Respiratory Distress Flashcards
(47 cards)
What are the questions you ask in the history of a child presenting with respiratory distress?
Establish what the parent or carer is worried about.
Note what symptoms there are and how long they have been going on for.
Specifically find out about recent activities suggesting foreign body ingestion (make no assumptions relating to a young baby’s age: an older toddler may try to ‘feed’ the new baby) and anaphylactic reaction.
Foreign body ingestion
Specifically find out about past respiratory disease.
Complete usual paediatric history. When enquiring about social history in a young child, enquire about smokers in the house (relatives, frequent visitors).
What are the suggestive features of foreign body ingestion?
Suggestive features: witnessed episode, sudden onset of coughing or choking, recent history of playing/eating small objects.
Effective coughing suggested by: crying or verbal response to questions, being able to take breath in before coughing, loud cough, fully responsive child.
Ineffective coughing suggested by: inability to vocalise, quiet or silent cough, inability to breathe, cyanosis, decreasing level of consciousness
Which questions do you ask about a past history of asthma?
Previous severe asthma.
Previous hospitalisations.
Dependence on inhaled or systemic corticosteroids.
Non-compliance with medications.
Labile asthma with pronounced diurnal obstruction.
Brittle asthma with unexpected sudden deterioration of airway function.
Chronic asthma with depressive symptoms/manipulative use of asthma.
What do you assess in an examination for respiratory distress?
General observations.
Respiratory system
- Assess chest expansion and auscultate beware of the silent chest (this means that very little air is going in and out).
- Pulse oximetry should show an oxygen saturation close to 100% in normal healthy children breathing air.
- Acute severe asthma is defined by an SpO2 ≤92%, respiration rate raised and the child being unable to talk in normal sentences
Other systems - these need assessing to gauge to what extent the respiratory distress has affected them:
-Cardiac system - tachycardia is generally seen (the heart rate should roughly be four times the normal respiratory rate) - eg, pulse ≥140 beats per minute (bpm) (2-5 years) or ≥150 bpm (≥5 years old) in acute severe asthma.
NB: bradycardia occurs in the presence of severe or prolonged hypoxia and is a pre-terminal sign.
- Skin colour - pallor occurs initially. Cyanosis is a late and pre-terminal sign.
- Agitation ± drowsiness. This may be difficult to assess and the parents will need to be consulted in the case of the very young child or baby.
What are the signs of respiratory distress?
Tachypnoea: very slow RR in children suggest imminent respiratory arrest or poisoning with narcotic drugs.
Intercostal and sternal recession: Intercostal and abdominal muscles are drawn in with each inspiration. This is seen more easily in very young children; therefore, it is particularly significant if seen in the child over 6-7 years of age.
Use of accessory muscles: look for the head bobbing up and down in infants.
Tripodding or anchoring: The child may sit forward and grasp their feet or hold on to the side of the bed.
Nasal flaring: particularly seen in infants
Inspiratory/expiratory noises:
- Stridor: high-pitched inspiratory noise - sign of upper airway obstruction.
- Wheezing: tends to be louder on expiration - sign of smaller-calibre lower airway obstruction.
- Grunting: exhalation against a partially closed glottis - sign of severe respiratory distress in infants.
What are the causes of respiratory distress?
Laryngomalacia.
Foreign body ingestion.
Laryngeal oedema: anaphylaxis, inhalation injury.
Upper respiratory tract infection: epiglottitis, croup, retropharyngeal abscess.
Lower respiratory tract causes: asthma, bronchiolitis and bronchitis, pneumonia, acute respiratory distress syndrome.
What are the clinical clues to alternative diagnoses other than asthma in wheezy children?
Symptoms present from birth or perinatal lung problem: cystic fibrosis, chronic lung disease of prematurity, ciliary dyskinesia, developmental lung anomaly.
Family history of unusual chest disease: cystic fibrosis, neuromuscular disorder.
Severe upper respiratory tract disease: defect of host defence, ciliary dyskinesia.
Persistent moist cough: cystic fibrosis, bronchiectasis, protracted bacterial bronchitis, recurrent aspiration, host defence disorder, ciliary dyskinesia.
Excessive vomiting: gastro-oesophageal reflux (with or without aspiration).
Paroxysmal coughing bouts leading to vomiting: pertussis.
Dysphagia: swallowing problems (with or without aspiration).
Breathlessness with light headedness and peripheral tingling: dysfunctional breathing, panic attacks.
Inspiratory stridor: tracheal or laryngeal disorder.
Abnormal voice or cry: laryngeal problem.
Focal signs in chest: developmental anomaly, post-infective syndrome, bronchiectasis, tuberculosis.
Finger clubbing: cystic fibrosis, bronchiectasis.
Failure to thrive: cystic fibrosis, host defence disorder, gastro-oesophageal reflux.
Focal or persistent chest radiological changes: developmental lung anomaly, cystic fibrosis, post-infective disorder, recurrent aspiration, inhaled foreign body, bronchiectasis, tuberculosis.
