Respiratory Flashcards

1
Q

List 5 causes of airway compromise in kids?

A
  1. Anaphylaxis → oedema, urticaria, shock, diarrhoea
  2. Epiglotittis → need immediate anaesthetics and ENT support → give ceftriaxone + adrenaline – don’t upset the
    child
  3. FB
  4. Diphtheria
  5. Croup → viral infection → dexamethasone, if severe, give adrenaline nebs
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2
Q

What do the following suggest:

  1. Wheeze alone →
  2. Creps alone →
  3. Wheeze and Creps →
A
  1. Wheeze alone → asthma
  2. Creps alone → pneumonia
  3. Wheeze and Creps → Bronchiolitis
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3
Q

What are the most common causes of tonsillitis? How do you distinguish
.

A

commonly group A β haemolytic streptococcus and EBV.

More likely to be bacterial if → there is constitutional disturbance (headache, apathy, abdo pain), white exudate, cervical lymphadenopathy
o Not possible to clinically distinguish between the two

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4
Q

What are the first line ivx for tonsillitis?

A
  1. Throat culture
  2. Rapid strep antigen test -

This test should be ordered in children over 3 years old and adults with high probability of group A beta-haemolytic streptococci (GABHS) infection, as assessed by at least three Centor criteria.
Lower sensitivity than culture. So confirm with culture. But faster result

If suspecting ebv:
Blood film - Atypical activated lymphocytosis - ebv
Serology- ebv IgM
FBC - Anaemia, low platelets
Mono spot test - positive
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5
Q

How do you treat tonsillitis? What must be avoided n why?

A

If not due to alpha haemolytic strep. - pain killers

Give ABX if severe / alpha strep→ Phenoxymethylpenicillin

or erythromycin/clarithromycin if pen allergic

  • Avoid Amoxicillin as can cause maculopapular rash if infectious mononucleosis (EBV)
  • Low threshold to give ABX in infants, immunosuppressed

If not severe but:
o If group A streptococcus (GAS) has been confirmed → after rapid antigen testing or strongly suspected after applying a FeverPAIN score (4 or 5) or Centor score (3 or 4) and results of throat cultures are pending → consider prescribing ABX

severe recurrent tonsillitis → more than 7 in 1 year or more than 5 per year for 2 years, with no clear explanation → refer to ENT to consider tonsillectomy

• Advise adequate fluid intake, ibuprofen/paracetamol, salt water gargling/lozenges with LA for pain relief

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6
Q

How does otitis media present? What would you see on otoscopy?

A

May present with otalgia, irritability, decreased hearing, anorexia, vomiting, or fever, usually in the presence of an ongoing viral respiratory infection.

NO DISCHARGE

Otoscope:
Bright red bulging tympanic membranes - can be white, yellow, pink or red, loss of normal light reaction ± perforation and pus

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7
Q

What are the most common causes of acute otitis media?

A

The most common bacteria responsible for AOM are
Streptococcus pneumoniae (approximately 40%),
non-typable Haemophilus influenzae (25% to 30%),
Moraxella catarrhalis (10% to 15%)

Remember these follow, respiratory viral infections - URT
o RSV
o Rhinovirus

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8
Q

What is the pathophysiology of acute otitis media?

A

Viral and bacterial co infection:

Kids get an URT, this affects nasal passages. Exudates forms in middle ear and becomes infected with nasopharyngeal bacteria

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9
Q

What is the admission criteria in otitis media?

A

: <3 months with temperature 38+ (suspected meningitis); 3-6 months with temperature 39+ or systemically unwell

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10
Q

How is otitis media managed?

A

Paracetemol or NSAID for pain and fever
• Ideally NO ABX or delayed ABX prescribing

o Can give a 5 day course of
amoxicillin PO to parents to give if no improvement in symptoms after 4 days of onset of symptoms or if there is significant worsening → if pen allergic
give clarithromycin or erythromycin

Give immediate ABX if systemically unwell
or other co-existing condition which may increase risk of serious complications

2nd line → Co-Amoxiclav

Recurrent - ENT referral. Don’t swab chronic OM

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11
Q

Dull retracted eardrum with fluid meniscus, flat trace on tympanometry, conductive loss on audiometry is indicative of?

A

The result of recurrent AOM infection :

otitis media with effusions (glue ear) with decreased hearing (eustachian tube dysfunction)

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12
Q

What is chronic supprapurative otitis media? presentation. and ivx? treatment?

A

Chronic suppurative otitis media (CSOM) is defined as ‘a chronic inflammation of the middle ear and mastoid cavity, which presents with recurrent ear discharges (otorrhoea) through a tympanic perforation’. CSOM is assumed to be a complication of acute otitis media (AOM).

not the same as glue ear!

-> will NOT have fever or pain!!

Otoscope: perforated eardrum
Weber’s test: lateralises to that ear. hearing loss (difficulty in school).

Refer to ent don’t swab
Rex; abx, steroid - TOPICAL

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13
Q

What is a Grommet?

indications?

A

Grommets are tubes used for treating glue ear - otitis media with effusions.

OM/Effusion mx: arrange hearing test, leave for 3 months

Named grommets due to shape. Aka Tympanostomy tube.

