Obesity can mimic asthma, it affects respiratory symptoms and lung mechanics, but it can also overlap of course. Asthma is more often diagnosed in obese (misdiagnosed?). High birth weight is associated. , as is maternal obesity (and gestational weight gain) in pregnancy. Each BMI increase of 1kg/m2 increases risk by 2-3%!
Obesity is one of the factors associated with fatal asthma attacks (but note socioeconomic confounding).
Weight reduction leads to improved lung function, health status, symptoms and morbidity in adults. Not yet proven in adolescents.
Slightly increased risk of acute asthma attacks in obese adults and school age children.
=allergic rhinoconjunctivitis due to seasonal triggers, typically grass and/or tree pollen. First described by John Bostock in 1819! More likely if born in early months of year!
So itchy, swollen, watery eyes, runny and/or blocked nose, sneezing. Often itchy throat and ears too. Cobble stone appearance can be seen at the back of throat.
Not dangerous, but can seriously affect quality of life: poor sleep, poor concentration (exams usually at worst time of year), embarrassment about snot. One study showed children in England were less likely to get their predicted exam grades if they had hay fever, especially if prescribed sedating antihistamines. Moderate to severe hay fever also associated with worse, uncontrolled asthma. London study found hospital admissions for asthma 50% higher 3 days after high grass pollen levels (inconclusive for tree pollen). [Int J Biometeorol. 2017]Brussels study found similar, compounded by air pollution. Treatment of hay fever with intranasal steroids or class 2 antihistamines reduced admissions by up to 80%. [asthma res and pract2015]
Associated with other atopic conditions, such as food allergy and asthma. Under recognized as trigger for asthma exacerbations – pollen is too large to trigger the lower airways directly, rather, pollen exposure in the upper airways trigger inflammation that travels down (probably over a period of weeks) to the lower airways. An exception is when pollen grains are fragmented, as seen in thunder storm asthma where one night in Melbourne, 2016, several thousand acute respiratory presentations came to ED (up over 400%), ambulance service was overwhelmed, hospitals ran out of inhalers. 10 deaths implicated. [Australia, Clin Exp Allergy. 2018;48:1421‐1428]. Complex though, rain/moisture probably contribute to pollen grain rupture, and atmospherics bring surges of pollen down to ground level.
There are many different species of grass, but if allergic to one you tend to be allergic to all of them. Trees on the other hand vary, you tend to be allergic to specific groups of trees. In Europe the most important are birch (northern Europe) and olive (Southern Europe). Birch is related to alder, hazel, beech and oak. Olive is related to ash. Weeds belong to various unrelated families.
Hazel trees can start producing pollen in January! Weeds such as nettle can continue producing pollen through September! Moulds seem more associated with asthma than hay fever. Cypress blooms in winter!
It’s not just pollen count – the amount of allergen carried by the pollen (“pollen potency“) varies too. Correlates pretty closely but varies by time and place, 4-5 fold difference geographically (especially grass). France has the highest yearly average grass pollen potency, 7-fold higher than Portugal. Olive pollen from two locations 400km apart varied 4-fold in their allergen potency – in Portugal there are times when pollen from Spain probably more of a problem for triggering hay fever than pollen from “local” trees! [Health Impacts of Airborne Allergen Information Network (HIALINE project)]
Watch the pollen count, and choose activities inside or outside accordingly. There are apps that can help with this. But note that the time of day is important too – for grass pollen, the risk is greatest in the first half of the morning and again from about 4pm in the afternoon, until late evening. But can persist into the early hours if temperatures remain high, this effect is particularly noticeable in the cities of the south of England. For tree pollen, the risk is usually during daylight hours only.
Closing windows, or at least not sitting near windows should help. Wash your hair more regularly. Don’t dry clothes outside. Pollen barrier balms available (evidence?). Big, wrap around sunglasses?
Choose when and where you are going on holiday carefully, so you get away during the worst period. North of Scotland and the islands have a short, late grass season (late June, early July). Coastal areas likely to be best (although often there are fields just back from the coast, so it may depend on the wind direction!). For tree pollen, season is earlier for most (see above), and there are parts of Scotland (Orkney, Lewis, Caithness, Sutherland) with very few trees. For holidays abroad, see World pollen data.
Antihistamines – oral or nasal. Various, some people find one works better than another Sedating antihistamines eg Chlorphenamine should be avoided except at night. Nasal steroids useful if used correctly. Combination steroid/antihistamine available. Leukotriene receptor antagonist licensed for hay fever in children with asthma.
Short courses of oral steroids might be justified for special occasions.
Immunotherapy available – deaths reported in asthmatics with poor control.
Sublingual – age not important cf ability to hold in mouth for 2 minutes. Not approved by SMC in Scotland yet. Combined grass and house dust mite coming.
