o  Associated with mild hearing loss.

·        Treatment:

o  Effusion common after an ear infection.  Watch and wait

o  If bubbles behind ear drum then it‟s resolving itself

o  Drugs: antibiotics and decongestants not very effective

o  If persisting > 3 – 6 months:

§  Test hearing

§  Limit passive smoke exposure

§  Treat underlying allergic rhinitis/adenoidal enlargement with intra-nasal steroids

o  Refer after 3 – 6 months if hearing loss and:

§  Failure to respond to antibiotics

§  Recurrent acute otitis media

§  Persistent otalgia

§  Retraction pockets

§  Expressive/receptive language delay

§  Underlying cranio-facial abnormalities (eg Down syndrome) 

o  ENTs say grommets are the treatment of choice: Aerate middle air (®¯ CO2 ®¯squamous metaplasia ®¯goblet cells ®¯effusion). Extrude over 18 months – 2 years. Take out if still there 5 yrs later. May take out adenoids at same time ® ­eustachian tube function (Paediatricians say adenoidectomy is treatment of choice). 

o  Precautions with grommets:

§  Plug ears when washing hair and bathing

§  Can swim in clean fresh water but no diving below the surface 

·        Chronic Suppurative Otitis Media – with hole in drum. Treatment: get rid of infection then surgical repair



·        Almost 100% given broad-spectrum antibiotics.  Inappropriate in 90% of cases

·        Pathogens: 

·        Viruses: Adenovirus, also rhinovirus, coronaviruses, RSV, Parainfluenza virus, influenza, enteroviruses, EBV 

·        Bacteria: S Pyogenes (GABHS = Group A Beta-Haemolytic Strep) in about 20 – 30% of cases, predominantly in those over 4 years

·        Differentiating (at best 70% predictive accuracy):

·        Exudative tonsillitis: Adenovirus, GABHS, EBV 

·        > 4 years, enlarged tender anterior cervical lymph nodes and diffusely inflamed pharyngeal structures (+ exudates) suggests S Pyogenes 

·        Diffuse, sandpaper-like red rash, accentuated in skin creases (Pastia lines) suggest Scarlet Fever. See Streptococcus Pyogenes (Group A, b Haemolytic) 

·        Nasal discharge, cough, hoarseness, conjunctivitis or diarrhoea +/- fever +/- tonsillar exudates suggests virus

·        Throat swabs: usually identify organism, but 10 – 50% are carriers

·        Treatment: 

·        Aim: Prevent acute rheumatic fever, suppurative complications (peri- or para tonsillar abscess) and hasten recovery

·        But

o   Only benzathine penicillin has been shown to reduce RF – and this was in military personnel

o   No convincing data which shows antibiotics reduce the risk of rare suppurative complications

o   Antibiotics reduce symptoms by 8 hours only 

o   Reinforces the notion that antibiotics are effective and increases the likelihood of their future use for trivial illnesses 

·        If high risk for RF (eg Maori, PI, > 4 years of age) take swabs or treat empirically. However, prescribing penicillin for sore throat hasn‟t altered the rates of RF, and many children with RF haven‟t consulted their doctor 

·        S Pyogenes: penicillin, 500 – 1000 mg BID for 10 days (Allergy: erythromycin)


Acute Sinusitis


·        Uncommon.  Bacterial sinusitis complicates 0.5 – 5% of viral upper respiratory tract infections 

·        With most colds, nasal discharge and obstruction are improving after 2 weeks. Children with acute sinusitis will not be improving

·        A minority present with high and persistent fever, periorbital swelling, facial and dental pain

·        Imaging:

o   Plain x-rays don‟t differentiate well between common cold and sinusitis

o   CT more useful.  Air-fluid levels, opacification, mucosal thickening > 4 mm 

·        Maxillary and ethmoid sinuses present at birth (although small). Frontal and sphenoid sinuses begin at 4 – 6 years of age

·        Pathogens: S pneumoniae (30 – 70%), H influenzae (20%), M Catarrhalis (20%), virus alone (10%)

·        Treatment:

o   High spontaneous cure (60% by 10 days vs 85% with amoxycillin)

o   Treat for S Pneumoniae in children with persisting symptoms which are not improving 

o   Amoxycillin 15 – 30 mg/kg TID for 5 days. Higher limit if < 2 years, attend child-care, or have received antibiotics in the last month in areas with > 10% penicillin resistance 

o   Consider Augmentin, co-trimoxazole, cefuroxime or ceftriaxone if no improvement after 48 – 72 hours




·        Inflammation in bronchial mucosa ® productive cough

·        Most cases are from viruses (eg RSV) 

·        Numerous studies have not found any evidence to support antibiotic treatment (but they‟re usually prescribed….) 

