Paediatric Respiratory Disease Flashcards

1
Q

What features make children susceptible to respiratory failure?

A

Compliant chest walls, poorly developed respiratory muscles = particularly susceptible to
respiratory failure; Early detection and prevention is cornerstone to mgmt

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2
Q

Which groups of paediatric patients are particularly susceptible?

A

Preterm infants, BronchoPulmonaryDysplasia, haemodynamically significant congenital heart disease, muscle weakness causing diseases, Cystic Fibrosis, Immunodeficiency

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3
Q

Presentation of URTI

A

Coryzal symptoms, sore throat, earache, sinusitis or stridor

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4
Q

Presentation of LRTI

A

Cough, wheeze, respiratory distress
o Moderate Distress – Tachypnoea, Tachycardia, Flaring, Accessory muscle use, Intercostal and subcostal recession, Head Retraction, Inability to feed
o Severe Distress – Cyanosis, Fatigue from work of breathing, LOC, <92% sats despite oxygen therapy
• NB: Signs of respiratory distress become less marked as exhaustion occurs

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5
Q

Stridor

A

Extrathoracic airway obstruction exaggerated during inspiration
o Inspiration is an active process; Contraction and downward movement of diaphragm with outward movement of ribs to generate negative pressure
o Airway walls are pulled apart to create negative intrathoracic pressure
o Leads to degree of inward collapse of large airways where pressure external pressure is atmospheric; hence worsens Stridor

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6
Q

Common cold

A

Most common infection in childhood; Clear/Mucopurulent discharge, nasal blockage; Most commonly Rhinovir, Coronavir, RSV
o Self-limiting, no specific curative treatment
• Analgesia by Paracetamol or Ibuprofen; Abx unnecessary as secondary infection uncommon; Cough may persist up to 4/52

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7
Q

Causes of sore throat

A

Pharyngitis

Tonsillitis

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8
Q

Pharyngitis

A

Pharynx and Soft Palate inflamed, Local LN enlarged and tender
o Viral infections – Adenovir, Enterovir, Rhinovir
o In older child, Group A haemolytic strep is a common pathogen (Pyogenes)

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9
Q

Tonsillitis

A

Form of Pharyngitis with intense Tonsillar inflammation, often Purulent
o Commonly Group-A Strep and EBV (Infectious Mononucleosis)
o Difficult to establish clinically whether viral or bacterial
o Bacterial Infection more likely to cause constitutional disturbances – Headache, Apathy, Abdominal Pain, White Tonsillar Exudate, Cervical LN

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10
Q

How to manage pharyngitis/tonsillitis

A

• Abx – Pen V or Erythromycin if Pen Allergic; Although only 1/3 are Bacterial infections
o 10 days to eradicate and prevent Rheumatic Fever
o Amoxicillin avoided as may cause widespread Maculopapular rash if EBV
• Admit if unable to swallow – IV Abx, Analgesia

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11
Q

Scarlet Fever, Group A Strep

A

Group A Strep can lead to Scarlet Fever – Most common 5-12yrs; Fever before headache and tonsillitis; Maculopapular rash with Flushed cheeks and Perioral sparing; White coated tongue, Sore and Swollen
o Only childhood rash caused bacterium; Pen V or Erythromycin to prevent complications e.g. Acute GN, Rheumatic Fever

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12
Q

Acute Otitis Media

A

Most common 6-12/12 age; 20% will have 3 or more episodes; Most common due to poor Eustachian tube shorter, more horizontal, poor function
o Otalgia, Fever; All children with fever must have ears examined

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13
Q

Acute Otitis Media O/E

A

Bright red, bulging TM with loss of normal light infection

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14
Q

Causes of Acute Otitis Media

A

Commonly caused by RSV, Rhinovir, Pneumococcus, Haemophilus, Moraxella

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15
Q

Glue Ear O/E and Management

A

Bulging appearance with pus with less inflammation; Peri-AOM
o Asymptomatic apart from decreased hearing; Commonly 2-7yrs; May cause conductive hearing loss – Interfere with development
15
o Ventilation tube insertion (Grommet)
o Adjuvant Adenoidectomy and Reinsertion Grommet if persist – Possible benefit