It drains fluid away from the middle ear and keeps the eardrum open/airated.

Indications;
Chronic otitis media with effusions for 6months (1 ear)
- for 3 months (both ears)

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14
Q

What presents as :

  • Barking cough, harsh stridor, hoarse voice
  • Preceded by fever and coryza, onset is over days
  • No drooling

Cause?

A

Croup - Viral laryngotracheobronchitis

Most commonly due to parainfluenza virus
(also RSV, human metapneumovirus, influenza*)

eg HiB - haemophilus influenza B

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15
Q

How do the different levels of croup present?

A

Mild croup: barking cough
Moderate: + stridor/sternal recession at rest
Severe: + agitation/lethargy, sternal/intercostal recession

stirdor - is on inspiration

0-2pts (mild); 3-7pts (mod); 8-11pts (severe); Westley croup severity score.

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16
Q

What are the signs of Impending respiratory failure - in croup ?

Admission criteria?

A

12-17 pts on Westley croup severity score.

↑ obstruction, asynchronous chest wall and abdominal movement, ↑RR of 70, pallor, cyanosis, ↓ consciousness

Admit if: moderate or severe illness; RR>60; other co-existing conditions, < 3 months, concern regarding carer’s ability to cope.

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17
Q

How is croup managed?

A

PO Dex OR nebulised budesonide,
Nebulised adrenaline if more serious

If severe → supplementary O2
• If respiratory compromise → oral dexamethasone (0.15mg/kg)
• If too unwell → consider IM dexamethasone or inhaled budesonide to reduce severity and duration

• If moderate → adrenaline nebs can provide transient improvement
o Risk of rebound 2h later so needs close monitoring
o Observe on day unit until respiratory distress settles

• If mild → oral dex, advise that symptoms usually resolve within 48h, encourage fluid intake and check on child
regularly (overnight)

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18
Q

What are the complications of UPPER RESPIRATORY TRACT INFECTIONS in kids?

A

Complications
• Difficulty in feeding in infants as their noses are blocked, obstructing breathing
• Febrile seizures
• Acute exacerbation of asthma

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19
Q

What is the Most common infection of childhood? Pathophysiology?

A

Rhinitis / common cold:

inflammation of URT mucosa, involving nose, throat, sinuses or larynx

Rhinoviruses (50%); coronaviruses (10%);
influenza (5%); parainfluenza (5%); respiratory syncytial virus, RSV (5%)

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20
Q

What is the management of rhinitis? Complications?

A

Health education → Self-limiting, no specific treatment → may reduce anxiety and unnecessary visits to Dr
• Pain → paracetamol or ibuprofen
• Potentially decongestants or antihistamines

Cough may last 4 weeks after cold

Complications - otitis media, acute sinusitis

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21
Q

How does acute sinusitis present ? Rx?

A

Majority of cases in adults and children are of viral aetiology.
Duration of symptoms more than 10 days often indicates bacterial cause.

Purulent nasal discharge (brown, yellow etc), nasal obstruction/ stuffiness

If they get a 2ndary bacterial infection due to the viral infection → pain, swelling, tenderness over cheek due to infection of maxillary sinus

Frontal sinuses NOT involved / developed

Rex: pain relief, abx (if immunocompromised or severe)
- saw in GP; dont get ent referall unless >7 in 1yr

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22
Q

Which condition presents as follows:

Hoarseness, dysphagia, sore throat, odynophagia, cough, GORD, rhinitis, fever, lethargy, fatigue
• Lymphadenopathy (ant cervical chain), post- nasal drip, SOB

Risk factors and ivx?

A

Laryngitis

Risks:
incomplete or absent Haemophilus influenzae type B (Hib) vaccination or Diphtheria, contact and travel,
preceded by urti !!!

Ivx:
clinical Dx mostly, BUT laryngoscopy (± biopsy)

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23
Q

List causes of laryngitis? Rx?

A

Causes may be infectious or non-infectious (e.g., vocal strain, reflux laryngitis, chronic irritative laryngitis).

Haemophilus influenzae is one of the most frequently isolated bacteria. Other causes include tuberculosis, diphtheria, syphilis, and fungi

Viral
o Supportive care – voice rest and hydration
o Paracetemol
o Guaifenesin – expectorant
o Codeine sulphate – antitussive

• Bacterial
o Same as above, with Abx – phenoxymethylpenicillin

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24
Q

What is acute epiglottitis? How does it present?

A

It is an URTI

Life-threatening emergency – high risk of AIRWAY obstruction.

Caused by haemophilus influenzae type B (universal Hib imm has led to a 99% reduction).

Very acute onset (over hours)- so may be well in the morning and shortly afterwards is unwell

no preceding coryza
high fever in ill or TOXIC looking child, absent cough

  • Subcostal, intercostal recession or sternal retraction (pic)
  • Unable to drink, speak, swallow, drooling saliva (due to pain in throat)

soft INSPIRATORY stridor

• Child sitting immobile, upright, mouth open, tripod positioning (they do this to open airway)

Pertinent diagnostic criteria include the classic ‘tripod’ seating position of the patient, drooling, high fever, and a toxic appearance.

