Common, typically young children with minor infections.
Due to decreased clearance, probably, carbohydrate side chains changed, affecting recognition – characteristic iso enzyme pattern on electrophoresis (ie not usual bone/liver forms).
Can be as high as 50x normal upper limit viz 10 000+! Can last up to 6 months.
Just show that other liver function tests normal, normal calcium/phosphate and no suspicion of myositis, rickets.
See BTS/SIGN/NICE 2025 guidance on asthma, asthma prevention, asthma and obesity
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!
Spacer best for everyone! Orange aerochamber is small mask, up to 18 months, yellow is 1-5yrs. Green is 5+, blue is adult. You can get blue with mask, not green.
200 doses in an MDI. 2 puffs BD exhausts an MDI in 50 days. Multidosing 5 puffs 4hrly will exhaust it in 6 days.
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.
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:
See MyLungsMyLife.org website for self management.
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. Early interventions have been disappointing. Curiously, food allergies and eczema often improve through childhood – this seems less common with asthma.
There are different risk groups. Environmental exposure to allergens and microbes in early life is one factor. Farm environment protects (exposures and/or dietary).
Most studies show dog ownership protective. Weaker evidence for cats. House dust mite sensitisation in early life predicts asthma in school age. Primary prevention of HDM sensitisation has conflicting evidence – Isle of Wight study showed mite avoidance prevented sensitisation and asthma; Canada study showed effectiveness but Dutch study did not. Manchester study reduced early wheezing but had higher rates of sensitisation. Australian study no effect overall but depended on age.
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. So impact of more RSV and other vaccines could be fascinating.
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). TSLP gene on chromosome 5q22 encodes for a master regulator for TH2 processes. But another well recognised gene region on chromosome 17q12-21 (including ORMDL3 and GSDMB) seems to be involved in airway dysregulation after virus infection, rather than allergy.
Increasing evidence that respiratory health is influenced by parental exposures that occur long before conception. The strongest evidence relates adolescent tobacco smoking and overweight in future fathers to increased asthma and lower lung function in their offspring, supported by evidence on parental preconception occupational exposures and air pollution. Antenatal and postnatal (passive) smoking important. Role of breast feeding vs formula still controversial.
No evidence for asthma preventer treatment as an early intervention – cf JIA and other inflammatory conditions.
Grass immunotherapy for rhinitis in children reduces the incidence of later asthma and need for asthma medication. Presumably house dust mite immunotherapy would help too? HDM antigens have allergenic but also endotoxin and enzymatic effects! Jurgen’s study of HDM SLIT in infancy found reduced sensitisation (to anything, but def HDM – but only 11% difference and active group had more pets…); at 3 yrs, no difference in clinical outcomes, unfortunately – in fact, more wheeze…
Spanish RCT of oral bacterial extracts (6 different ones for 6 months) significantly reduced number of wheeze episodes (40%) for up to 1 year. 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!).
Probably 60% of infections are mixed viral/bacterial! Pneumococcus, Haemophilus (non capsulated), Moraxella catarrhalis. Group A Strep is characterized by older age, higher local aggressiveness (ie tympanic perforation and mastoiditis) but lower rates of fever and respiratory symptoms.
AOM is associated with dummy use, adenoids/tonsillitis.
60% of placebo treated children were pain free within 24 hours of presentation [Cochrane 2004, PMID 14973951]. Antibiotics do not increase this proportion. At 2-7 days after presentation, antibiotics reduce by a third the number of children who still have pain (only 14% of the original number), giving a NNT of 15. Too few cases of complications eg mastoiditis to be able to comment on whether antibiotics are useful for preventing such complications.NICE clinical knowledge summary gives NNT of 4000 to prevent 1 case of mastoiditis!
Management is therefore primarily good analgesia. No role for decongestants/antihistamines (Cochrane/NICE).
SIGN guideline 66 on AOM in primary care does not recommend routine antibiotics (but if used, Amoxicillin or co-amox for 5 days recommended). SIGN warns that evidence is poor in infants or in severe disease.
NICE clinical knowledge summary states that at initial presentation, pain and fever should be treated with paracetamol or ibuprofen, at maximum doses if necessary. No benefit from using both (though poor quality evidence). For most children antibiotics can be delayed until day 4 of illness (mean duration of illness is 4 days).