[Sian Ludman, St Mary’s]
For symptoms all year round (perennial), triggers such as house dust mite and pets are more likely.
Diagnosis is about probability – high probability is recurrent episodes of cough, wheeze, breathlessness, chest tightness plus documented wheeze, atopic history, documented variable PEF or FEV1. Isolated episodic cough is not sufficient. Episodes typically triggered by viral infections, cold air, exertion, laughter or emotion. Start treatment, “typically” 6 weeks inhaled corticosteroids (ICS). If good response to treatment, then diagnosis is confirmed.
If intermediate probability then spirometry with reversibility is preferred initial test for children old enough to do it (Grade D recommendation). If spirometry normal, then do challenge tests and/or Fractional exhaled nitric oxide (FeNO) measurement. For younger children, watchful waiting or trial of treatment.
FeNO has reasonable positive predictive value, but false positives in allergic rhinitis, rhinovirus and dietary nitrates, plus overlap in values between asthmatics and normal population (especially children).
Red flags –
Focal chest signs
Abnormal voice or cry
Failure to thrive
Self management education, written personalized plan. Assess control – consider using Asthma Control Test (ACT) questionnaire or similar.
Assess risk of future attacks. Co-morbid atopic conditions, younger age, obesity, and exposure to environmental tobacco smoke are markers of increased risk (some of these strongly socioeconomically linked, of course).
Ask specifically about medication use and assess prescriptions. Explore attitudes to medication as well as practical barriers to adherence.
Not for routine house dust mite avoidance measures. Avoid smoking and second hand smoke.
Weight loss (including dietary and exercise programmes) for overweight and obese. Breathing exercise programmes can be offered as an adjuvant to pharmacological treatment for adults.
ICS are recommended preventer. An asthma attack in the previous 2 years, symptoms 3 days a week, or using reliever 3 days a week, or waking 1 night a week are indications. Give twice daily at least until good control established.
Start at dose appropriate for the severity of the disease. In mild to moderate asthma, no benefit in starting at high dose and weaning. In children, “reasonable” starting dose is Very Low (100mcg twice daily of Clenil or equivalent).
5yrs and over, if add-on is required then choice between inhaled long acting beta agonist (LABA) or leukotriene receptor antagonist (LTRA). Only then increase dose of ICS from very low (100mcg Clenil or equivalent twice daily) to low (200mcg twice daily).
For exercise induced symptoms, generally just a sign that inadequate control! But if otherwise well controlled then give inhaled short acting beta agonist immediately prior to exercise. Then choice between LRTA, LABA, cromoglicate or theophylline.
Acute Severe Asthma
Sats under 92%
PEF 33-50% of best or predicted
Can’t complete sentences in one breath, or too breathless to feed
HR >140 (under 5), >125 (over 5)
RR>40 (under 5), >30 (over 5)
Life threatening defined as:
Exhaustion, poor resp effort [tautology?]
MDI plus spacer if mild/moderate
If refractory to beta agonist, add ipratropium 250mcg mixed into beta agonist [same dose for everyone]
“Consider adding 150mg magnesium sulphate to each neb in first hour if symptoms started <6hrs and presenting with sats <92%” [Recommendation based on MAGNETIC trial – no overall benefit but better Asthma Severity Score at 1 hour for this subgroup – see below] – 2.5ml of 250mmol/ml (1000mg made up to 16ml)
Give oral steroids early, dose by age.
Second line treatment –
Consider single IV bolus of salbutamol (15mcg/kg over 10mins)
Consider aminophylline for severe asthma unresponsive to maximal doses of bronchodilators and steroids.
Consider IV MgSO4 40mg/kg/d
Systematic review of IV Magnesium in children (2018) – pulmonary function improved, hospitalization and further treatment decreased. MAGNETIC trial of Magnesium nebs did not show a clinically significant improvement in mean asthma severity scores in children with acute severe asthma. Best clinical response was seen in children with saturations <92% at presentation and those with preceding symptoms lasting less than 6 hours [Lancet 2013].
According to the 2010 Global Disease Burden Assessment, outdoor air pollution caused more than three percent of the annual disability and life lost. Rising due to urbanisation. Responsible for 50 000 deaths annually in the UK.
Air pollution associated with low birth weight, smaller heads, developmental disorders eg autism, type 2 DM, strokes, heart attacks (atherosclerosis), cognitive decline, slower development of lung function with reduced adult capacity (implication for COPD), onset of asthma, wheeze. Not just exacerbations of chronic lung disease!
Different kinds of pollution – particulates (different sizes eg PM1), nitrogen dioxide, sulphur dioxide. Most PM10 from traffic, but natural sources too eg pollen, soil. Wood burners! NO2 and SO2 falling as fewer power stations and less industrial output, but NO2 particular problem for urban centres where most commercial vehicles run on diesel.