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25
How do we ivx acute epiglottitis?
: Laryngoscopy (Dx and therapeutic - because can establish airway - do in theatre); Lateral neck X-ray - thumbprint sign cultures; - neutrophilia/ left shift oximetry and monitoring; gases
26
How do we manage acute epiglottitis?
Urgent hospital admission – senior anaesthetist, ENT, paeds • Secure airway, then supplementary O2 → visualise & intubate with GA * Then, blood cultures and IV ABX (ceftriaxone/cefuroxime or local guidelines) * ± dexamethasone
27
What causes whooping cough?
gram negative bacterial, Bordetella pertussis.
28
How does whooping cough present? Risk factors?
An URTI with severe cough Initial symptoms may be similar to a cold, with rhinorrhoea and lacrimation, or a dry cough followed by episodes of severe coughing. Fever may be absent or low-grade. Week long coryza (catarrhal phase), then paroxysmal cough followed by inspiratory whoop ± vomiting (post gussied vomiting) ± epistaxis Early phase - Rhinorrhea 1-2wks later - cough 3wks+ - inspiratory whoop * Symptoms worse at night, child may go red/blue in face * Infants may have apnoea rather than a whoop Inspiratory whooping is a characteristic symptom in children but may be absent in infants, adolescents, and adults. * Symptoms gradually decrease (covalescent phase) but can persist for months * RF: not vaccinated (should have DTaP at 2, 3 and 4 months), contact with infected
29
Admission threshold in whooping cough?
• Admit if <6 months and acutely unwell, significant breathing difficulties (severe paroxysms, apnoea episodes, cyanosis) o Need isolation on ward - remain culture positive 3-4 weeks even with vaccine / rx. can affect adults
30
What are the ivx for whooping cough?
1. per-nasal swab/ nasopharyngeal swab AND culture Culture of the bacterium Bordetella pertussis from nasal secretions can confirm the diagnosis, especially early in the course of the disease. A negative culture does not exclude the diagnosis 2. Pcr of above More sensitive 3. Can consider serology
31
List some Other Bordetella species that may rarely cause pertussis or pertussis-like cough
include B parapertussis, B bronchiseptica, or B holmesii; these species are not vaccine-preventable
32
What are the Three identifiable stages typical in childhood pertussis? How do they present?
catarrhal, paroxysmal, and convalescent -> *
33
How do we manage pertussis?
• Macrolides - Azithromycin or Clarithromycin if started in catarrhal phase, onset of cough within previous 21 days * Give prophylaxis to close contacts, advise rest/fluids/paracetamol * Avoid school or nursery until 48 hours of ABX • Inform that even with ABX, whooping cough is likely to cause a protracted non-infectious cough that may take several weeks to resolve completely
34
What are the most common causes of pneumonia by age group?
* Viruses are more common in younger children, and bacteria in older children * Newborn eg <1month (group B strep), * Infants (mainly RSV, but also Strep pneumoniae, pertussis, H influenzae) - but note viral causes more common that bacterial (until age 5) so rsv> strep p * 5y+ (mycoplasma pneumoniae, streptococcus pneumoniae, chlamydia pneumonia
35
How does pneumonia present in kids?
* Fever, difficulty breathing, preceding URTI, cough, lethargy, poor feeding, ↑ RR, nasal flaring, chest indrawing * Consolidation → dull percussion, ↓ breath sounds, bronchial breathing
36
How do we manage paeds pneumonia? what is the admission criteria?
Supportive care → fluids, O2, analgesia Community acquired: Non-severe (based on clinical judgement - no scores) Kids 1 month + 1st line - Amoxicillin TDS 5 days Clarithromycin - if mild / pen allergic / atypicals Severe Co-amoxiclav TDS 5 days ``` o Broad spectrum IV ABX for infants – cannot be sure if viral or bacterial? Admit if o O2 sats <93% o Severe tachypnoea o Grunting o Apnoea o Not feeding o Increased drowsiness o Severe chest recessions o RR > 60 o Age <3 months o Temp 38+ ```
37
How do we ivx pneumonia in a child?
Cxray Your response exam and it’s components eg cyanosis etc Do we do sputum etc? *
38
Causes and epidemiology of RSV?
Bronchiolitis is the leading cause of hospital admission in infants under 1 year of age. Affects children <1yo; 30% of infants will get it → age from 0 months to 24 months • 80% are respiratory syncytial virus → RSV
39
How does bronchiolitis present ? Main differentiators from others?
Coryzal symptoms preceding a dry cough and increased breathlessness, feeding difficulty ± recurrent apnoea • ↑ RR, subcostal/intercostal recession, Differentiators: hyperinflation of chest (prominent sternum, displaced liver) * Fine end-expiratory crackles, high pitched wheeze, exp > insp, cyanosis or pallor * Worse on day 4-5 then starts getting better, lasts 10-14 days
40
Who is particularly at risk of bronchiolitis?
Premature borne, | bronchopulmonary dysplasia, underlying lung disease, CF, CHD (congenital heart disease)
41
How do we ivx bronchiolitis? Admission criteria?
Resp stuff- Degree of agitation, signs of cyanosis/accessory muscles, RR, HR, BP, hydration status, O2 sats • Admit if → agitation, severe respiratory distress, RR > 70, central cyanosis, sats <92 Not necessary but can do: • Virus can be identified by PCR of nasopharyngeal aspirate • CXR not indicated in straightforward cases but would show hyperinflation and air trapping
42
How do we manage bronchiolitis? prognosis?