Management of respiratory distress
Life-threatening respiratory distress warrants immediate initiation of life support measures and immediate ambulance transfer to hospital.
Children with moderate-to-severe respiratory distress should be referred to the local paediatric team.
Where the decision is made to treat the child at home, parental education and frequent reviews are mandatory.
Almost all ill (or injured) children will benefit from high-concentration oxygen therapy. The only small group of infants to be careful with are those with duct-dependent congenital heart disease.
It is usually counterproductive to make an unwilling child wear an oxygen mask. Avoid any other action that may agitate the child (which worsens the respiratory distress) unless the child is critically ill.
Most of the assessment and initiation of treatment can be done with the child in their parent’s arms.
Do not put anything (including a thermometer) in the mouth of a child with stridor as this may precipitate complete respiratory obstruction).
What is croup?
Croup is a common childhood illness causing symptoms which may involve a harsh barking cough, hoarse voice and (inspiratory) stridor.
It is usually caused by inflammation of the upper respiratory tract (predominantly the larynx and trachea but it may affect the bronchi) as a result of viral infection.
What is the pathophysiology of croup?
Viral upper respiratory tract infection (URTI) causes nasopharyngeal inflammation that may spread to the larynx and trachea, causing subglottal inflammation, oedema and compromise of the airway at its narrowest portion.
The movement of the vocal cords is impaired leading to the characteristic cough. Occasionally, fibrinous exudation with pseudomembrane formation may occur, causing further airway compromise.
It is thought that some children who experience recurrent bouts of spasmodic croup have a primarily allergic rather than infective aetiology for subglottal oedema
What are the causative organisms for croup?
Parainfluenza virus types I, II, III and IV (thought to be responsible for about 80% of cases - type I causing 50-70% of severe cases).
Respiratory syncytial virus.
Adenoviruses.
Rhinoviruses.
Enteroviruses.
Measles.
Metapneumovirus.
Influenza A and B (type A is associated with severe disease).
Mycoplasma pneumoniae (rare cause).
What are the risk factors for croup?
Croup most often affects children aged 6 months to 3 years.
More prevalent in autumn and spring.
Genetic studies suggest that the C/C variant of the CD14 C-159T gene has a significantly lower prevalence of croup.
Presentation of croup
Croup normally starts with nonspecific symptoms of viral URTI, such as runny nose, sore throat, fever and cough.
This progresses over the course of a couple of days to include the characteristic barking cough and hoarseness. These symptoms tend to be worse at night.
There is a high degree of variability in clinical findings. There may be a mild-to-moderate fever. Check vital signs (including temperature, pulse and blood pressure).
A barking cough and hoarse cry are nearly always present.
Stridor (harsh, low-pitched noise heard during inspiration) may be heard at rest or only when the child is agitated or active.
Chest sounds are usually normal but can be decreased in volume where there is severe airflow limitation.
Respiratory distress with marked tachypnoea and intercostal recession may be noted.
It should be recognised that a child whose stridor appears to be improving and in whom intercostal recession has disappeared may in fact be deteriorating with worsening airways obstruction. Such a child may be at high risk of complete airway occlusion.
Drowsiness, lethargy, and cyanosis despite increasing respiratory distress should be considered as red flags for impending respiratory failure.
The illness tends to last for about 3-7 days but can persist for up to two weeks.
Differentials for croup
Epiglottitis Inhaled foreign body Inhaled noxious substance Acute anaphylaxis Bacterial tracheitis Diphtheria Laryngomalacia Peritonsillar abscess (quinsy) Retropharyngeal abscess Angioneurotic oedema Vocal cord paralysis
Which scoring system is used to assess the severity of croup?
Westley clinical scoring system.
• The modified Westley clinical scoring system for croup
Inspiratory stridor:
o Not present - 0 points.
o When agitated/active - 1 point.
o At rest - 2 points.
Intercostal recession: o Not present - 0 points. o Mild - 1 point. o Moderate - 2 points. o Severe - 3 points.
Air entry:
o Normal - 0 points.
o Mildly decreased - 1 point.
o Severely decreased - 2 points.
Cyanosis:
o None - 0 points.
o With agitation/activity - 4 points.
o At rest - 5 points.
Level of consciousness:
o Normal - 0 points.
o Altered - 5 points.
Possible score 0-17: 0-3 = mild croup, 4-6 = moderate croup, >6 =severe croup.
When is immediate hospital assessment for croup indicated?
Moderate or severe croup, or impending respiratory failure.
Any suspicion of epiglottitis, bacterial tracheitis, peritonsillar abscess, retropharyngeal abscess, or laryngeal diphtheria.
Any suspicion of inhaled foreign body, angioneurotic oedema, hypocalcaemic tetany, or ingestion of corrosives.
When is admission to hospital required in a child with croup?
History of severe obstruction, previous severe croup, or known structural upper airways abnormalities (eg, laryngomalacia, tracheomalacia, vascular ring, Down’s syndrome).
Age less than 6 months.