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16
Q

Management of Acute Otitis Media

A

Serious complications include Mastoiditis and Meningitis;
• Analgesia – Paracetamol, Ibuprofen; Regular Analgesia more effective and may be needed for up to 1 week for inflammation to resolve
• AOM mostly resolves spontaneously – Abx reduces pain duration but does not reduce HL
o Amoxicillin given if child remains unwell 2-3/7 later
o Decongestants nor Antihistamines not useful

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17
Q

Sinusitis

A

Infection of Paranasal Sinuses in Viral URTI; Secondary bacterial infection can occur with pain, swelling and tenderness over maxilla; Antibiotics and Analgesia for Acute Sinusitis
• Frontal sinuses do not develop until late childhood; Infection is uncommon in first decade

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18
Q

Stridor2

A
Harsh, musical sound due to partial obstruction of lower portion of upper airway (Upper Tracheal, Larynx); Most commonly laryngeal and tracheal infection
o Mucosal inflammation and swelling can rapidly cause life-threatening obstruction
• Assessed based on – Characteristic (None, Only on crying, At Rest, Biphasic Stridor), Degree of
Chest Retraction (None, Only on crying, At Rest)
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19
Q

Presentation of obstruction

A

o Severe obstruction leads to Tachypnoea, Tachycardia, Agitation
o Central Cyanosis, Drooling or reduced LOC suggest impending complete obstruction
o SpO2 reliably detects hypoxaemia but is only lowered in later disease
• Total obstruction might be precipitated by examination of throat using spatula; Avoid examination unless full resuscitation is available on hand

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20
Q

Causes of Acute Stridor

A
Croup
Epiglottitis 
Foreign body 
Anaphylaxis
Smoke Inhalation 
Trauma 
Lymph node swelling
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21
Q

Croup

A

Laryngotracheobronchitis
• Viral Croup – 95% Laryngotracheal infections; Parainfluenza most common but others e.g. Rhinovir, RSV and influenza also similar clinical picture
• 6/12 to 6yrs of age; Peak incidence 2yrs, most common in Autumn

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22
Q

Presentation of Croup

A

Coryza and Fever; Hoarseness (due to vocal cord inflammation), Barking Cough (Tracheal Oedema
and Collapse), Harsh Stridor, Variable degree of Chest Retraction, Nocturnal symptoms
Recurrent Croup might be related to pattern of atopy

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23
Q

Management of Mild Croup

A

Mild – Stridor and Recession disappears at rest; Home management; Observe for deterioration; Admit if poor access to hospital, <12/12, parental confidence etc
• Inhaled warm moist air – Conventional but no evidence for use
• Oral steroids – Dexamethasone, Prednisolone or Neb steroids (Budesonide) reduce severity and duration of disease
o First line if chest recession noted at rest

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24
Q

Management of Croup in Severe Upper Airways Obstruction

A

Neb Epinephrine, Oxygen by face mask
o Rapid but transient improvement; Observe 2-3hrs after
o Intubation is unusual after steroid therapy

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25
Q

Acute Epiglottitis

A

Intense swelling of Epiglottis and surrounding tissues, associated with Sepsis
o Life-threatening emergency – High risk of Respiratory Obstruction
o Most common 1-6yrs but can affect all groups
• Caused by HiB; Immunisation has led to 99% reduction of disease

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26
Q

Presentation of Acute Epiglottitis

A

High Fever, Intense Throat pain (Drooling due to painful swallow), Soft Inspiratory Stridor, rapidly increasing Respiratory Distress; Immobile, Upright with Open mouth