Most cases are mild and self-limiting, and supportive care is the only indicated therapy. if very young and struggling with breathing : -> Give O2 (nasal cannula, can be humidified) (target sats above 92) . note if sats are high enough - dont need to give this! -> ± fluids (give orally if not tolerated - nasogastric, then IV) see bronchiolotic podium -> next card if older: o ± paracetamol or ibuprofen o May need oral steroids - if prior hx of wheeze o Don’t smoke in the house Prophylaxis: Palivizumab IM- humanised monoclonal antibody that binds to the F protein of respiratory syncytial virus (RSV) and inhibits viral infection and replication. - for the <1y/o & predisposed. Or <2 and immunosuppresed • Prognosis → most recover in 2 weeks – largely self-limiting
43
What is the bronchiolitic podium?
Escalation steps in regards to breathing and feeding Breathing 1. No support 2. O2 3. CPAP a. To open up heavy mucus airways closing at end of expiration b. CPAP will hold these open when max breath out c. Preopens airway – give when child is grunting (this is child self-creating CPAP) 4. Intubate and ventilate Feeding 1. Little and often 2. NG tube a. Still risk of vomiting and aspiration 3. IV fluids a. Completely removes pressure of having to feed on top of breathing 4. Intubate and ventilate
44
What is the aetiology of cystic fibrosis?
Defective CFTR (cystic fibrosis transmembrane conductance regulator) – cAMP dependent chloride channel, gene on Chr7 Delta F508 locus
45
What is the screening schedule for cystic fibrosis?
Newborn o Screening; heel-prick test (Guthrie) - you find; o Increased IRT (immunoreactivity trypsinogen) detected by - If raised then screened for common CF gene mutations - IRT wont be elevated anymore after 5 weeks of age Gold standard: Sweat test - for raised cl- ions
46
What is the presentation / complication of cystic fibrosis by age?
``` Infancy o Meconium (10-20%), prolonged jaundice, FTT, recurrent chest infections (pseudomonas aeruginosa), malabsorption, steatorrhoea ``` • Young child o Recurrent chest infections → leading to bronchiectasis, abscesses (persistent cough and purulent sputum), rectal prolapse, nasal polyp, sinusitis • Older child o ABPA, diabetes mellitus, cirrhosis, distal intestinal obstruction, pneumothorax, sterility (males) 90% have pancreatic exocrine insufficiency (lipase, amylase, protease) → maldigestion and malabsorption → decreased elastase in faeces -> presents with steatorrhea, poor growth etc.
47
How do we ivx cystic fibrosis?
Diagnostic test is the sweat test to confirm elevated chloride levels (60-125mmol/L in CF, normal is 10-40) • Confirmation with genetic testing • Can be diagnosed either o An Asymptomatic infant with IRT confirmed with sweat and gene, clinical manifestations and sweat and gene o OR clinical manifestations alone • CXR: hyperinflation, peribronchial shadowing, bronchial wall thickening, ring shadows
48
How is CF managed?
Have to monitor systems: Resp, Nutrional deficiencies, Metabolic (pancreas), Gonads (fertility), Psycological sx Respiratory o Increased monitoring with spirometry and symptoms watches. o Physiotherapy twice a day → airway clearance manoeuvres and devices + encourage physical activity o ± prophylactic oral ABX (azithromycin), prompt IV ABX with any symptoms or signs of infection o If end stage CF lung disease – transplant is the only option • Mucoactive agents if lung disease → hDNase1 (dornase alfa) if FTC>40% or mannitol dry powder for inhalation • Nutrition → regular assessment of dietary status, ORAL pancreatic enzymes (enteric coated pancreatic replacement therapy) to be taken with all meals and snacks, high calorie diet, fat soluble vitamins * Advise → managing risks of cross infection, fertility, implications for school/employment * Routinely monitor and watch for complications Insulin if diabetic. Fertility counselling. Transplant if needed.
49
What is the outpatient management of asthma?
Over 5: Step 1: SABA Salbutamol inhaler as required – SABA Consider stepping up when using salbutamol inhaler more than 3x a week Step 2: SABA + Low dose ICS (preventer) - Low dose inhaled steroid - budesonide Step 3: SABA + Low dose ICS + LTRA Step 4: SABA + Low dose ICS + LABA - Add in LABA – long acting B agonist (salmetarol) if 5y+ or oral Montelukast if <5y (leukotriene receptor antagonist - LTRA) ? Step 5: SABA + MART* * combined reliever, low dose ICS + maintenance Step 6: SABA + MART* - *with moderate dose ICS Step 7: SABA + MART - High dose ICS 4. Oral steroid in lowest dose to maintain control – usually prednisolone, managed by specialist ``` Under 5: 1. SABA 2. SABA+ Mod dose ICS try for 8 weeks. if not working think of diff diagnosis 3. SABA + Low dose ICS + LTRA 4. stop LTRA - > refer to specialist ```
50
Child is not coping well on basic outpatient management of asthma. What is next?
Check inhaler technique • What exactly has the parent tried, and how did they give it? • Do they know there are different inhalers and what they are for? * Try SPACER if there is no O2 need (sats >94%) * If they need O2 (sats<92%) then go for nebulised salbutamol. * Between 92 – 94 is a grey area and dependent on individual. - Maintain sats 94-98% ``` generally: if moderate - SABA by spacer (10 puffs via spacer - BURST technique - 1 puff every 30-60seconds ) If severe - nebulised SABA ```
51
How is severe/ life threatening acute asthma managed in over 2 years old? name some tehcniques used
