Respiratory Flashcards
croup
asthma
bronchiectasis
COVID 19
whooping cough notifiable
yes
epidemiology whooping cough
cases in older children and adults tend to be much milder, whilst infants remain most at risk of hospitalisation and death due to pertussis (5). The incidence of pertussis tends to peak every 3-4 years for reasons that are poorly understoo
vaccines whooping cough
pertussis vaccines - 2, 3 and 4 mths of age, booster at 3 yrs and 4 mths
bacteria whooping cough
bordatella pertussis
gram negative bacillus
spreads by aerosolised droplets
bacteria attaches to respiratory epithelium and produce toxins which paralyse cilia and promote inflammation, impairing clearance of secretions
risk factors whooping cough
non vaccination
exposure to an infected individual
clinical features whooping cough
- catarrhal phase - 1-2 weeks
Rhinitis
Conjunctivitis
Irritability
Sore throat
Low-grade fever
Dry cough - paroxysmal phase - 2-8 weeks
severe paroxysms of coughing followed by inspiratory gasp, can result in vomiting
if <3mths apnoea more common - convalescent phase - 3 mths
decreases in frequency and severity
ddx whooping cough
bronchiolitis
mycoplasma pneumonia
bacterial pneumonia
management whooping cough
duration of cough <21 days= macrolide
Clarithromycin for those under 1 month, azithromycin or clarithromycin for those over 1 month
Co-trimoxazole is the 2nd line antibiotic where macrolides are contra-indicated or poorly tolerated
Further management is supportive, including paracetamol and / or ibuprofen for symptomatic relief and adequate fluid intake to prevent dehydration
can take up to 3 mths to reolve
hospital admission whooping cough indications
Who are under 6 months of age and acutely unwell
With significant breathing difficulties, e.g. apnoeic episodes, cyanosis, respiratory distress or severe paroxysms of coughing
Feeding difficulties
With significant complications, e.g. pneumonia or seizures
whooping cough avoiding school ?
The child should avoid nursery or school until they have had the cough for 21 days or have had antibiotics for 5 days
investigations whooping cough
<2 weeks - culture of nasopharngeal aspirate or swab…PCR testing
>2 weeks - anti pertussis toxin IgG serology, oral fluid testing for anti pertussis toxin
FBC - lymphocytosis
whooping cough complications
Secondary bacterial pneumonia (up to 20% of infants)
Seizures
Encephalopathy (rare)
otitis medis
bronchiolitis definition
viral infection of the bronchioles
most commonly caused by RSV
RSV
respiratory syncytial virus
bronchiolitis epidemiology
children <2 yrs
1/3 will develop in first year of life
occurs during winter and spring months
pathophysiology bronchiolitis
Proliferation of goblet cells causing excess mucus production
IgE-mediated type 1 allergic reaction causing inflammation
Bronchiolar constriction
Infiltration of lymphocytes causing submucosal oedema
Infiltration of cytokines and chemokines
risk factors bronchiolitis
Being breast fed for less than 2 months
Smoke exposure (eg. parents’ smoke)
Having siblings who attend nursery or school (increased risk of exposure to viruses)
Chronic lung disease due to prematurit
clinical features bronchiolitis
Low-grade fever
Nasal congestion
Rhinorrhoea
Cough
Feeding difficulty
examination bronchiolitis
Tachypnoea
Grunting
Nasal flaring
Intercostal, subcostal or supraclavicular recessions
Inspiratory crackles
Expiratory wheeze
Hyperinflated chest
Cyanosis or pallo
ddx bronchiolitis
pneumonia
HF
croup
CF
investigations bronchiolitis
nasopharyngeal aspirae or throat swab
blood and urine culture
FBC
ABG
CXR - Hyperinflation
Focal atelectasis
Air trapping
Flattened diaphragm
Peribronchial cuffing
urgent referral bronchiolitis
Apnoea
Child looks seriously unwell
Severe respiratory distress eg. grunting, marked recessions, respiratory rate >70
Central cyanosis
Oxygen sats < 92%
Hospital referral should be considered if any of the following are seen (4):
Respiratory rate > 60
Inadequate fluid intake (50-75% of usual volume)
Clinical dehydration
bronchiolitis hospital management
Give oxygen if sats < 92% in room air
Give fluids via nasogastric or orogastric tube if inadequate oral intake
Consider CPAP if there is impending respiratory failure
Perform upper airway suctioning if there are upper airway secretions or apnoea
discharge bronchiolitis
Clinically stable
Taking adequate oral fluids
Maintaining sats > 92% for more than 4 hours
complications bronchiolitis
Hypoxia
Dehydration
Fatigue
Respiratory failure
Persistent cough or wheeze (very common and parents should be counselled that their child may cough for several weeks)
Bronchiolitis obliterans – Airways become permanently damaged due to inflammation and fibrosis
prognosis bronchiolitis
lasts for 7-10 days
cough can last for 6 weeks
CF definition
an autosomal recessive disease caused by a mutation in the CF transmembrane conductance regulator gene (CFTR) resulting in multisystem dysfunction. In 2000 the life expectancy of a child born in 2000 was 50 years
epidemiology CF
approximately 1 in 25 Caucasian Europeans are carriers of a CF gene with approximately 1 in 2500 live births having CF. p.Phe508del (ΔF508) is the commonest mutation in the UK with this accounting for at least one mutation in 90% of people with CF in the UK, with 50% of those with CF in the UK are homozygous for this mutation
CF respiratory tract
The CTFR gene encodes the CFTR protein – a chloride channel that is present in numerous epithelial tissues. Chloride is driven against its concentration gradient using ATP.