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27
Q

Management of Acute Epiglottitis

A

Do not examine without expert; Total airway obstruction can occur
• Urgently admit; Bleep Senior Anaesthetist, Paediatrician and ENT surgeon; Transfer to ITU/Anaesthetic room
o Intubation with general anaesthetic; Rarely urgent tracheostomy is life-saving
• Only after secured airway – Blood cultures, IV Abx (E.g. Cefuroxime)
o Tracheal tube can be removed 24hrs after; Abx given 3-5/7 course
• Prophylaxis of close household contacts with Rifampicin offered

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28
Q

Other causes of stridor

A

Bacterial Tracheitis (Pseudomembranous Croup) – Similarly to Severe Epiglottitis; High Fever, Severely Unwell, Rapidly progressive obstruction with copious, thick airway secretions
o Typically, S aureus; IV Abx, Intubation, Ventilation as required
• Consider Anaphylaxis or FBO in absence of apparent infection
• Chronic Stridor – Structural problems (Intrinsic narrowing/collapse, or Extrinsic compression)

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29
Q

Bronchiolitis Presentation/Symptoms

A

Preceding Coryzal symptoms; Dry wheezy cough, tachypnoea, tachycardia, subcostal and intercostal recession, hyperinflation, fine end-inspiratory crackles, high-pitched wheeze (expiratory > inspiratory)

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30
Q

Bronchiolitis: Causative Organism

A

RSV is causative in 80%, remainder would be Parainfluenza, Rhinovirus, Adenovirus, Influenza and Human Metapneumovirus
o Co-infection will be more severe; RSV plus HMPV

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31
Q

Bronchiolitis: When to Admit

A

Apnoea, <90% RA, Inadequate fluid intake-less than 50% of normal intake, Severe respiratory distress or Tachypnoea >70, <4 weeks old, safety netting is not enough, in presence of other illnesses; CXR and Blood gases only if respiratory failure suspected

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32
Q

Management of Bronchiolitis

A

Supportive Management; Humidified Oxygen as guided by sats, Monitoring for Apnoea; No evidence from use of mist, nebulised hypertonic NaCl, Abx, Steroids or Bronchodilators
o Fluids by NGT or IV if poor intake
o NIV with CPAP, or mechanical ventilation based on severity
o Infection control (RSV is highly contagious) – hand hygiene, gowns, gloves

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33
Q

Prognosis and Follow up of Bronchiolitis

A

Most recover within 2/52, but as many as half will have recurrent; With adenovirus infections, rarely can lead to permanent damage – Bronchiolitis Obliterans
• Prevention by IM Palivizumab (Anti RSV) reduces number of admissions in high-risk preterm infants, but NNT=17; expensive and multiple injections required

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34
Q

Viral Episodic Wheezing

A

Only in response to infection; Most common
o Narrowing of small airways due to immune response and inflammation
o Often have small airway diameter at birth; Typically resolves at 5yrs presumably due to increasing airway size
o RF: Maternal smoking, family history; More common in males

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35
Q

Multiple Trigger Wheeze

A

More likely to develop into Asthma over time

o Frequent wheeze triggered by not only viruses but cold air, dust, dander, exercise

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36
Q

Atopic Asthma

A

Recurrent wheeze associated with symptoms between viral symptoms (interval) plus evidence of allergy to one or more inhaled allergens (e.g. HDM, Pollen, pets)
o Evidence based on skin prick or serum IgE
o Strongly associated with other atopic diseases such as Eczema, Rhinoconjunctivitis and Food Allergy

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37
Q

Other causes of recurrent childhood wheeze

A

Non-atopic asthma, Recurrent anaphylaxis (food allergy related), Chronic aspiration, CF, BPD, BO, Tracheo-bronchomalacia

38
Q

Pathophysiology of Asthma

A

Genetic predisposition, atopy and environmental triggers like allergens, smoking, cold air and exercise lead to bronchial inflammation: oedema, excessive mucus production, infiltration with eosinophils leading to bronchial hyperresponsiveness to stimuli leading to airway narrowing with reversible airflow obstruction leading to wheezing, cough, breathless ness and chest tightness