Hospital admission 1. High flow O2 - if sats <94% 1a. SABA - nebulised Salbutamol 5mg - repeat in 20-30mins as needed 1b. Oral Prednisolone - given for all exacerbations - OD for 3-5 days - If cant take oral then IM - can cause vomiting so IV hydrocortisone may be used instead. If above fails add to SABA: 2. Nebulised Ipratropium bromide If above fails add: 3a. IV MgSO4 - if sats below 92% - single bolus 3b. PICU admission + IV salbutamol (bolus -> infusion) 4. IV Aminophylline - bronchodilator - if max doses of above don’t work Intubation/Ventialtion last line Mnemonic: O SHIT Me Oxygen, salbutamol, hydrocortisone, ipratropium bromide, Theo/aminophylline, magnesium
52
How is severe/ life threatening acute asthma managed in under 2 years old?
Hospital admission High flow O2 - is sats <94% 1. SABA - nebulised Salbutamol 2.5mg - repeat in 20-30mins as needed *note salbutamol are given with the O2 2. Nebulised Ipratropium bromide + nebulised? SABA (2.5mg) 2b. Oral Prednisolone 3. Speak to PICU / specialists
53
What are the paediatric criteria for severe asthma? and life threatening asthma? Near fatal asthma NICE guidelines
Severe acute asthma Can’t complete sentences in one breath or too breathless to talk or feed; SpO2  140/minute in children aged 1–5 years; heart rate > 125/minute in children aged over 5 years; Respiratory rate > 40/minute in children aged 1–5 years; respiratory rate > 30/minute in children aged over 5 years. Life-threatening acute asthma Any one of the following in a child with severe asthma: SpO2
54
What is the cause of the following in asthma: Transient wheezing Recurrent wheeze
Transient early wheezing. o Viral induced wheeze – small airways are more likely to narrow and obstruct with inflammation and aberrant immune response to viral infection. o Episodic nature resolves by 5y (pre-school wheeze) - usually rhinovirus - no future risk asthma You cant diagnose someone under 4yo with asthma - instead it is called viral induced wheeze. • Persistent and recurrent wheezing o Presence of IgE to common inhaled allergens, persistent wheezing past pre-school → atopic asthma, associated with other atopic diseases and FHx o Small number of non-atopic asthma
55
What are the clinical characteristics of asthma?
Expiratory polyphonic wheeze • Symptoms worse at night or early morning • Triggers → exercise, dust mites, pets • Interval symptoms – between acute exacerbations • Personal or FHx of atopy
56
In childhood, what may be the cause of a SLEEP RELATED BREATHING DISORDER?
upper airway obstruction secondary to adenotonsillar hypertrophy • Predisposition → hypotonia, muscle weakness, anatomical problem
57
How are SLEEP RELATED BREATHING DISORDERS investigated?
Overnight pulse oximetry to identify frequency and severity of periods of desaturation (92%) • ± limited polysomnography if more complex – add in HR, RR, airflow, PCO2
58
What is the atopic March?
Eczema and food allergy in infancy | • Allergic rhinitis and conjunctivitis and asthma in preschool
59
What are features of IgE mediated allergy?
Early phase, within minutes of exposure, due to release of histamine and other mediators from mast cells • Uriticaria, angioedema, sneezing, bronchospasm • Then last phase response may occur after 4-6 hours, with nasal congestion in upper airway, cough, bronchospasm in lower airway Non-IgE mediated immune response have delayed onset and more varied clinical course
60
How do we manage anaphylaxis starting in the community?
ABCDE assessment Call for help - Sit up - breathing difficulties - lie supine and lift legs; hypotensive - recovery position ; unconscious IM adrenaline (under 6 - 150mcg. 6-12 = 300mcg. >12 = 500mcg) Hospital: IV Fluids, high flow O2, IM Chlorpheneramine, IM hydrocortisone (follow the order above strictly!) Maybe salbutamol
61
What is food intolerance?
Non-immunological reaction caused by enzyme deficiencies, pharm agents or naturally occurring substances.
62
How do we manage allergic rhinitis and conjunctivitis?
1. 2-5y → give oral antihistamine (cetirizine, loratadine) as required, if 5y+ consider Azelastine (intranasal) 2. If persistent → advise to avoid causative allergen 3. Consider → intranasal corticosteroid 4. Consult again in 2-4w if symptomatic and inadequately controlled Can get syrup antihistamine for younger kids.
63
What is the aetiology and treatment of chronic urticaria?
Chronic urticaria → lasting more than 6 weeks. o Usually non-allergic, due to local increase in permeability of capillaries or venules o Changes dependent on activation of skin mast cells o Treatment: No airway involvement : - 2nd generation non- drowsy anti-histamines: loratidine, citirizine. Avoid allergen. Airway involvement: - + adrenaline
64
What is primary and secondary allergy and their causes?
Usually primary → child has failed to ever develop immune tolerance o Infants → milk, egg, peanut o Older children → peanut, fish, shellfish Can be secondary → initially tolerate, then become allergic later o Usually due to cross-reactivity between proteins in fruit/nuts and pollen → “oral allergy syndrome”
65
How does non-IgE food allergy present?
Non-IgE mediated → erythema, atopic eczema, GORD, change in frequency of stools, blood/mucus in stools, abdo pain, FTT, infantile colic, constipation, food aversion, pallor ASSOCIATED WITH FEEDS • Ask for personal or FHx of atopy, details of food avoidance, feeding history (age of weaning, breast/formula)
66
How do we investigate food allergy?
1. Skin prick allergy testing AND RAST (measurement of specific IgE antibodies) - only used if IgE mediated • Non-IgE are harder, rely on clinical history and exam 2• Can trial elimination of suspected allergen for 2-6 weeks then reintroduce 3• Consider endoscopy, intestinal biopsy Gold standard → exclusion of relevant food under dietician supervision followed by double blinded placebo controlled food challenge
