Category Archives: General paediatrics

Onion and garlic allergy

Alliums, as are leeks, shallots and chives. Part of same bigger family as asparagus but probably not co-sensitivity.

The main issue with onion is the chemicals released from cut surfaces, which can trigger eye/nose reactions and potentially asthma. But there’s actually some evidence that onion has an anti-allergy action.

With garlic, there is a well recognised contact dermatitis relating to chopping it.

Otherwise, allergy is very rare. Potentially part of celery-spice-mugwort syndrome.

As with that syndrome, the problem for the allergic person is that not only is it not one of the 14 UK recognised allergens for food labelling and restaurants, but it can be included under “spices” if less than 2% of the overall product, without further detail.

Food allergy

Mixed up with “intolerance” and “sensitivity” – intolerance is a vague term for any kind of reaction, agnostic to cause (most commonly used for gastrointestinal symptoms); “sensitisation” has a specific meaning (see allergy diagnosis) so not to be confused. Allergy is where there is an immune mediated problem (based ideally on history and testing) – but sometimes hard to know the mechanism.

2 basic types of food allergy, you can have both at the same time – type 1 (IgE mediated), and non-type 1 (non-IgE mediated – possibly type 4 hypersensitivity).

Most commonly (in Scotland – but varies across UK, especially with different ethnic groups), and varies widely across the world):

  • Milk
  • Egg
  • Peanut
  • Tree nuts
  • Legumes/Pulses
  • Sesame
  • Wheat
  • Crustaceans/molluscs
  • Various fruits

Birch pollen sensitization in Northern Europe changes the kinds of allergies you get – cross sensitivity with fruit and nuts (pollen food syndrome) – whereas in the rest of Western Europe you get more fruit and seed allergies based on LPS.

Allergy has increased over recent decades – “hygiene hypothesis” has now been developed further to address entire “exposome“. Eczema increases the risk of food allergies 6-fold, via genetic and environmental factors (esp filaggrin mutations, and IL-4 receptor alpha chain polymorphisms).

Hospital admissions for food allergy in the UK have increased 3 fold over the last 30 years, with the biggest increase in children [BMJ 2021; 372: n251]. In big English study of primary care records, estimated incidence of probable food allergy doubled between 2008 and 2018; prevalence highest in children under 5 years (4·0%). Rate in children aged 5–9 years 2·4%, 15-19 years 1·7%. In those with previous food anaphylaxis, only 64∙0% of children and young people had at least one prescription for adrenaline autoinjector, and only 50.3% had them on repeat. Adrenaline autoinjectors prescription was less common in those resident in more deprived areas. 93.3% of first health care encounters for children regarding allergy were in primary care, with 2.2% in emergency departments. Only 7.4% of children had been seen for allergy in a hospital clinic. 92.2% of children had only ever been seen for food allergy in primary care (and looking at those prescribed AAIs, 93.5% only ever seen in primary care!).[Lancet Public Health 2024, Paul Turner]

If you ask people about their children’s allergies, up to 28% of infants will report allergies! Lifetime and point prevalence of self-reported food allergy 20% and 13%, respectively – point prevalence of sensitization as assessed by sIgE stands at 17%, skin prick test 6%, and food challenge positivity 1%. Based on clinical history or positive food challenge, food allergies have increased from 2.6% in 2000–2012 to 3.5% in 2012–2021. Point prevalence for under 16s for self reported but physician diagnosed food allergy is 3.75%. Patterns vary across European regions but not in a consistent way. [Spolidoro and Venter 2022]

Having a child with a food allergy has a significant effect on the quality of life for the whole family. One study suggested that having a peanut allergic child had a worse effect on a family than having a child with diabetes, even though with diabetes you also have restrictions on eating and the potential for serious adverse events. A similar study found the same comparing food allergic families with families where a child had a rheumatological diagnosis. The main domains affected were social. Patient/parent feedback pretty consistent across the world however (although most studies done in Europe and English speaking countries), and across time:

  • Parents lived in fear after the first reaction, often perceiving it as traumatic, and often feeling guilt too
  • They tried to live an ordinary family life and had to learn how to be one-step ahead and understand early signs.
  • The family’s social life was also influenced.
  • Parents asked for support and information from health professionals
  • More knowledge and skills increased parents’ confidence (and by implication quality of life – Knibb 2015)

Mothers tend to report greater impact on the child’s quality of life and experience more anxiety and stress than fathers. Mothers tend to shelter the child, whereas fathers more often express a desire to expand their child’s life, and these differences are often greater where parents are separated.