39
Q

Presentation of Asthma in Children

A

Suspected in any child with wheeze on more than one occasion, particularly if interval symptoms; more common if personal or family atopy history
o Wheeze can be described as whistling in the chest when child breathes out
o Needs to be differentiated from transmitted upper airway noises
o Polyphonic noise (due to airways of different sizes being affected), typically expiratory, coming from the small airways
• Nocturnal or Early Morning worsening
Non-viral triggers, Interval symptoms (symptoms between acute exacerbations), positive response to asthma therapy

40
Q

What do you need to establish in a suspected asthma presentation

A

Need to establish – Frequency, Triggers, Sleep disturbance, Severity of Interval Symptoms, and Social aspects

41
Q

What would you look for on examination in suspected asthma

A

Look for Eczema and examine nasal mucosa for Allergic Rhinitis; Monitor growth (should be normal unless severe disease)
• Wet cough, sputum production, finger clubbing or poor growth would suggest condition characterised by chronic infection e.g. Cystic Fibrosis

42
Q

How is asthma diagnosed in children

A
  • Younger children – History and Examination; Parental description of disease
  • Skin-prick testing for common allergens to aid diagnosis of atopy
  • If uncertainty in diagnosis or severity monitoring, PEFR – Less sensitive than Spirometry for exchanges in airway calibre but more convenient
  • Poor control leads to increased PEF variability
  • Response to bronchodilator is most helpful – Improvement of PEF or FEV1 of more than 12% indicates bronchodilator reversibility, characteristic of asthma
43
Q

Management of Asthma

A

Always monitor growth of asthmatic children, especially if taking regular steroids
• Inhaled Beta Agonists = Relievers; LABA not to be used without Inhaled steroids, particularly useful in exercise induced asthma
• Ipratropium bromide – Useful when other bronchodilators ineffective, or mgmt acute
• Inhaled Corticosteroids – Prophylaxis on regular use; Used in conjunction with LABA or LTRA; no clinically significant effects in low dose but can cause reduced high velocity but will have catch up growth in late childhood
o High doses can lead to impaired growth, adrenal suppression and altered bone metabolism; Use lowest dose possible for control

44
Q

Complete Control of Asthma

A

Absence of daytime or night time symptoms, no limits on activities and exercise, no need to use reliever, normal lung function and no exacerbations requiring hospital or oral steroids in 6/12

45
Q

Pharmacological Management of Asthma

A

SABA to start; Add ICS, or consider LTRA instead for <5yrs
o Add on <5yrs: ICS+LTRA, if LTRA ineffective increase ICS dose
o Add on >5yrs: ICS+LABA, if partial LTRA response increase ICS, if no response, stop LABA, increase ICS and consider LTRA or Theophylline

46
Q

Types of Inhaled Therapy

A

Pressurised Metered Dose Inhaler and Spacer (all ages; mask if <3yrs), Breath-actuated Metered Dose (6+yrs), Dry Powder Inhaler (4+yrs, needs good inspiratory flow), Nebuliser (Only for Acute or Rapid-Onset Severe = Brittle)

47
Q

When is oral prednisolone given?

A

typically given alternate days to minimise adverse effects on growth; Only in severe persistent asthma and as last resort

48
Q

When are anti-IgE Mabs given?

A

severe atopic asthma under specialist case; Allergen immunotherapy effective if single allergen implicated; risk of systemic allergic response in treatment

49
Q

What advice should be given in chronic severe asthma and about therapies

A

Advise on second-hand smoke; psychological intervention might be useful in chronic severe
• Antihistamines and Nasal steroids for the use of Allergic Rhinitis
• No evidence for use of Antibiotics or Cough Medicines

50
Q

How does acute asthma present

A

Wheezy SOB, Tachypnoea (poor guide to severity), Tachycardia

51
Q

What is important to note in presentation of acute asthma?