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When do we Refer to specialist or secondary care in allergy?
if o FTT with GI symptoms, not responding to single-allergen elimination diet o More than 1 acute systemic reaction o More than 1 severe delayed reaction o Confirmed IgE mediated allergy and asthma o Negative tests but persistent clinical suspicion o Multiple allergies
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How do we manage allergy? anaphylaxis?
Avoid relevant foods • Advice from paediatric dietician to avoid nutritional deficiencies • Teach family and child how to manage an allergic attack o Written info + adequate training o Anti-histamines if mild o EpiPen – IM adrenaline if severe Anaphylaxis: 1. A-E approach* 2. 1:1000 IM Adrenaline 3. Check response at 5 minutes 4. Repeat IM as needed if inadequate 6. Consider Antihihstamine and steroid; IV chlorphenamine 20mg IV hydrocortisone 200mg - to prevent rebound anaphylaxis *may need O2, IV fluid
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What is cows milk allergy? Epidemiology? Types?
Cows' milk allergy (CMA), also called cows' milk protein allergy, is one of the most common childhood food allergies. It is estimated to affect around 7% of babies under 1, though most children grow out of it by the age of 5. CMA typically develops when cows' milk is first introduced into your baby's diet either in formula or when your baby starts eating solids. Not lactose intolerance More rarely, it can affect babies who are exclusively breastfed because of cows' milk from the mother's diet passing to the baby through breast milk. There are 2 main types of CMA: immediate CMA – where symptoms typically begin within minutes of having cows' milk. IgE mediated delayed CMA – where symptoms typically begin several hours, or even days, after having cows' milk. Non IgE
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How does cows milk allergy present?
A diagnosis of IgE-mediated allergy should be suspected, particularly if symptoms are multiple, persistent, severe, or treatment-resistant. Typical symptoms include urticaria, angio-oedema, itching, cough, hoarseness, wheeze, or breathlessness after cow's milk ingestion. A diagnosis of non-IgE-mediated allergy should be suspected if: There are one or more symptoms such as gatro-oesophageal reflux disease, abdominal discomfort, constipation, diarrhoea (+- bloody stools), or atopic eczema, particularly if symptoms are treatment-resistant. Anaphylaxis
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How do we manage cows milk allergy?
Refer to specialist allergy clinic Rid of cow milk from diet If your baby is formula-fed, your GP can prescribe special infant formula. If your baby is exclusively breastfed, the mother will be advised to avoid all cows' milk products. Reassess every 6-12 months if have outgrown it
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What is laryngomalacia?
Congenital abnormality of the larynx cartilage which predisposes to dynamic supraglottic collapse during inspiration of respiration → results in upper airway obstruction and stridor. • Most frequent congenital stridor in infants and cause ‘noisy breathing’ in infancy. NOT an infectious cause
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How is laryngomalacia investigated?
Monitor O2 sats ± flexible laryngoscopy if diagnostic difficulty to assess anatomy and comorbidities
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What is the management and complications of laryngomalacia?
Manage conservatively with close observation • Regular review and monitoring of growth • Tend to resolve by 18-24 months (although may initially worsen with age, max at 6-8 months) – 70% resolve by 1 year old Complications: respiratory distress, failure to thrive, cyanosis Endoscopic supraglottoplasty if airway compromise or feeding disrupted sufficiently to prevent normal growth.
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What are the causes of persistent pulmonary htn?
``` Usually associated with birth asphyxia, meconium aspiration, septicaemia, respiratory distress syndrome, may also be primary. ``` • As a result of high pulmonary vascular resistance → there is right to left shunting within the lungs and at atrial and ductal levels
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How does persistent pulmonary htn present and how do we ivx?
Cyanosis after birth Decreased 02 sats Absent heart murmurs and signs of HF Bradycardia, hypotension Resp distress: grunting, tacchypneoa, tacchycardia, etc IX: 1• Urgent Echo to visualise constricted pulmonary vessels to confirm DX, and rule out congenital HD 2• Can do CXR too→ normal heart size ± pulmonary oligaemia also check sats
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How do we manage persistent pulmonary htn?
Management: • Give O2 → refer to PICU • Most require mechanical ventilation eg CPAP and circulatory support * ± inhaled NO (vasodilator) * ± ionotropic support (adrenaline/ dopamine - to help heart beat harder to overcome bradycardia) * ECMO if severe but reversible – very specialist * Continuous monitoring of O2, BP, temp * Will also need NG tube for nutritional support * Then slow weaning off support and step down Prognosis → serious condition, mortality <10%, 25% likely to have some impairment such as learning difficulties, deafness
