Incomplete bladder emptying cannot be diagnosed on a single post-void residual urine on ultrasound, due to significant intra-individual variability. Two post-void residual urine tests are recommended; larger volumes are seen if the bladder has been over distended (eg initial volume greater than 115% of expected), and in younger children. Greater than 20 ml is more specific than 10% bladder capacity. [J urology 2009 (182):1933]
Bladder capacity is = (Age +1) x 30 (ml) max 390ml.
Exclamation mark hairs (thin proximally, at scalp, normal distally) suggest alopecia areata, but may be seen in trichotillomania, so not very predictive.
Pull test – gentle traction on about 20 (some people say 60) hairs in 3 different locations. Positive if more than 3-5 hairs extracted – confirms active hair loss but not very specific. Usually telogen effluvium but can be early alopecia areata.
Developmental Co- ordination Disorder (DCD), as outlined in DSM IV (American Psychiatric Association 1994):
It is essential that early referral is made in order that children do not develop behavioural difficulties due to their frustration at not being able to carry out the same tasks as their peers.
Clues are:
N.B Most children in their early school years will demonstrate one (or more) of these areas of difficulty but this does not mean they all have DCD! Children with DCD will present with many of the difficulties above for a prolonged period.
A common issue for babies and infants. But not that common – in EAT study, symptoms (vomiting, colic, eczema) related to milk reported by 13% of parents, but only found in 0.7%!
“Intolerance” suggests that cow’s milk causes adverse effects (generally gastrointestinal) but without committing to an underlying mechanism.
If there is reason to think the adverse effects are immune mediated (because there are signs/symptoms outside the GI tract, for example) then it is preferable to use “cow’s milk allergy” (which then divides into type 1, non type 1, or mixed).
Can even affect exclusively breast fed infants if sufficient milk proteins transmitted in breast milk, but probably over diagnosed (as challenge after 2-4 weeks not done).
Not the same as lactose intolerance – lactose is a sugar, intolerance to it is due to malabsorption and effects of undigested sugar in colon eg bloating, diarrhoea. NOT rash, vomiting. Usually post-gastroenteritis, transient. No useful test other than lactose restriction for 2 weeks then rechallenge.
Some parents feel milk leads to more respiratory problems – there is some evidence that milk allergy is associated with more respiratory/GI infections and that an elimination diet (although supplemented by pre/probiotics) lead to reduced infections and less antibiotic use.
Can be IgE mediated (immediate, histamine release, potentially anaphylaxis), else non-IgE mediated (typically more chronic, delayed symptoms, predominantly gastrointestinal, possibly a threshold level below which a patient is asymptomatic) but can be both. Non-IgE mediated symptoms include:
Note that the first 4 problems are very common and cow’s milk protein intolerance may only be a factor in a small proportion of such patients. Best predictor of whether symptoms are due to milk allergy appears to be the background of the health care professional, not the history, age or family history of atopy! See Imperial College review of evidence (Munblit and Perkins 2020).
ESPGHAN 2023 guidance does detail trial of exclusion for reflux. For colic, very strict – only when Rome IV research criteria satisfied (3hrs per day, without obvious cause, cannot be prevented or resolved by care givers, 3 days a week, confirmed with prospective diary) AND suspected on basis of additional symptoms.
In patients with eczema, a mixture of IgE mediated and non-IgE mediated reactions can be seen (and immediate reactions may be seen on re-introduction even when only delayed reactions seen initially).
Well baby with blood +/- mucus in stool, usually in first few weeks of life. Associated with eczema and family history of food allergies. Mixed feeding appears to protect. Benign – in exclusively breast fed infants, ESPGHAN says no dietary intervention for first month. Even for formula fed babies controversial, as large study in Boston found elimination increased risk of later type 1 milk allergy by factor of 5!
DRACMA 2022 guidelines from WAO quote small Brazilian study showing 80% tolerant by 6 months so earlier reintroduction presumably possible if you do exclude. Calls for more research.
So depends on severity/frequency – and if you eliminate, definitely challenge early.
Prescriptions for specialist formulas increased massively in early part of century – 10-12x higher than expected in England, for example. Estimated prevalence is 1% in the UK, less than 0.3% in Germany and Greece.
With delayed reactions, diagnosis depends on history, and then dietary exclusion followed by re-challenge after 2-4 weeks. In the case of FPIES, re-challenge may need to be done in hospital. Sometimes the diagnosis is only made at endoscopy.
Dietary exclusion has been shown to affect long term taste preferences. Also significantly restricts diet, with potential impact on calcium intake (and also riboflavin, niacin, zinc).
For immediate reactions, skin prick testing (SPT) more specific than IgE blood testing. 3mm SPT wheal considered positive in infants, but low specificity; when doing IgE/SPT tests, also check egg allergy (high cross-reactivity) and soy (for formula substitution). If IgE/SPT negative, needs challenge (ideally double blind).