Diesel engines also produce polycyclic aromatic hydrocarbons eg BaP (Benzo pyrene), maternal exposure a concern as linked to mental health and neurodevelopmental problems in children. Some also carcinogenic.
Particulates a problem for respiratory conditions. Often contain spores and pollen. Ozone associated with airway hyperresponsiveness.
Not just about degree of pollution – metereological factors (temperature, atmospheric pressure, low humidity etc) complicate. In Taiwan, pollution synergistic with dust mites for development of asthma.
Carbon deposits found in fetal side placental macrophages.
MRSA and stenotrophomonas colonization in CF associated with maternal PM levels.
European study of 325 000 adults found mortality increased proportionally with levels of particulate matter, nitrogen dioxide and black carbon – even at levels below current EU/US/WHO standards. [BMJ 2021;374]
Southern California reduced PM levels and found less severe chronic lung problems.
1 hour commuting in Sao Paolo estimated to be equivalent to 5 cigs/d. In London, travel to school is bulk of exposure (plus school breaks! Note locations!) esp stationary traffic.
What cars produce in lab tests is not the same as in the real world, even when manufacturers don’t cheat!
Low emission zones generally exclude cars, and may just divert traffic elsewhere, not much evidence that they help. London low emission zone has reduced NO2 slightly only. Plan for ultra low zone.
Severe acute respiratory syndrome – caused by one of the coronavirus group, see also MERS and COVID19. The virus probably originated in bats, then crossed into humans via masked palm civets.
The virus spread beyond its original outbreak in China when a businessman became unwell on his flight out of China and died in Vietnam in 2003. Further outbreaks appeared rapidly, as far afield as Toronto. Eventually led to 8000 cases globally, but rapid surveillance and isolation measured brought the epidemic to an abrupt end within 4 months.
Super shedders exist, who have much higher infectivity (1 case on a plane infected 120 others, whereas another plane had 4 cases on board, but no secondary cases occurred!). On the other hand, there is no documented transmission by asymptomatic cases, or between children.
Incubation period is 5-7 but up to 14 days. Spread is by respiratory, fomites, and faecal-oral routes. Peak shedding occurs at peak of clinical disease hence outbreaks were often among health care workers.
Symptoms are ‘flu-like, and non-specific. Fever is universal. Those who do badly have sudden deterioration on 10th day, with ARDS. Mortality is around 10%, but very age dependent, reaching over 50% in the over 65s. Children have lower viral loads, and generally have a benign course. Compared with adults, they perhaps get more gastrointestinal symptoms than respiratory.
Children under 5 yrs are hardly affected at all – perhaps because recent coronavirus infection protective, perhaps because of reduced immune reactivity.
No long term morbidity seen in children.
The diagnosis is suggested by the paucity of clinical signs (mild crepitations only, if anything) with an abnormal chest radiograph (non-specific), and laboratory evidence of leucopenia, lymphopenia, and thrombocytopenia. Raised AST/ALT also seen.
Definitive diagnosis is by ELISA or PCR, neither of which is very sensitive, or useful early on in disease.
Interferon alpha appears to be of benefit in vitro. Otherwise supportive.
Personal Protective Equipment effective if used properly – so buddy system.
Infection control – encourage self isolation, dedicated staff etc.
Middle East respiratory syndrome, caused by a coronavirus (MERS-CoV) . See also COVID19 and SARS.
Reported 2012. More than 2000 cases so far, mostly related to Arabian peninsula, but a single case of MERS-CoV in a returning traveller led to an outbreak involving 186 cases across 16 hospitals in the Republic of Korea.
36% mortality, mostly people with co-morbidities. More than 2000 cases so far.
One of WHO blueprint priority diseases – potential for serious outbreak, no treatment or vaccine (6-7 others: SARS, Crimean-Congo HF, Ebola, Lassa etc).
Incubation time 2-5 days but up to 14. Median onset to hospitalisation 4 days.
Risk factor appears to be camel contact – milk, meat, urine.
Management based on experience of SARS etc.
Infection control – negative pressure, dedicated staff, cleaning, PPE for suspected cases, self isolation for close contacts.
Hogmanay 2019 WHO were informed of cluster of cases of Pneumonia of unknown cause in Wuhan city, Hubei province, China.
Novel coronavirus identified, named SARS-CoV-2. COVID19 is associated disease. Distinct from coronaviruses responsible for SARS (severe acute respiratory syndrome) and MERS (Middle East respiratory syndrome) but of course these are both similarly capable of causing severe disease, whereas many coronaviruses pretty benign.
By end of February 2020, more than 70 000 cases reported across China, 2500 fatalities. Pandemic was declared by WHO on 11th March.
Cruise ships including the Diamond Princess in Japan (over 700 cases) and the Zaandaam were particularly hard hit.