The concern for the child’s safety affected eating outside the home, with birthday parties and visits to peers’ homes particularly threatening. School and nursery are a major source of concern and often led to more parental work, preparing safe lunches.

Parents often felt they had to teach themselves about allergies, due to the lack of early information provided by health care, and then ended up having to teach family, friends and educational institutions too.

Adolescence is a particularly stressful time, as parents recognize the need for the child to become more independent, at the same time that the adolescent can see the parents as excessively controlling (at least with respect to peanut allergy). Supportive friends particularly important for adolescents.

[Larsen Moen, J Ped Nursing 2019]

Hyperkalaemia

Usually due to renal failure. Causes arrhythmia and death…

Treatment

  • Slow injection of calcium – note calcium chloride and gluconate both available so potential for confusion. Dose is 0.11 mmol/kg, to be given over 5–10 minutes, maximum 4.5 mmol (0.11 mmol/kg is equivalent to 0.5 mL/kg of calcium gluconate 10%). Repeat as necessary if ECG changes do not improve.
  • Bicarbonate indicated if hyperkalaemia due to acidosis or renal failure. 
  • Insulin/dextrose – 10ml/kg 10% dextrose (so 5x usual dose for hypoglycaemia!), plus 0.1u/kg insulin (max 10 units), give over 5 mins. Likely peak action at 30 mins.
  • Dialysis.
  • Hydrocortisone if suspected Addisons. 
  • ECG monitoring
  • Repeated salbutamol nebs

Frusemide and calcium resonium only for asymptomatic!

Bronchiolitis

NICE guidance updated 2021.

Seasonal lower respiratory tract infection of young children, typically caused by Respiratory syncytial virus (RSV) but can be others or mixed.

Classically wheezy cough, wheeze and/or crackles, reduced feeding and increased work of breathing.

Fever not usually high (“consider pneumonia if over 39”)

Diagnosis

Clinical. You would probably have to do 133 Chest x-rays before you found something that would change diagnosis – overuse of CXR associated with increased (and inappropriate) use of antibiotics.

Swabbing for virus identification can help with cohorting and avoidance of nosocomial infection, which can be a major problem.

Management

Ex-prems, chronic lung disease, neuromuscular disorders, haemodynamically significant congenital cardiac disease, immunodeficiency at higher risk, of course.

Admit if sats under 90% if 6/52+ (92% if underlying health problem or under 6/62) – and start oxygen if persistently low.

Admit if feeds less than 50-75% of usual volume, or severe respiratory distress, or reported/observed apnoeas.

NG or orogastric feeds if required – no preference but in theory obstructing nostrils could be unhelpful…

And UTI

Bacteriuria is not uncommonly seen with bronchiolitis, not always clear if this is true urine infection.

Prognosis

Initial coryza 1-3 days. Symptoms peak at 3-5 days. Cough resolves within 3 weeks in 90% but can persist for longer (but perhaps recurrent viruses?).

Prevention

RSV passive immunisation for high risk babies with paluvizimab (Synagis). Limited benefit but does appear to reduce incidence of severe bronchiolitis.

Vaccination in pregnancy effective – antibodies cross, but also prevents Mum getting it and passing it on!

There’s an important story about the dangers of vaccine development.

JCVI recommended Nirsevimab be used first line in 2023 – single injection (half life 71 days). HARMONIE trial – 83% reduction in RSV hospitalisation, 75% reduction in “very severe” disease. Spain and US doing. Fight for global supply so not available…

2025 – programme for high risk babies extended to include all babies born <32/40 (regardless of whether mum received vaccine in pregnancy).