Immunocompromised.
Inadequate fluid intake.
Poor response to initial treatment.
Uncertain diagnosis.
Significant parental anxiety, late evening or night-time presentation, the child’s home is a long way from the hospital, or the parents have no transport.
What are the investigations for croup?
A low SaO2 on pulse oximetry (<95%) indicates significant respiratory impairment.
It is important to weigh the benefits of investigations such as CXRs and blood tests against the risks of distressing the child and making the symptoms worse.
A rapid influenza A test can be performed if it is considered vital to do so but even this investigation (which requires a throat swab) can distress the child.
Direct or indirect laryngoscopy is not usually required but may be employed where the course of the illness is atypical or there is reason to suspect a congenital or other alternative cause for upper airway obstruction.
What is the management of croup?
Do not give antibiotics unless there are sound clinical reasons to suspect secondary bacterial infection.
Keep the child as calm and as comfortable as possible. Allow the child to remain in a parent’s arms and avoid any unnecessary painful interventions. Persistent crying increases oxygen demands and respiratory muscle fatigue and worsens the obstruction.
Use paracetamol or ibuprofen to control any discomfort from symptoms or fever.
Ensure an adequate fluid intake.
Do not advise humidified air (eg, steam inhalation).
Mild croup is largely self-limiting but treatment with a single dose of a corticosteroid (eg, dexamethasone 150 micrograms/kg) by mouth may be of benefit.
More severe croup (or mild croup that might cause complications) requires hospital admission. A single dose of a corticosteroid (eg, dexamethasone 150 micrograms/kg or prednisolone 1-2 mg/kg by mouth) should be administered before transfer to hospital.
In hospital, dexamethasone 150 micrograms/kg (by mouth or by injection), prednisolone 1-2 mg/kg by mouth or budesonide 2 mg (by nebuliser) will often reduce symptoms. The dose may need to be repeated after 12 hours if necessary
Nebulised adrenaline (epinephrine) is usually reserved for patients in moderate-to-severe distress.
Nebulised adrenaline (epinephrine) solution 1 in 1,000 (1 mg/mL) should be given with close clinical monitoring in a dose of 400 micrograms/kg (maximum 5 mg) repeated after 30 minutes if necessary
What are the complications of croup?
Bacterial superinfection may result in pneumonia or bacterial tracheitis. The most frequent organism is Staphylococcus aureus, followed by group A streptococcus, Moraxella catarrhalis, Streptococcus pneumoniae, Haemophilus influenzae and anaerobes.
Pulmonary oedema, pneumothorax, lymphadenitis and otitis media have also been reported.
Inability to maintain adequate fluid intake may lead to dehydration.
What is anaphylaxis?
Anaphylaxis is a severe, life-threatening, generalised or systemic hypersensitivity reaction which is likely when both of the following criteria are met:
• Sudden onset and rapid progression of symptoms.
• Life-threatening airway and/or breathing and/or circulation problems.
Skin and/or mucosal changes (flushing, urticaria, angio-oedema) can also occur but are absent in a significant proportion of cases.
What is the cause of an anaphylactic reaction?
An anaphylactic reaction occurs when an allergen reacts with specific IgE antibodies on mast cells and basophils (type 1 hypersensitivity reaction), triggering the rapid release of stored histamine and the rapid synthesis of newly formed mediators.
These cause capillary leakage, mucosal oedema and ultimately shock and asphyxia.
Anaphylactic reactions can vary in severity and rate of progression - they may progress rapidly (over a few minutes) or occasionally in a biphasic manner.
Rarely, manifestations may be delayed by a few hours (adding to diagnostic difficulty) or persist for more than 24 hours.
Anaphylactoid reactions are not IgE-mediated but cause similar mast cell activation.
What are the triggers of an anaphylactic reaction?
Foods: o Peanuts o Pulses o Tree nuts such as almond and hazelnut o Fish and shellfish o Eggs o Milk o Sesame
Venom:
o Bee stings
o Wasp stings
Drugs: o Antibiotics o Opioids o NSAIDs o IV contrast media o Muscle relaxants
What is the presentation of anaphylaxis?
There is often (but not always) a history of previous sensitivity to an allergen, or recent history of exposure to a new drug (eg, vaccination).
Initially, patients usually develop skin symptoms, including generalised itching, urticaria and erythema, rhinitis, conjunctivitis and angio-oedema.
Signs that the airway is becoming involved include itching of the palate or external auditory meatus, dyspnoea, laryngeal oedema (stridor) and wheezing (bronchospasm).
General symptoms include palpitations and tachycardia (as opposed to bradycardia in a simple vasovagal episode at immunisation time), nausea, vomiting and abdominal pain, feeling faint - with a sense of impending doom; and, ultimately, collapse and loss of consciousness.
Airway swelling, stridor, breathing difficulty, wheeze, cyanosis, hypotension, tachycardia and prolonged capillary filling suggest impending severe reaction.
If no history is available in a collapsed patient, use an ABCDE advanced life-support approach.
