Category Archives: Common

Hay fever

=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.

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 over a period of weeks to the lower airways. An exception is when pollen grains are fragmented, as seen in thunder storm asthma [Australia, Clin Exp Allergy. 2018;48:1421‐1428]

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 February, weeds can continue produce 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 varies too. Correlate pretty closely but varies by time and place. Pollen potency varies (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 accordingly. Pollen levels fall in evening in countryside, but in cities not until 1am!

Closing windows, or at least not sitting near windows, washing hair, not drying clothes outside, pollen barrier balms.

Choose where you are going on holiday carefully!

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.

BTS/SIGN Asthma guidance

Latest revision 2019.

Diagnosis is about probability – high probability is recurrent episodes, documented wheeze, atopic history, documented variable PEF or FEV1. 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 FeNO measurement. For younger children, watchful waiting or trial of treatment.

Red flags –

  • Focal chest signs
  • Abnormal voice or cry
  • Failure to thrive
  • Vomiting
  • Wet/productive cough
  • Nasal polyps


Self management education, written personalized plan.

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.


ICS are recommended preventer. Give twice daily until good control established.

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 to low.

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:

  • PEF <33%
  • Exhaustion, poor resp effort [tautology?]
  • Hypotension
  • Cyanosis
  • Silent chest
  • Confusion

Treat –

  • Oxygen
  • 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 short duration of symptoms and presenting with sats <92%” [Recommendation based on MAGNETIC trial, benefit for those with short duration of symptoms – 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


According to NICE, 3 or more loose or liquid stools in a day (or more frequently than is normal for the individual) counts as diarrhoea.

Persisting for more than 14 days makes it chronic.

Acute typically gastroenteritis. Presence of blood and/or mucus suggests more invasive inflammation, viz colitis.

In kids, can occur with pretty much any illness!

Vomiting with diarrhoea makes a primary gut cause more likely, but still not specific.

Prolonged Jaundice

Physiological is because Long chain FAs in breast milk compete with Glucuronyl transferase! Dehydration and poor feeding contribute (jaundice FOLLOWS, does not cause). But can also be seen in bottle fed babies.

Prolonged jaundice defined as 21/7 if well, term according to American Academy of Pediatrics. After that, investigation probably appropriate.

Unconjugated vs Conjugated bilirubin is important – do direct bilirubin. Conj bili >20 may indicate significant disease, esp if unconj not high. Low albumin suggests prenatal onset.


  • Haemolysis (so liver function tests normal): eg rhesus disease (diagnosis: Direct Coombs Test Positive), ABO, irregular antibodies (Kell, Duffy; varying significance), hereditary sphero/elliptocytosis, G6PD deficiency, DIC. G6PD in baby can be precipitated by maternal drugs/infection. Enzyme assay false negative because of high retic count, so test mother for carrier status.
  • Crigler Najjar is unconjugated. Uridine Di Phos Glucuronyl transferase deficiency (Dubin Johson/Rotor only present >2 yr). Recessive form is severe, assoc with kernicterus; dominant can be treated with phenobarb.
  • Hypothyroidism
  • Galactosaemia – in the first week of life can be unconjugated but always features liver dysfunction cf Crigler Najjar so unlikely to be any confusion.


Suggests hepatitis. Note that Alk phos in normal neonates is often high in isolation. See BSPGHAN protocol.

  • Congenital Biliary Atresia
  • Choledochal cyst: assoc with East Asians, PKD (Caroli’s disease). Cystic mass below liver. Can rupture and cause ascites, cause obstruction +/or cholangitis. Late carcinoma risk.
  • Spont CBD perforation – discoloured umbilicus, paracentesis diagnostic. Rx Surg
  • Gallstones – possible!
  • Congenital viral infection (TORCH), enteroviruses (esp ECHO, assoc with fulminant hepatitis), sepsis (eg UTI, listeria assoc with hepatic abscesses).
  • Cystic fibrosis and bile plug syndrome
  • Inherited Metabolic Disorders: galactosaemia, Zellweger’s, haemochromatosis, etc.
  • Alpha -1 antitrypsin deficiency
  • Alagille’s syndrome
  • Endocrine disorders: congenital hypothyroidism (1 in 60 000), pituitary/adrenal underactivity.

SIGN/BTS Asthma guidance 2016

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.

ICS doses

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.


An added sound heard when listening with a stethoscope, distinct from heart sounds or other clicks or snaps.

Can indicate a structural abnormality.  But can be heard in normal hearts too, esp kids.

Still’s murmur

Or “innocent” murmur.  Characteristic vibratory, crescendo-decrescendo sound, loudest along left sternal border.  Never louder than grade 3.  Typically gets quieter when child stands up (you would not expect a murmur caused by a structural abnormality to change).