A

Duration of symptoms, Treatment already given, Course of previous attacks;

52
Q

Other causes of SOB

A

Pneumonia/LRTI, FBO, Anaphylaxis, PTX, Effusion, Metabolic acidosis (DKA, IEM, Lactic), Severe Anaemia, HF, Panic attack

53
Q

Life threatening red flags

A

<92% Sats, Predicted PEF <33%, Accessory muscle use, Poor respiratory effort and Silent chest, Hypotension and Arrhythmia, LOC and exhaustion

54
Q

When to admit in acute asthma presentation

A

Admit if despite high-dose inhaled bronchodilator therapy: inadequate clinical effect, appear to become exhausted, Marked PEF or FEV1 <50%, or <92% sats
o CXR is unusual, non-asthmatic picture e.g. asymmetry suggesting PTX, Lobar collapse or signs of severe infection
o Blood gases if life-threatening or refractory cases; only affected if in extremis

55
Q

Management of Acute Asthma

A

High dose inhaled bronchodilators, steroids and oxygen (if <92% sats)
o Beta agonist dose and frequency based on severity of attack by spacer unless severe or life-threatening asthma
▪ High-flow Salbutamol Neb otherwise
o Addition of Neb Ipratropium to initial therapy in severe asthma
o Short course Oral Prednisolone (3-7/7) expedites recovery from asthma attack

56
Q

What if inhaled therapy are not working as poor delivery to poorly ventilated lung

A

o IV Mg Sulfate (most evidence), Aminophylline (loading dose then continuous infusion, skip loading if patient already on theophylline) or Salbutamol can be useful
o SE Theophylline: Seizures, Severe Vomiting, Fatal Cardiac Arrhythmias

57
Q

What should you be monitoring in management of acute asthma

A

Monitor ECG for arrhythmia due to Salbutamol or Aminophylline, check U/Es

58
Q

When do you give abx in acute asthma

A

Abx given only if evidence of bacterial infection

59
Q

What happens if inadequate response in acute asthma

A

Escalate to mechanical ventilation if inadequate response

60
Q

What should be done on discharge from acute asthma

A

Patient Education on discharge – Medication review, Inhaler technique, Personalised Asthma Management Action Plan

61
Q

What is Cystic Fibrosis

A

Most common Life-limiting Autosomal Recessive condition in Caucasians (1 per 2500, 1 per 25 carrier rate); Life expectancy likely into 40s
• Consider in all children with Recurrent Infection, Loose Stools or Faltering Growth
• Defective CFTR gene due to mutation Ch7, 78% due to ΔF508; Chloride channel
o Prenatal detection and carrier detection for wider family
o Some genotypes can be associated with milder disease with pancreatic sufficiency
o Genotype specific treatment – CFTR Potentiators and Correctors

62
Q

Pathophysiology of Cystic Fibrosis

A

Abnormal Ion transport across epithelial cells leads to multiple systemic issues
• Airways – Reduction of airway surface liquid layer, increased viscosity leads to Impaired Ciliary Function; Retention of Mucopurulent secretions; Chronic Infection (Specific organisms include S aureus, HiB, Pseudomonas, Burkholderia spp.
o Leads to Bronchial Wall Damage, Bronchiectasis, Abscess Formation
• Dysregulation of Inflammation and Infectious defence
• Thick Viscid Meconium – Meconium Ileus (10-20% of affected infants) and MIES
o Vomiting, Abdominal Distention, Failure to pass Meconium in first /7 of life
o Surgery usually required; Gastrografin enema may relieve
• Blockage of pancreatic ducts – Insufficiency → Malabsorption; Excessively salty sweat
o 90% of CF patients have exocrine deficiency (Lipase, Amylase, Proteases)
o Pancreatic insufficiency can be diagnosed by low Faecal Elastase