Lockdown declared in UK on 23rd March.
Binds to ACE2 – potentially explaining particular susceptibility among people with hypertension and Africans (nearly double rate of whites) and Asians (although Indian rates lower than Bangladeshi/Pakistani). Rates among Chinese females actually lower than among Whites! [UK data]
At least 3% of severely affected people have known or previously unrecognised genetic defects in type 1 interferon production (especially TLR3 and IRF7 which amplify production).
Risk of “critical illness “ from COVID-19 RR 1.44 if overweight, 1.97 if obese. UK OpenSAFELY analysis. Death 1.27 if BMI 30-39, 2.27 if BMI>40. ACE-2 higher in obese. Plus different immune responses and challenges to ventilate.
London has double the age standardised mortality of any other part of the UK (Birmingham next), as high as 144 per 100 000 in Newham. Glasgow’s rate is about 80 [UK data].
Diabetes, cancer and poorly controlled asthma associated with death in primary care records study. Residential care homes, health care workers, social deprivation, Black/Asian groups also seem to be particularly at risk of death.
Bronx worse hit than Manhattan, despite similar population density. Higher attack and death rates among Afro-Americans. Role for air pollution too?
Pregnancy increases risk slightly, not much risk to baby although elective preterm delivery may be part of management of sick mother.
Acute neurological presentations in adults, including stroke and Guillain Barre syndrome.
Transmission from asymptomatic cases seems to be less important than symptomatic and pre-symptomatic (1-2 days).
Probably more severe than SARS but still children tend to be less severely affected than adults. Cross protection from immunity from other coronaviruses? Differences in ACE2? Some asymptomatic.
Wheeze uncommon. Asthma does not appear to increase risk (in China).
X-ray more often negative; CT more sensitive.
Can present with GI symptoms.
One baby born to an infected mother developed severe complications.
Neutrophil and LDH counts go up, lymphocytes go down.
A small series of children with COVID-19 has shown a greater prevalence of peripheral halo (halo-sign) lung consolidations on CT.
The criteria for the definition of Acute Respiratory Distress Syndrome (ARDS) and septic shock, the guidelines for the management of sepsis and septic shock and the use of non-invasive ventilation in children are different from those of adults.
Children desaturate more easily during intubation; therefore, it is important to pre-oxygenate with 100% O2 with a mask with a reservoir before intubating.
A rectal swab may be useful in children to determine the timing of the termination of quarantine.
[Chengdu and Italian experience, from PIPSQC]
WHO supports use of dexamethasone in patients with acute respiratory presentation and hypoxia (sats<90%), tachypnoea, or severe respiratory distress. RECOVERY trial continues to study dexamethasone in neonates, plus roles for azithromycin and toculizimab.
Remdesivir is licensed in hospitalised patients in oxygen, over 12 years and over 40kg and can be considered in this age group for patients with high-risk comorbidity,
Paediatric multi inflammatory syndrome associated with COVID19 (PIMS-TS)
Neutrophilia (most), lymphopenia, single or multiorgan dysfunction. Possibly Kawasaki criteria. Exclude other infectious cause including shock syndromes and myocarditis (but don’t delay seeking advice).
Abnormal fibrinogen, d-dimer, ferritin, hypoalbuminaemia. Other features eg coagulopathy variable.
WHO refer to PIMS-TS as Multisystem Inflammatory Syndrome in Children (MIS-C), case definition is similar but requires at least 3 days of fever and either evidence of COVID-19 on PCR or serology or a likely contact with COVID-19.
Length of PICU
stay generally short, some require ECMO, majority survive.
For suspected asthma, where child unable to do spirometry, then watchful waiting or trial of treatment for specified time period. Choice of treatment depends on severity and frequency of symptoms – “typically 6 weeks inhaled steroid”, “very low dose”.
Start regular preventer treatment or escalate treatment if you are getting frequent symptoms, viz:
three times a week or more, or
using your blue inhaler three times a week or more, or
if your asthma is waking you up once a week or more.
Start regular preventer if asthma attack in previous 2 years!
Same table for all ages now, and same steroid doses!
Step 1 – very low dose inhaled corticosteroid (ICS). OR leukotriene receptor antagonist (LRTA) if under 5.
Step 2 – Add LRTA if under 5, else inhaled long acting Beta agonist (LABA) if 5+.
Step 3 – If no response to LABA, stop and increase ICS dose. If some benefit from LABA continue and increase ICS dose, or consider trial of LTRA.
Step 4 – high dose therapies: increase ICS dose to medium, or add slow release theophylline. Refer for specialist care.
Very low dose is 50mcg 2 puffs twice daily of beclometasone. Low dose is double that, medium 200mcg 2 puffs twice daily.
QVAR and fluticasone are double the efficacy of beclometasone so doses are halved. Ciclesonide is somewhere in between.