Venous hum

Another innocent one, a rumble heard in the upper chest, disappears when lying down, or when neck turned or neck veins occluded gently.

Pulmonary flow murmur

Pulmonary valve closest to anterior chest wall, which might explain why you sometimes hear this.  Might be confused with pulmonary stenosis or subaortic membrane.


Baby strains and cries to pass stool but it comes out soft or not at all.  Functional gastrointestinal disorder thought to occur in 0.9 – 5% of infants under 6 months (Rome IV criteria).

Due to poor co-ordination of pelvic floor muscles with increased intra-abdominal pressure generated during stooling. Seen in babies up to 9 months.

Studies have reported symptoms of discomfort around passing normal stool in up to 18% of babies, not all of these children will strictly meet the diagnostic criteria for dyschezia.

Differentiating from true constipation etc requires a clinical history and a normal clinical examination, with the key difference being that the stool is not hard in dyschezia.

No medication (or any form of rectal stimulation) required, can be expected to resolve spontaneously.


See BTS/SIGN guidance on asthma, also asthma prevention.

National asthma guidance conflicting – NICE recommends both spirometry and Fractional exhaled nitric oxide to confirm diagnosis, has rejected “trial of treatment” and de-emphasized peak flow monitoring.

FeNO is expensive and available in only a minority of GP practices and hospital services.  Requiring it means GPs can no longer make diagnosis themselves.

Spirometry results in most primary care patients with asthma are normal!

Other difference from SIGN/BTS is Leukotriene Receptor Antagonist (LRA) as first choice add on rather than Long acting Beta agonist (LABA), on basis of marginal benefit but increased cost.

Primary care respiratory society UK has produced advice on how to deal with conflicting national guidelines – reasserts prime importance of good clinical method and regular reassessment, prioritises peak flow monitoring alongside trials of treatment if necessary.

[BMJ editorial 2017]

Spacer best for everyone!

200 doses in an MDI.   2 puffs BD exhausts an MDI in 50 days. Multidosing 5 puffs 4hrly will exhaust it in 6 days.

Stage 3 for over 5yrs is LABA. Montelukast is only recommended as an option in older kids if failure to respond to LABA.  The other option is slow release theophylline.

Growth Restriction

Children who use inhaled steroids for asthma grow slower than their peers in the first year of taking the medication, by about half a centimetre per year. Metanalysis of 25 trials, various types of steroid.  Seems to be most obvious in initial year of treatment.  Only 1 study followed children into adulthood – budesonide, used for average of 4 years – reduction in final height of  1.2cm (Kelly, PMID 22938716).

Should therefore be prescribed at the lowest effective dose. Cochrane 2014 found significant difference between low dosing (50-100 Clenil equivalent) and medium dosing  of 0.2cm per year but noted that the  majority of trials did not report height data.

However, the small effect on growth needs to be weighed against the proven benefits of these drugs in controlling asthma, and ensuring children’s lungs grow to their full capacity.   Undertreated asthma is much more likely to have a harmful effect on a child’s development than a small reduction in growth.

Newer Therapies

Xolair=Omalizumab, monoclonal vs IgE. Subcut, 2-4 weekly, for age 6+ where conventional therapy not working.  Other criteria are total igE >30, positive tests for aeroallergens, FEV1<80%.

Airsonett is evidence based, temperature controlled laminar flow system for bedroom. Noisy!


See National review of asthma deaths.  Recommendations include:

  • Refer specialist if >=2 courses oral steroids within 12 month period
  • Follow up after every ED/OOH attendance
  • Hospital follow up after every hospital attendance
  • Annual inhaler technique check
  • Personal asthma plan for everyone

See website for self management.

Asthma prevention

Atopy is not a single phenotype, the idea of an “atopic march” from infantile eczema through food allergy to asthma and rhinitis is way too simplistic.

There are different risk groups.  Environmental exposure to allergens and microbes in early life is one factor.  Farm environment protects.  Indoor allergen exposure at 1yr of age is protective against recurrent wheeze at 3 yrs.  Reduced bacterial diversity is a risk factor for asthma and atopic wheeze – certain bacteria esp bacteroides and firmacutes seem to be protective.

Viruses also play a role.  RSV is associated with later asthma regardless of existing atopy or not, although perhaps not with asthma persisting into adulthood; rhinovirus wheezing in first 3yrs is similarly associated with persistent wheeze, especially in atopic persons.

Heritability of asthma accounts for less than 50% of patients so gene-environment interactions are at least as important.  A gene has been found that is associated with early childhood asthma with severe exacerbations (CDHR3).

Animal experiments have already shown that oral administration of bacterial extracts prevents bronchial hyperreactivity.  We should therefore encourage less Caesarean sections, more breast feeding, less antibiotic use, more green spaces, more “natural” food preparation and distribution (ie less plastic!).