63
Q

Presentation of Cystic Fibrosis: Newborn

A

Screening detected or Meconium Ileus
o All UK newborns screened; Reduce risk of faltering growth or established infection
o Immunoreactive Trypsinogen (IRT) raised in CF; Routine heel-prick
o Screened for gene mutations, Confirmation by Sweat Test (Cl 60-125mmol/L in sweat, compared to 10-40 in normal children)

64
Q

Presentation of Cystic Fibrosis: Infancy

A

Prolonged Jaundice, ↓Growth, Recurrent Chest, Malabsorption, Steatorrhoea

65
Q

Presentation of Cystic Fibrosis: Young child

A

Bronchiectasis, Rectal Prolapse, Nasal Polyp, Sinusitis

o Productive purulent cough, coarse inspiratory creps and expiratory wheeze

66
Q

Presentation of Cystic Fibrosis: Older child/adolescent

A

Allergic Bronchopulmonary Aspergillosis, DM, Cirrhosis, Portal HTN, MIES, PTX, recurrent Haemoptysis, Males: Sterility
o Finger clubbing in established disease

67
Q

Respiratory management of Cystic Fibrosis: Mucus Clearance

A

Spirometry (FEV1 indicates clinical severity, declines with progression)
o With regular treatment, no respiratory symptoms in infancy and childhood
o Twice daily PT to clear secretions; Chest Percussion, Postural Drainage, Controlled Deep Breathing Exercises and other PT devices in older children
o Physical exercise is useful and encouraged

68
Q

Respiratory management of Cystic Fibrosis: Mucus Clearance

A

• Continuous Prophylactic Antibiotics – Typically Flucoxacillin; Also rescue oral Abx if any increase in respiratory symptoms or decline in lung function

69
Q

Respiratory management of Cystic Fibrosis: Persistent Symptoms

A

• IV therapy if persistent symptoms; 2/52 course via PIC line

70
Q

Respiratory management of Cystic Fibrosis: Pseudomonas Infection

A

Daily Nebulised Antipseudomonal Abx for Chronic Pseudomonas infection

71
Q

Respiratory management of Cystic Fibrosis: Mucus Viscosity

A

• Nebulised DNase or hypertonic saline – Decrease sputum viscosity, increased clearance

72
Q

Respiratory management of Cystic Fibrosis: Respiratory Exacerbation

A

• Azithromycin decreases respiratory exacerbations due to immunomodulatory effect

73
Q

Respiratory management of Cystic Fibrosis: End Stage Lung Disease

A

• Bilateral Sequential Lung Transplantation for End-stage Lung Disease; 50% survival at 10yrs
o Requires MDT assessment, Optimise for Co-Mords and Micro, Psychological preparation and Timing, Expert Post-Transplant Care

74
Q

Aim of Respiratory Management in Cystic Fibrosis

A

At least Annual Review in specialist centre; Aim to prevent progression of lung disease, maintain adequate nutrition and growth

75
Q

Nutritional Management of Cystic Fibrosis

A

Assess regularly; Oral, Enteric coated Pancreatic Replacement Therapy with all meals
o Dose according to clinical response
• High calorie diet (150% of normal); Overnight feeding via Gastrostomy can be used
• Fat soluble vitamin supplementation

76
Q

Cystic Fibrosis in Later Life

A

• DM more common due to decreasing endocrine function
• 1/3 of adolescent patients have liver disease, hepatomegaly on palpation, abnormal LFTs or ultrasound due to poor biliary flow
o Ursodeoxycholic Acid can improve
o Progression to Cirrhosis, Portal HTN and Liver Failure rarely; For Transplant
• MIES – Oral laxatives usually sufficient
• Normal fertility in females; Males need ICSI to have children
• Psychological and Emotional Support; Transfer to Specialist Adult CF care