Eardrops containing analgesia and anaesthetic (phenazone and lidocaine = “Otigo”) work within 10 minutes – they also significantly reduce the number of people who go on to have antibiotics. Not to be used instead, however, and not to be used where perforation/discharge.
Antibiotics should be offered however at presentation to people who are systemically unwell. Depending on severity, antibiotics should be considered where child is under 2yrs with bilateral otitis media, or if there is perforation and/or discharge in the ear canal. This advice is also reflected in the British National Formulary for children.
Delaying antibiotics certainly reduces prescriptions, metanalysis of 4 studies in Cochrane did not find any significant difference in pain at 3-7 days, although all but 1 reported some benefit in the immediate treatment group.
A study comparing delayed antibiotics with vs without a prescription (ER based) found high and comparable parental satisfaction rates with both approaches [Chao Peds 2008 PMID 18450878]. In the Cochrane review of delayed antibiotics for URTI, which looked at both adults and children, immediate antibiotics were felt to be more likely to confer modest benefits than delayed antibiotics, with no differences in complication rates between immediate vs delayed antibiotics. Immediate antibiotics had slightly higher levels of patient satisfaction than delayed antibiotics but of marginal clinical significance (92% versus 87%). Concluded that as no evidence for benefit of delayed vs no prescription, best to offer nothing (likely to result in the least antibiotic use). [Cochrane 2011 Delayed antibiotics in URTI, PMID 17636757]
BNFc does suggest antibiotics if:
BNFc also suggests that perforation of the tympanic membrane usually heals spontaneously without treatment; but treat if there is no improvement (eg pain or discharge persists).
Lancet 2006 [pmid 17055944] meta-analysis supports the idea of treating under 2s with bilateral signs (NNT=4), but unlike the BNFc supports treating otorrhoea (NNT=3), as does Cochrane!
Exponential increase in drug resistance and multiresistance. Given how effective placebo is, an effective drug has to do considerably better! Amoxicillin no longer useful (but still recommended by NICE), cefaclor and TMP-SMX not good for borderline resistant pneumococci, azithromycin does not achieve MIC for Hib/Pneumo in ear (although cure rates may not be all that bad…). Co-amox in double dose ie 90 mg/kg/d in 2 divided doses is effective, but increasing resistance.
Treatment leads to higher numbers of resistant species in nasopharynx, esp dually resistant bugs. Azithromycin persists in body for several weeks so is excellent for inducing resistance. Despite overall trend towards reducing antibiotic usage in AOM, most reduction in amoxicillin, with increased prescribing of quinolones and azithromycin. So don’t treat at all unless added features (unless under a year). [Ron Dagan, Beersheva]
Lots of potential complications:
Very wide range of risk factors and causes for aphthous ulcers including any sort of physical or chemical irritation, there are probably genetic factors.
Minor vs major vs herpetiform: how big and painful! HSV is possible but tends to affect lips and produce crusts.
There is some suggestion that iron, Folic Acid and B12 deficiencies can trigger it.
Food triggers: acidic foods such as tomato, citrus. Nuts, chocolate, wheat and spices.
Cinnamon and benzoates – Glasgow study of adults with RAS or Orofacial granulomatosis and other oral mucosal diseases found significantly higher rates of positive patch testing in both groups (70%, cf 60% of controls!), esp food additives (benzoic acid, salicylic acid, tartrazine, glutamic acid, butylated hydroxytoluene, butylated hydroxyanisole, propylene glycol, sorbic acid and sodium metabisulphite), – 41% contact urticaria cf 22% controls – with high rate for benzoate, Perfumes and flavourings 40.7% overall, vs 9% controls – of which cinnamaldehyde most important (32.4%). Chocolate was mentioned specifically but actually only 3.7% positive. [QJM. 2000 Aug;93(8):507-11. PMID 10924532]
Aphthous ulcers can be a sign of an underlying problem including inflammatory bowel disease, coeliac disease, Behcet’s and PFAPA syndrome but you would expect other signs and symptoms.
The less obvious cause would be cyclic neutropaenia.
Aphthous ulcers can be a lifelong problem although they tend to be less of an issue after teenage years.