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What is the aetiology and epidemiology of NEWBORN RESPIRATORY DISTRESS SYNDROME?
AKA surfactant deficient lung disease * Lack of surfactant, so high surface tension in lungs * Air sacs collapse, so increased energy required for breathing * ± development of interstitial oedema and increased pulmonary HTN • Babies start producing surfactant at 24-28 weeks GA with enough to breathe by 34 weeks GA o More common in premmies – 50% if 28-32w GA o Also seen with diabetic mothers and LBW hyaline
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How does NEWBORN RESPIRATORY DISTRESS SYNDROME present?
* Cyanosis * Increased RR * Signs of respiratory distress * Emergency * CXR → distinct cloudy appearance of lungs
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What is the management and complications of NEWBORN RESPIRATORY DISTRESS SYNDROME?
``` Antenatal o Give steroids (dex) to mother if risk of delivery less than 34 weeks o Also tocolytics to delay premature birth if possible ``` • Postnatal o Transfer to neonatal unit for supplementary O2 or mechanical ventilation to keep sats between 91- 95% o + Artificial surfactant via ET tube !!! (otherwise alveolar collapse) + fluids, nutritional support * Increased risk of pneumothorax, pulmonary haemorrhage, lung scarring (BPD) * Brain damage due to hypoxia – risk of developmental disabilities.
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What is meconium aspiration and what are the risk factors?
* 8-10% will pass meconium before birth - should usually be after * Rare in preterm, increased risk the greater the gestational age * Can occur in response to fetal hypoxia ``` • RF: o GA > 42 weeks o Maternal history of HTN/PET/smoking/substance abuse o Fetal distress o Oligohydramnios o Meconium stained amniotic fluid o Chorioamnionitis ``` * Infants inhale thick meconium → lung irritant resulting in mechanical obstruction and chemical pneumonitis * Plus predisposing to infection
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How does meconium aspiration present? What is the ivx?
Present with respiratory distress (increased RR, chest retraction and hypoxia) Dx confirmed by CXR o Overinflated lungs with patches of collapse and consolidation • Increased incidence of air leak, pneumothorax and pneumomediastinum • FBC/CRP/Culture to rule out infection
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How do we treat meconium aspiration?
* Give O2 by hood or nasal cannula to keep sats >92% * IV fluids, NG feeds ± ABX (ampicillin, gentamicin) * Artificial ventilation often required * Increased risk of persistent HTN; * TX with inhaled NO and ECMO (extracorporeal membrane oxygenation)
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What is Bronchopulmonary dysplasia (BPD; formerly chronic lung disease of infancy) ?
Lung disease most common in preterm infants - who received help with breathing Prolonged high oxygen delivery in premature infants causes necrotizing bronchiolitis and alveolar septal injury, with inflammation and scarring. This results in hypoxemia common in infants with low birth weight (LBW) and those who receive prolonged mechanical ventilation to treat respiratory distress syndrome (RDS) There’s different levels of this from mild - severe
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How does Bronchopulmonary dysplasia present? What are the findings on ivx?
Physical findings: ``` hypoxemia; hypercapnia; crackles, wheezing, & decreased breath sounds; increased bronchial secretions; hyperinflation; frequent lower respiratory infections; delayed growth & development; ``` cor pulmonale; CXR shows with hyperinflation, low diaphragm, atelectasis, cystic changes.
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How do we manage bronchopulmonary dysplasia?
Diuretics O2 - if low O2 sats Viral immunisation
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What is QUINSY? How is it managed?
A quinsy is a peritonsillar abscess, a rare complication of bacterial tonsillitis. It is not inflammation of the tonsils, rather an abscess around the area. Patients present with a severe sore throat (worse unilaterally), with associated severe odynophagia. Associated symptoms include stertor - noisy breathing and trismus - lock jaw; in children, they can present in similar ways. On examination (often difficult due to trismus), there will be extensive erythema and soft palate swelling, with the anterior arch being pushed medially and a deviated uvula (Fig. 3). Patients should be admitted and started on intravenous antibiotics, with regular analgesia and topical analgesic throat sprays. All peritonsillar abscess will require either needle aspiration (following topical local anaesthetic) or an incision and drainage (with further opening via use of Tilley’s forceps) ABCDE approach, senior peads, ENT
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what might cause upper airway obstruction? what are possible signs?
Edema of airway above or below glottis. Foreign body signs: stridor, sternal recessions, suprasternal retractions
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suglottic edema will be a finding in which condition?
croup
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what might cause lower airway obstruction?
infection bronchospasm allergen - > inflammation
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what are the signs of lower airway obstruction?
prolonged expiratory phase of breathing wheeze Fast RR / tachypnoea
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list causes of pneumothorax in infants?