77
Q

Pneumonia in children

A

Incidence peaks in infancy and old age, but relatively high in childhood; Major cause of mortality in lesser developed countries
o In 50% of cases causative organisms is not identified
o Viruses – Most common cause in young children, while Bacteria – More common in older children; Difficult to distinguish in clinical practice

78
Q

Causative Organisms of Pneumonia: Newborn

A

Maternal Genital Tract organisms, especially Group B Streptococcus, Gram negative Enterococci and Bacilli

79
Q

Causative Organisms of Pneumonia: Infants and Young Children

A

Respiratory Viruses (e.g. RSV) and specific bacterial pathogens (S pneumo, HiB, Bordetella pertussis, Chlamydia trachomatis; Less common but serious S aureus
o HiB is less common due to immunisation
o Pneumococcal vaccine (13 strains) still under study; decreased septicaemia, meningitis and severe URTI but no reduction in bacterial pneumonia

80
Q

Causative Organisms of Pneumonia: >5 years

A

Mycoplasma pneumo, S pneumo, Chlamydia pneumo

81
Q

Other causative organisms

A

At all ages TB should be considered for at-risk populations

82
Q

Presentation of Pneumonia

A

Fever, Cough, Tachypnoea
• Lethargy, Poor feeding and generally unwell; Cough might be absent
o Also, Nasal Glaring, Chest Recession
o Most sensitive clinical sign is Tachypnoea (c/f Asthma)
o End respiratory crackles, Dullness on percussion on consolidated area, decreased AE
• Localised chest, abdominal or neck pain characteristic of pleural irritation – Bacterial infection
o Consider pneumonia in all children with neck stiffness or acute abdominal pain
• Small proportion of children develop pleural effusion; even rarer effusions develop into empyema with septations due to fibrin formation

83
Q

Management of Pneumonia

A

CXR to confirm diagnosis – Cannot reliably differentiate viral and bacterial
• NPA may identify viruses; blood markers not useful for differentiation
• Most children can be managed at home

84
Q

When to admit a child with suspected pneumonia

A

Admit if Sats <92%, Recurrent Apnoea, Grunting, Inability to feed/fluid intake

85
Q

Management as inpatient in suspected pneumonia

A

Oxygen if <92%, Analgesia if pain is present, IV fluids to correct dehydration and maintain
o PT effectiveness has not been evaluated
• Abx – Based on child’s age, severity of illness; No advantage for using IV Abx if mild/moderate
o Newborn – IV broad-spectrum Abx
o Older infants – Oral Amoxicillin; Co-Amox if non-responsive or complicated
o >5yrs – Amoxicillin, Oral Macrolide (e.g. Erythromycin)

86
Q

How to treat parapneumonic effusion s

A

1/3 of children; may resolve with Abx
o If not resolved despite 48hrs Abx suggestive of Pleural Effusion requiring US-guided percutaneous drainage (chest drain, fibrinolytic agent)
o Refractory cases require VATS, Thoracotomy, Decortication

87
Q

When to investigate for chronic lung infection

A

Children with persistent ‘wet sounding’ cough require further investigations

88
Q

Persistent Bacterial Bronchitis

A

Chronic infection driving persistent lower airway inflammation commonly due to HiB or Moraxella catarrhalis
o May be precursor to Bronchiectasis if undermanaged
o Specialist respiratory care is required; Growth from culture of sputum or BAL
o Treated with High-dose Abx and PT

89
Q

Bronchiectasis

A

Permanent dilatation of the bronchi; Generalised or Lobar; Generalised might be due to CF, PCD, Immunodeficiency or Chronic Aspiration; Focal might be due to previous severe pneumonia, congenital lung abnormality or FBO
o HRCT required to identify extent of bronchiectasis; For focal disease Bronchoscopy to exclude structural cause

90
Q

Pulmonary TB

A

Dx either Tuberculin skin test (difficult to interpret if BCG vaccinated) or blood tests (IGRA); CXR Hilar or Paratracheal LNA highly suggestive