·        Production, colour or culture or sputum does NOT predict aetiology

·        Consider treatment if: 

o   Prolonged cough in older child: ?M pneumoniae ® erythromycin

o   Pertussis and cough < 4 weeks: erythromycin (or co-trimoxazole) reduces infectivity

o   Cystic fibrosis/other chronic lung disease: tailored antibiotics 

o   Prolonged cough (> 8 – 12 weeks and not from URTI): investigate for asthma, Tb, pertussis, CF, foreign body, Subacute-sinusitis, psychogenic cough




·        = Laryngotracheobronchitis 

·        Pathogens: Usually viral: Parainfluenza 1 and 2 are the most common. Measles and influenza are the most severe. Don‟t give antibiotics

·        Presentation:

o   Child < 5 years

o   Coryza and fever over 1 – 2 days 

o   Then characteristic harsh “barking” cough, hoarseness +/- signs of upper airway obstruction (stridor, respiratory distress), inspiratory stridor

o   Worse at night, and peak on 2nd or 3rd night. Varies hour to hour (ie don‟t send them home just yet…)

o   Lasts 3 – 4 days then changes to sound productive.  May last for another 2 weeks

·        Differential:

o   Epiglottitis: Absent/minimal cough, low-pitched expiratory snore

o   Bacterial tracheitis: toxic appearing, older child, high fever, brassy cough, stridor, tender trachea

o   Laryngeal foreign body: sudden onset, unable to vocalise

o   Angioneurotic oedema: associated signs usually present

o   Retropharyngeal abscess: High fever, dysphagia, hyperextension of neck

·        Assessment:

o  Severe if restless, anxious, pallor, lethargy, tachycardia, tachypnoea, indrawing, cyanosis or ¯breath sounds 

o  Loudness of stridor is not a reliable guide to severity of obstruction 

o  ­Risk of obstruction if: pre-existing upper airway narrowing (eg sub-glottic stenosis) or Down Syndrome 

·        Management:

o  Avoid distressing the child, settle them on parent‟s lap

o  Blood tests, pulse oximetry, O2 masks and nebulisers rarely needed

o  Mild:

§  Not distressed, no stridor at rest 

§  No treatment, management at home, return if signs of ­obstruction, lots of comfort

§  Paracetamol

o  Moderate: 

§  Frequent barking cough, distressed, persistent inspiratory stridor, tracheal tug or sternal retraction at rest, but no signs of hypoxia

§  Observe or admit 

§  Steroids (Dexamethasone or betamethasone 0.6 mg/kg orally or im, prednisolone 1 mg/kg) orally. May be repeated 12 – 24 hours later (but consider alternative diagnoses first)

§  Disturb child as little as possible

o  Severe:

§  Signs of obstruction, hypoxia (restless, irritable, anxious, cyanosis), ¯breath sounds

§  ?ICU admission

§  Nebulise adrenaline + Steroids (Prednisolone 1 mg/kg/day)

§  Monitor closely




·        Caused by Haemophilus Influenza Type B

·        Incidence ~ 20 cases pa (dropped from 160 in 1992 prior to vaccination)

·        Presentation:

o  Incubation for 2 – 4 days

o  Acute, febrile illness, toxic looking child 

o  Snore, mouth always open, drooling, prefers to sit upright. Soft inspiratory stridor, louder expiratory stridor

o  No cough (cf croup)

·        Management:

o  Blood cultures

o  Intubate first, then give iv antibiotics (if given first, pain ® panic ® respiratory arrest) 

o  Cefotaxime 25 – 50 mg/kg/8hr iv (max 2g) due to ­penicillin resistance

o  Amoxycillin 50 mg/kg/4 hr iv (max 2g) if penicillin sensitive

·        Other illnesses caused by H Influenzae type B: 

o  Meningitis: 5% mortality, 10% with sequalae (retardation, seizures, hearing loss, etc), 20 – 30% have functional disabilities (eg learning difficulties)

o  Also pneumonia, empyaema, septic arthritis, periorbital or facial cellulitis

·        Vaccination: 

o  Prior to immunisation was the most common cause of life threatening bacterial infection < 5 years of age. 

o  Herd immunity now works well

o  Subunit vaccine is 95% effective.  Few side effects (< 5% with local reactions)

o  Notifiable disease




·        Bordetella Pertussis = Whooping Cough

·        Epidemiology:

o  Highly contagious.  Regular epidemics every 3 – 5 years in NZ

o  Incidence: up to 5000 cases a year (only a small proportion notified)

o  In first year of life 80% are hospitalised and 0.2% die

·        Presentation:

o  Phases:

·        Incubation 2 – 3 weeks

§  Coryzal phase: ~ 1 week

§  Paroxysmal phase: 

·        Develops into paroxysmal bouts: unprovoked cough followed by inspiratory gasp (whoop), apnoea, vomiting. 