Apart from Bonjela, Difflam spray, chlorhexidine mouth rinse. Cholinesalicylate dental gel (not licensed under 16 years).
Steroids: Hydrocortisone dissolving tablets, else a steroid inhaler sprayed in to the mouth or Betametasone soluble tablets as mouthwash (unlicensed).
BNFc mentions doxycycline rinsed in mouth!
Salt water rinses, applying teabags or Aloe juice directly to the ulcers!?
Can be continuous. Phonophobia, photophobia, nausea are possible, but if more than one present, and particularly if vomiting or severe nausea, then migraine would be preferred diagnosis.
Often spreads into or arises from neck.
Chronic tension-type headache – as above but on >/15 days/month for at least 3 months. But gets messy – it is possible that a patient can have both this and Chronic migraine, viz only two of the four pain characteristics are present and associated with mild nausea. In all these cases consider Medication-overuse headache.
Common problem in children, as well as adults!
Distinguish primary from secondary.
Most headaches get worse with exertion so that’s not a discriminating feature. Headaches that get worse on standing suggest a CSF leak; worse on lying down suggests a tumour. See NICE CKS.
International Headache Society 2004 Migraine without aura def:
Aura – Hemianopia or spreading scintillating scotoma. Note that migraine with aura is a contraindication to treatment with combined oral contraceptives.
Some specific types:
Neuronovascular condition – baseline hyperexcitability in cortex.
Double the risk if you had infant colic, which is not true for tension headache! Sleep disruption as common factor? [JAMA 2013;309:1607-12]
Several genetic links found eg C677T mutation of the methylenetetrahydrofolate reductase gene (MTHFR), EAAT2. [J Headache Pain. Jan 2012; 13(1): 1–9. doi: 10.1007/s10194-011-0399-0]
Beware Occipital epilepsy!
American Academy of Neurology recommendations are that neuroimaging should be considered in:
[CurrOpPeds Dec 2004]
Although popular perception is that migraine is caused or at least triggered by dietary factors, there is a wide variation in reporting of dietary triggers. Certainly migraine is associated with obesity, and dietary habits seem to be as important as specific foods, and there is probably a cycle of inconsistent nutrition and poor control of migraine.
My colleagues talk about 4Cs (chocolate, cheese, coffee, citrus) but I have found no evidence for this. Awareness of possibility of dietary triggers actually has greater influence on perception of personal triggers than personal experience! See below.
Some evidence for lipid intake esp PUFA (decreased ingestion of lipids was associated with a decrease in the frequency, intensity, and duration of migraines and a decrease in the use of medication) but confounded by obesity, weight reduction, and changes in nutrient intake. Another study found reduced migraine spells among children subjected to a diet rich in fibre. Not much evidence for cheese at all! [Nutrition Reviews. 70(6):337-56, 2012 Jun. UI: 22646127]
Trial of cyanocobalamin, folate, and pyridoxine (2 mg of folic acid, 25 mg vitamin B6, and 400 microg of vitamin B12) in patients with MTHFR gene defects found a reduction of homocysteine levels and improvement of migraines. [Pharmacogenetics and Genomics. 22(10):741-749, October 2012]
Paracetamol, ibuprofen, and nasal-spray sumatriptan are all effective symptomatic treatments for episodes of migraine (peds sys rv 2005). Migraleve is paracetamol, codeine (8mg), buclizine – for 10yr plus. Paramax, with metoclopramide, for 12 yr plus. Anti-emetic improves pain killer absorption so potential benefit even if no nausea!
Sumatriptan was previously contraindicated for hemiplegic migraine, but this was probably a theoretical concern, and there is evidence that it works. No caution or contraindication mentioned in BNF now.
Mefenamic acid for menstrual, esp with dysmenorrhea.
CGRP receptor antagonists – olcegepant, telcagepant [not in BNF]. Now erenumab [monthly subcut injections, BNF says specialist use only, minimum 4 migraines per month – SMC approved with restrictions], eptinezumab etc vs same calcitonin gene-related peptide receptor. Significant improvement in headaches in 40%, about 3 less headache days per month.