infection eg pneumocystis pneumonia PCP trauma mechanical ventilation; causes damage to lung parenchyma, forcing air out
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list signs of pneumothorax in infant?
assymetrical chest rise absent sounds in field of lung teension pneumothorax; distended neck veins - venous congestion hypotension poor perfusion
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difference between wheeze and stridor?
○ Stridor § Caused by EXTRAthoracic airway narrowing - upper airway issues § Predominantly INspiratory ○ Wheeze § Caused by INTRAthoracic airway narrowing - lower airway issues - Predominantly EXpiratory
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how do we ivx asthma?
O2 sats PEF (if over 5) ABG (if normal or high = exhaustion! concerning)
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what are the criteria for safe discharge from hospital for a kid with acute asthma ? what advice to give?
1. They are using inhaled SABA < 4hourly Advice: - Parent; monitor PEF - Safety net advice - must have GP follow up within 48hours of discharge: 1. will review sx, check inhaler technique, 2. currrent medications for optimisation (may quadruple ICS dose or prescribe oral steroids - usually specialist though) 3. Create a personalised asthma action plan
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if you had to increase dose of ICS for child and asthma is now well controlled more thhan 3 months, what should you do?
reduce dose of ICS gradually 25-50% each time every 3 months can stop ICS if good control + only taking ICS as maintenance
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how do we mx viral induced wheeze
Depends if already have asthma or not If not: Prescribe SABA + Spacer - PRN If asthma: Prescribe short course prednisolone PO If bacterial infection: Prescribe antibiotics safety net: check on kid regularly especially at night come to AnE if high RR, Work of breathing, reduced consciousness/ hard to rouse, poor feeding, worse fever Advice: parent stop smoking Follow up: Within 48 hours; check sx & PEF (>5ys)
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What is otitis externa?
diffuse inflammation of the external ear canal, which may also involve the pinna or tympanic membrane
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What is the cause and presentation of otitis externa?
Most commonly caused by Pseudomonas aeruginosa and Staphylococcus species. Presents with rapid onset of ear pain, (generally within 48 hours) of symptoms within the past 3 weeks, coupled with signs of ear canal inflammation. May be otorrhoea tenderness, itching, aural fullness, and hearing loss. tragal tenderness
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What are some risk factors for otitis externa?
external auditory canal obstruction swimming local trauma allergy diabetes immunocompromised prolonged used of topical antibacterial agents chemical irritants
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How do we treat otitis externa?
initial treatment in otherwise healthy people 1st line: antibacterial otic drops (Ofloxacin otic) adjunct: pain management refractory to initial treatment, or diabetic or immunocompromised 1st line: topical and systemic antibacterial therapy adjunct: pain management
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What are some risk factors associated with foreign body aspiration?
disorders associated with dysphagia and impaired cough reflex Young age
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How does foreign body aspiration present?
Inhalation of a foreign body into the larynx and respiratory tract. sudden onset of respiratory distress associated with coughing, gagging, or stridor. Choking crisis and intractable cough Unilateral wheezing and unilateral breath sounds suggests partial obstruction of the main or distal bronchi because: wheeze - lower airway stridor - upper airway
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How do we ivx foreign bodies?
Clinical diagnosis 1st - CXR Other - bronchoscopy/ CT
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How do we manage foreign bodies?
conscious 1st line: encouragement of cough 2nd line: external manoeuvres 3rd line: removal of foreign body unconscious 1st line: secure airway - endotracheal intubation plus: removal of foreign body A. Flexible bronchoscopy B. Surgery C. Thoracotomy if destroyed segment If coughing is ineffective, back blows, chest thrusts for infants or abdominal thrusts (Heimlich manoeuvre) These actions create an 'artificial cough' to increase intrathoracic pressure and dislodge the foreign body
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how do we ivx cows milk allergy?
IGE mediated - skin prick test NON-IGE - if breastfed: Mum cut out cows milk form diet for up to 6 weeks - if not: hydrolysed feed.
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what are the most common causes of Neonatal Breathing Difficulty?
Common causes: Transient tachypnoea of the newborn (TTN) Sepsis Pneumonia Less Common: Meconium aspiration Pneumothorax Congenital anomaly (diaphragmatic hernia, tracheoesophageal fistula)
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how does Transient tachypnoea of the newborn (TTN) present? risk factors?
tachypnoea and recession In the first hours of life Resolves within 4 hours - if not consider another diagnosis eg sepsis Risks: C-section - as infant has had none of the stimuli to begin resorption of alveolar amniotic fluid