·        Thick tenacious sputum ® can‟t clear ® coughing spasm. Whoop may be absent in infant. If severe may need suction 

·        In between paroxysms looks well, is afebrile and has no chest signs

·        Median length: 6 weeks.  Can be up to 12 weeks

·        Infectious for 2 – 3 weeks of paroxysmal phase

o   Persistent cough for 3 – 4 months (convalescent phase – bacteria cleared) 

·        Treatment: if < 4 weeks duration: erythromycin. Doesn‟t impact illness after paroxysmal phase is established, but will ¯ infectivity

·        Admit if under 6 months and/or cyanosis or apnoea in paroxysms

·        Complications:

o   Anoxic seizures in 1 – 3% 

o   Encephalopathy in 0.1 – 0.3% ® retardation, spasticity and seizure disorders. Rate of severe neurological complications of immunisation negligible compared with the risk of encephalitis from whooping cough 

·        Vaccine: 

o   Whole cell vaccine effective in 60 – 90%, has higher efficacy for more severe outcomes, local reactions or fever in 50%. 1 in 1 million are associated with an encephalopathy (? No causal relationship established) 

o   Acellular pertussis has higher efficacy and is better tolerated (< 10 – 15% adverse reactions) – now being introduced




·        Epidemiology

o   Classically RSV 

o   Highly infectious acute viral respiratory illness in kids 2 weeks to 12 months of airways < 1 mm diameter

o   Epidemics every winter with RSV, also parainfluenza, influenza and adenoviruses

o   Major cause of URTI in kids: up to 50% of 1 year olds have had RSV infection

o   Seasonal in winter/spring

·        Presentation:

o   Short incubation: 3 – 4 days

o   Contacts: older siblings will have had nothing more than a snotty nose

o   Difficulty with expiration (cf Croup – inspiratory) 

o   Typical pattern: Starts as URTI - 1 day of runny nose, 1 day of cough, then wheeze. Illness/breathlessness worst on 4th day of wheeze (6th or 7th day of illness) 

o   Low-grade fever, non-toxic, cough, wheezy, difficulty feeding, hyperinflated chest, diffuse fine inspiratory crackles and expiratory wheeze 

o   If more severe then ­irritability, pallor, pulse > 160/min, respiratory rate 50 – 70/min, expiratory grunt (not stridor), head nodding, more marked retractions 

o   Respiratory failure in 1 – 2%: pallor, sweating, drowsiness, ¯respiratory effort, ¯breath sounds, apnoea. Cyanosis is a late sign 

o   Feeding a good indicator of respiratory distress (and one which parents can monitor at home)

o   Recurrence common (?hypoplastic airways and smoke exposure)

o   Usual recovery is 7 – 10 days 

o   Can get repeat viral illness – in which history suggests fluctuation – getting better, then got worse again, etc 

·        Distribution of LRTI from RSV:

o   Bronchiolitis: 40 – 90%

o   Pneumonia: 5 – 40%

o   Tracheobronchitis: 10 – 30%

·        Risk factors for severe presentation:

o   < 6 weeks old

o   Older siblings

o   Maternal smoking

o   Preterm delivery

o  Underlying conditions: congenital heart disease, chronic lung disease of infancy, congenital abnormalities, immunodeficiency

·        Differential: 

o  Recurrent bronchiolitis, history of eczema, strong family history of atopy Þ ?asthma. Trial of nebulised salbutamol. 

o  Persistent cough, failure to thrive Þ cardiac disease, cystic fibrosis, structural lung disease, aspiration, immunodeficiency 

·        Investigations:

o  Nasopharyngeal aspirate for culture and viral immunoflouresence

o  Bloods for culture and serology 

o  Imaging: CXR shows hyperinflation, peribronchial thickening, often patchy areas of consolidation and collapse. Hyperinflation and wheeze differentiate it from pneumonia

·        Treatment:

o  Not bronchodilators, steroids, ribavirin or antibiotics

o  Symptomatic treatment: O2, rehydration, minimal handling

o  Can go home if they‟re feeding OK and don‟t need O2 

o  Admit if respiratory distress, difficulty feeding, or adverse social circumstances. If sending home early in the illness, arrange for review within 24 hours 

o  Put on NG feeds: not hungry ® ¯distress 

o  If respiratory rate > 70/min and feeding poorly then IV or NG fluid at 50 – 75% of maintenance requirements (risk of SIADH) 

o  If oximetry < 92% then O2 

o  If severe, monitor blood gases, consider CPAP or ventilation (especially chronic respiratory/heart disease)

o  Maybe wheezy for 2 weeks and a cough for 4 weeks




·        Epidemiology: Peak incidence in first 2 years, and in Maori and PI children