For prophylaxis, Pizotifen does not work (grade I evidence, plus makes you fat), flunarizine (CCB) is the most effective (not in BNF), also amitriptyline (dangerous in overdose), propanolol (dizziness, sleep disturbance, depression etc, also dangerous in overdose). Encouraging data (grade IV) for anti-epileptic mediations topiramate, valproate, levetiracetam, zonisamide. Cyproheptadine? Candesartan (anti-hypertensive, in BNF for migraine prevention)?
Always increase preventer dose to maximum before giving up, note that often symptoms worsen after initial benefit.
Current evidence on the efficacy of percutaneous closure of patent foramen ovale (PFO) for recurrent migraine is inadequate in quality and quantity. The evidence on safety shows a small incidence of well-recognised but sometimes serious adverse events, including device embolisation and device prolapse (each reported in less than 1% of patients). Therefore this procedure should only be used with special arrangements for clinical governance, consent and audit or research. [NICE]
Combined oral contraceptives are contraindicated in migraine with aura. But may be useful if menstrual pattern to headaches if no aura.
50% migraine in childhood remits at puberty. Onset in adolescence associated with persistence.
Patient support at Migraine Trust.
Poor sleep associated with hyperactivity, obesity, poor school performance, depression. And affects parents, of course! Caffeine and Propranolol (as used for migraine prophylaxis) affect sleep!
REM (rapid eye movement) phase is light sleep. Usually in later part of night after deep sleep. Slow wave (deep) sleep is associated with increased anabolic hormone release, mitotic repair. Higher proportion of sleep in adolescence is slow wave. 60% of newborn sleep is REM.
Recommended sleep duration: [National Sleep Foundation]
Some sources suggest adolescents have increased sleep requirements.
Late insomnia (early morning waking) in depression. Cf early – mood disorders, anxiety (cortisol vs melatonin).
30 mins high intensity exercise is as good as melatonin. But ideally 3hrs before bed time!?
Sleep latency 19 min under 2yrs, 17-19 mins thereafter.
Night wakenings are normal! But parental response varies!
Excessive sweating seen in 11% of children, so considered normal. But beware weight loss, lethargy! Can also be associated with obstructive sleep apnoea.
For infants not going to sleep, options are extinction vs gradual retreat. Not appropriate for under 6/12 of age as may affect bonding. No adverse effects otherwise.
Melatonin does not increase total sleep time! Helps prepare brain for sleep – does not induce sleep, as such. Earlier waking as well!
Nocturnal seizures – stereotyped, multiple in one night, sudden stop and start, mostly after first third of sleep. Seen in BECTS.
Restless legs associated with iron deficiency!
Benign nocturnal leg pain common in children.
Teenagers generally do have different body clock, but not helped by major changes in bed/wake times at the weekend. Blue light from screens suppresses natural melatonin production besides distraction.
For autism – Hope for autism do not need diagnosis, others do. Waiting times? National Autistic Society page. Arch, Reach websites.
CAMHS won’t prescribe melatonin but do prescribe methylphenidate!?
Bio melatonin 3x the price, not approved by SMC. Modified release melatonin may be useful with or without standard if early waking in night.
In early part of night, likely to be non REM, cf later in night.
Classic non REM =
REM related =
Sleep hygiene, then consider melatonin and CBT (stress often provokes non-REM). Benzodiazepines can help non REM but can worsen REM.
Beware Narcolepsy – poor sleep quality at night, then daytime somnolence, plus hypnagogic/hypnapompic hallucinations, sleep paralysis, cataplexy (laughing causes collapse). Genetic, treatable with stimulants.
For culture, looking for urine infection, traditionally midstream urine, or at least clean catch. Hard if not toilet trained.
Ideally, avoid first portion of sample (easier if toilet trained), more likely to be contaminated.
Need to be well hydrated, of course.
In/out catheter and suprapubic aspiration are quick but invasive and unpleasant.
For babies, “Dangle-tap” urine collection method –
86% successful within 5 minutes, mean 57secs! Over 3 months hard as heavy and actively resisting.
Older babies – try Quick Wee – gentle suprapubic cutaneous stimulation using gauze soaked in cold fluid for 5 mins. 30% successful within 5 minutes.
[Madrid Infanta Sofia hospital, as reported in Arch Dis Child
2013;98:27-29 doi:10.1136/archdischild-2012-301872]]