Treatment

See here.

Moulds

Initial studies did not show any relationship between moulds/damp and health, as there was major confounding with socioeconomic status, and because it is hard to quantify mould exposure (with many different mould species).

Then there is the effect of climate, and the built environment – heating, ventilation, insulation, materials etc.

More recently systemic reviews have made it clear there is a link particularly with development of asthma, particularly in older children, and where there is already a family history of atopy.

Coroner ruled death of 2yr old Awaab Ishak in 2020 from granulomatous tracheobronchitis was due to environmental mould exposure from poor housing.

Longitudinal studies have suggested that there may be protective effects but data is limited.

Similarly there is evidence that higher exposure to moulds leads to more asthma exacerbations.

There are genetic polymorphisms that affect ability to break down the fungal protein chitin, and these have been linked to urgent medical care visits, which suggests a non-immune mechanism may be important.

Dampness is linked to mould growth but also to house dust mite, microbial volatile compounds, mycotoxins and endotoxin.

The most studied mould species are AspergillusPenicilliumAlternaria and Cladosporium.

Limited evidence that interventions to reduce mould make any difference.

[European respiratory review 2018]

Gynaecomastia

Common in newborns, presumably due to maternal hormones. Bud underneath the surface, plus swelling of areola/nipple area.

Another peak around puberty, can be unilateral, can be tender. Can progress to be cosmetically problematic.

Exclude a hormonal problem (including prolactinoma and other hormonal tumour):

  • Prepubertal
  • Delayed puberty with no development of penis/testes, no axillary/pubic hair
  • Galactorrhoea
  • Testicular mass

Transfusions

January 2022 – safety alert from MHRA/CMO regarding deaths where there was a delay in providing emergency transfusion.

Should be agreed criteria for rapid concessionary release of blood products.

One issue is Autoimmune haemolytic anaemia, where the presence of red cell antibodies will complicate cross matching (11% mortality!).

Another issue highlighted is failure to give Prothrombin complex concentrate to reverse warfarin (and some other anticoagulants) where severe or limb/sight threatening bleeding.

Nappy rash

Nappy rash is an irritant contact dermatitis affecting the skin where the moist nappy is in contact. It spares intertriginous areas.

Change nappies 6-8 times a day, dry thoroughly, use barrier eg zinc oxide cream.

Differential diagnosis:

  • candidiasis,
  • atopic dermatitis, seborrhoeic dermatitis
  • psoriasis,
  • Langerhans cell histiocytosis,
  • Acrodermatitis enteropathica (autosomal recessive zinc disorder), else nutritional zinc deficiency – +/- acral dermatitis, alopecia, malabsorptive diarrhoea)

Intertrigo (inflammation in the creases) can similarly be infective (bacterial or candidal), eczematous/seborrhoeic or psoriatic.

Blistering rashes

Common, typically vesicular rather than bullous:

  • Varicella – tends not to affect mouth or palms/soles cf below, but more toxic
  • Coxsackie – Enteroviruses such as coxsackie nearly always involve buccal mucosa and tongue (eg Hand-Foot-Mouth). If nowhere else, Herpangina tends to be posterior mouth ie tonsils, soft palate.
  • HSV stomatitis tend to be more unwell, higher fever, gingivitis, cervical adenopathy, no cutaneous lesions.
  • Gianotti-Crosti syndrome
  • eczema herpeticum ie HSV superinfection of eczema;
  • mycoplasma (but mycoplasma has been associated with every kind of rash!)

Rare:

  • disseminated zoster (starts in a dermatome, immunosuppressed);
  • disseminated HSV;
  • vaccinia

For more dramatic blistering:

  • Bullous impetigo
  • Stevens Johnson syndrome esp with plaques, conjunctivitis, lesions at mucocutaneous junctions
  • Urticaria (rarely)
  • Dermatitis herpetiformis
  • Pemphigoid (v rare in children)
  • Acrodermatitis enteropathica – genetic (recessive) disorder leading to Zn deficiency. Blistering rash esp peripheries, face and nappy; diarrhoea (Normal Zn is 10-23).