·        Presentation:

o  Initial prodromal coryzal symptoms for a few days

o  Fever, cough, tachypnoea, signs of consolidation 

o  Young children may present with predominantly systemic features: fever, lethargy, vomiting, abdominal pain 

o  Older children may have headache, pleuretic chest pain, irritating cough, maybe abdo pain if lower lobe or even signs of meningism if upper lobe

o  Severe if: 

§  Toxic: lethargy or ¯arousal, circulatory compromise, abnormal respiration (eg apnoea, cyanosis) 

§  Respiratory distress: pallor, restless, agitated, nasal flaring, grunting, head nodding, chest wall recession, paradoxical abdominal movement, difficulty feeding

·        Signs on exam:

o  In infants: may be few signs, usually limited to a few focal crackles 

o  Older children: ¯chest wall movement, ¯breath sounds, fine crackles, later dull to percussion and bronchial breath sounds 

·        Pathogens:

o  Viruses are the most common cause in infants and young children:

§  RSV and Parainfluenza 3 most common 

§  Suggested by: infant or young child, coryzal prodrome, mild or moderate constitutional disturbance, hyperinflation and diffuse inspiratory crackles, patchy consolidation on CXR 

§  Rarely, infections with influenza A, adenovirus 3, 7 or 21 can be severe leading to death or severe lung damage

o  Bacterial:

§  S pneumoniae most common bacteria

§  S aureus uncommon but severe, H influenzae uncommon 

§  M pneumoniae common in school age children, insidious onset including anorexia, headache, scattered fine inspiratory crackles, bilateral 

§  S pyogenes: typically follows Varicella, influenza A or measles, protracted course and often empyema

§  Chlamydia: in 1st 2 months. Vertical transmission + eye infection in first 5 – 7 days.

·        Investigations:

o   Imaging: CXR to:

§  Confirm diagnosis

§  Detect complications: pleural effusion, pyopneumothorax, lung abscess

§  Exclude other causes: congential lung lesions, lung abscesses

o   Blood cultures before antibiotics

o   Nasopharyngeal aspirate for RSV detection

o   Serology for M pneumoniae or RSV 

o   Aspiration of pleural fluid (assists diagnosis, and is therapeutic – antibiotics won‟t penetrate a large effusion)

·        Treatment:

o   Penicillin G is the treatment of choice for uncomplicated bacterial pneumonia (unless allergy). 

o   Despite 20% of S pneumonia‟s showing reduced sensitivity, concentrations in the serum and lung tissue exceed the MIC by several fold. More treatment failures are associated with erythromycin and co-trimoxazole 

o   Admit if any of:

§  < 2 years

§  Signs of toxicity, hypoxia, respiratory distress

§  Extensive consolidation or an effusion

§  Clinical or x-ray signs of Tb

§  Adverse social circumstances, no transport or no access to phone

§  If sent home, then review within 12 – 24 hours

o   For uncomplicated bacterial pneumonia: Penicillin G 25 – 30 mg/kg/6hr iv (max 2.4g) 

o   If not afebrile within 24 hours on penicillin G, then review microbiology results, repeat CXR, consider other causes and treatments. Treatment failure: consider Viral, Mycoplasma, S aureus, resistant H influenzae 

o   Supportive therapy: minimal handling, careful fluid management (max 50% of maintenance fluids if IV), O2 

o   Management of pleural effusion. Before antibiotics do diagnostic aspiration and urgent gram stain. Discuss with paediatric surgeon: 

§  Thin clear fluid: aspirate as much as possible

§  Thin purulent fluid: intercostal drain 

§  Thick purulent fluid: loculates so drain won‟t work Þ thoracotomy (consider flucloxacillin +/-Cefotaxime) 

§  Infected effusion = Empyema = pus in pleural cavity

§  Fibrous septae will form around empyema = loculated empyema


Tb Pneumonia


·        Rarely presents as acute pneumonia

·        Consider if:

o   Known exposure to Tb

o   Child or family born in an endemic area

o   > 4 week history of cough, especially if fever, sweats and weigh loss

o   Refractory pneumonia

o   Suggestive CXR

·        Nurse in respiratory isolation:

o   Virtually all child cases are primary and non-infectious with a small burden of disease 

o   But adolescents, those with extensive or cavitating disease, or infected visiting family are infectious

·        Investigations:

o   FBC, ESR, electrolytes, CR and LFT

o   Mantoux test 

o   Specimen collection: sputum if available. Early morning gastric aspirates better than lavage. Also consider urines, pleural biopsy and LP

·        Empiric treatment: isoniazid, rifampicin, pyrazinamide

·        Notify to Medical Officer of Health

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