In the airway, CFTR is present on airway epithelial cells and submucosal glands and when defective results in disruption to chloride ion movement and also affects sodium reabsorption (by disturbing the function of ENaC) which reduces the amount of water in secretions. This results in reduced airway surface liquid.
The airway surface liquid is an important component of the mucociliary escalator and also has key immunological functions. The effects of reduced airway surface liquid serve to impede mucus clearance.
The altered lung environment provides a niche for bacterial growth with the biofilm mode of growth providing ideal conditions to protect bacteria from the host immune system and the actions of antibiotics. The pro-inflammatory cascade contributes to tissue damage.
CF pancreas
In the pancreas the pancreatic duct is usually occluded in-utero causing permanent damage to the exocrine pancreas rendering patients with CF ‘pancreatic insufficient’. Pancreatic insufficiency is closely related to genotype. Over time, endocrine pancreas is affected with 28% of those older than 10 years requiring treatment for CF-related diabetes mellitus.
CF gi tract
In the gastrointestinal tract, the small intestine secretes viscous mucus which can cause bowel obstruction in-utero which can cause meconium ileus. In the biliary tree in-utero, CF can cause cholestasis which can result in neonatal jaundice. Later in life the same pathology can result in distal intestinal obstruction syndrome (DIOS) and CF-related liver disease (14% of patients)
CF repro tract
98% of men with CF are infertile due to a congenital absence of the vas deferens. In women nutrition is likely to be an important predictor of successful pregnancy. It is suggested that the timing of pregnancy be carefully planned, as pregnancy is often associated with a deterioration in lung health
risk factors
aut recessive
lots of mutations to teh CFTR gene
Different organs have different sensitivity to loss of CFTR protein function, with the vas deferens particularly sensitive in contrast to the lungs, which are less sensitive. Instead the lungs are more susceptible to other factors, like stochastic, environmental, and genetic modifiers-genes that modify the expression of CFTR protein
clinical features CF
Neonates
Meconium ileus – 10% of children present with abdominal distension, delayed passage of meconium and bilious vomiting in the first days of life.
Since the introduction of screening for CF in neonates (part of the Guthrie test) the majority of cases of CF are identified here (however it is important to note that it is a screening test and still needs diagnostic testing)4
Failure to thrive
Prolonged neonatal jaundice
Infancy
Failure to thrive
Recurrent chest infections
Pancreatic insufficiency: steatorrhoea
Childhood
Rectal prolapse
Nasal polyps (N.B. strongly suspect CF in children presenting with nasal polyps)
Sinusitis
Adolescence
Pancreatic insufficiency: diabetes mellitus
Chronic lung disease
DIOS, gallstones, liver cirrhosis
examination CF
Hands: finger clubbing
Face: nasal polyps
Chest: hyperinflated, crepitiations, portacath (indwelling vascular access device)
Abdomen: faecal mass (if constipated/DIOS), may have a scar from ileostomy (meconium ileus)
diagnosis of CF
A diagnosis of CF can be made if there is a fitting clinical history and a positive chloride sweat test which may be supported by the identification of two identified mutations
investigations CF
Chest radiograph: to assess for hyperinflation, there may be evidence of bronchial thickening (undertaken annually as part of annual assessment) Some units undertake CT scanning.
Chloride sweat test (at diagnosis and annually if in receipt of CFTR potentiator/corrector therapy)
Microbiological assessment e.g. cough swab/sputum sample (at every clinical encounter)
Glucose tolerance test (at annual assessment at teenage and beyond)
Liver function test and coagulation (at annual assessment)
Bone profile (at annual assessment)
Lung function testing – spirometry / lung clearance index
chloride sweat test
This test measures the electrolyte concentration in sweat
Sweat sample is collected by pilocarpine iontophoresis. Careful technique must be employed to ensure and adequate sample is collected to avoid inaccurate results. A common reason for failure of the test is an insufficient sample in a small baby (limit 3kg).
A sweat chloride >60mmol/L is suggestive of CF. A sweat chloride of 40-60mmol/L is borderline and should be repeated
A single sweat test is not sufficient to diagnose CF, a second test or identification of genetic mutation
Faecal elastase to assess pancreatic function
Chest CT (high resolution) to assess for bronchiectasis (where bronchial diameter would exceed that of accompanying pulmonary vessels)
Genetic analysis
management CF
patient and family education
twice daily physio
mycolytics - DNase, hypertonic saline
exercise
creon
fat soluble vitamins - A, D, E, K
monitor growth
nutrition as higher metabolic demands - build up milkshakes
sputum cultures - monitor for infections, with 2 weeks of abx
if pseudomonas - eradication
regular azithromycin
active segregation
minimise complications
annual review
organisms CF
Staphyloccocus aureus, Haemophilus influenzae and Pseudomonas aeruginosa
complications CF resp
allergic bronchopulmonary aspergillosis
bronchiectasis
haemoptysis
pulmonary HTN
pneumothorax
resp failure
nasal polyps
complications GI CF
rectal prolapse
distal intestinal obstruction syndrome
CF releated liver disease
complications endocrine CF
CF related diabetes - associated with rapid decline in lung function and disease progression - Clinical presentation can differ to typical type 1 DM and comprises weight loss, anorexia and fall in lung function
delayed puberty - avg of 2 yrs, reduced bone minteral density
other complications CF
arthritis
reduced bone mineral density
sub or infetility