Cow’s milk must be tried again to prove it is the causal agent, unless type 1 symptoms, or severe non-type 1 (FPIES). If symptoms return then continue elimination diet for at least 6 months, else 1yr of age, then re-introduce gradually. ESPGHAN says do IgE for milk first if type 1! Highlights that boiling more likely to hydrolyse proteins than baking, but ignores matrix idea. No evidence for further challenges but suggests every 6 months.
Exposure does encourage tolerance. In studies, after 6 months of oral desensitization, 11% had had positive food challenges cf 40% for abstainers. And in the abstainers, the threshold of sensitivity tended to be lower, and symptoms more severe [Eur Ann Allergy Clin Immunol. 2007 39:12-9. PMID 17375736].
Almost all non IgE milk allergy and most type 1 resolves by 1yr after diagnosis.
Reintroduction is typically done according to a “ladder” of 4 or more steps – baked milk, then boiled milk, then yogurt, then fresh raw milk. Baked milk is less allergenic due to the matrix of wheat – if wheat allergic, then gluten free cheese oatcakes (Nairns) or shortbread (Walkers/Asda).
IgE disease less likely to resolve if asthma, rhinitis, severe reactions or strongly positive results. Median age of tolerance 5yrs. According to Thermofisher, positive IgE Casein (Bos d 8) means less likely to tolerate baked milk or outgrow, as protein (casein) more heat stable (no consensus on component testing in ESPGHAN 2023).
You could argue for early introduction of weaning foods but this is only briefly mentioned in ESPGHAN 2023 and not yet recommended.
Final adult height has been shown to be reduced in milk allergy – this could be related to co-morbidities (asthma, eczema, steroid use, sleep disruption etc) or feeding difficulties (associated with elimination diets).
EAACI task force recommends against use of milk formula top ups in first week of life in breast fed babies. Low certainty, though. Also recommends avoidance of allergens (including milk but not limited to) in pregnancy and during breast feeding!
ESPGHAN discusses too. In a multivariate model, independent factors associated with milk allergy were family history of allergy (OR = 2.83), avoidance of dairy products during pregnancy or breastfeeding (OR = 5.62), and formula given at the maternity hospital (OR = 1.81). In an RCT of daily 10ml formula supplementation (n=504 breast fed) cf only soya formula if required, performed between 1 and 2 months of age, daily formula ingestion prevented nearly 90% of later milk allergy confirmed by OFC at 6 months (RR: 0.12). EAACI neutral on this – and regular top ups would never be supported by breast friendly clinicians. Overall however, ESPGHAN group decided there was insufficient evidence for any of these things.
See also EAT study, and GINI study.
66% of kids grow out cow’s milk allergy, even if they completely avoid it. But rate rises to nearly 90% if baked milk introduced. And less restrictive diet good for everyone, of course.
Salmivesi RCT from Finland 2012 – n=28, age 6-14. 81% using daily milk 6400mg protein at 12 months. First dose milk 0.06mg – 8 further observed doses (0.12mg day 8; 0.24mg day 15; 2.0mg day 36 [big jump!]; 4.0mg day 38 [2 days later!?]; 8.0mg day 42; 40mg [big jump again!] day 57; 80mg day 64; and 160mg on day 78) with other dose increases done at home. Monitored for 2hr in clinic. Final dose of 6400mg (=200ml) was given at home (!) on day 162.
Oral immunotherapy (OIT) for severe milk allergy (IgE >85 or low eliciting dose): at 1yr 36% tolerated 150ml, 54% 5-150ml (good enough for accidental exposure). 10% could not complete protocol. [reference?]
DRACMA update on milk immunotherapy (2021) mostly fresh milk used in research. Randomized trials looked at kids aged 2-14, mean 8. Non randomized had wider range. 67% tolerated 150ml (cf 2.2% of controls), 78% tolerated 5-150ml (=swig protection) (cf 3.3% of controls). Anaphylaxis rate of 5.5 per person-years (although not always defined, and not always usual definition). 63% used IM adrenaline!?
6.9% developed EOE but rarely biopsy confirmed. No deaths.
2–8 weeks after discontinuation of successful OIT, tolerance of cow’s milk persisted in only 36% (20%–91%). So you have to persevere life long, probably.
Quality of life badly reported – only 5 studies. 1 study found parents reported better QOL in 37%, worse in 26%, and unchanged in 38%! 2 conference abstracts reported improved QOL or at least reduced anxiety in general and reduced fear of unexpected reaction. Some studies found worse QOL! Certainty of evidence overall v low…
Only 1 trial and 2 non randomized studies of baked milk OIT! In the 1 RCT of baked milk, 73% achieved tolerance at 12 months (cf none of control group) – other studies did not find evidence of effectiveness however (meta-analysis of Anagnostou. Tolerance to heated or baked milk may be temporary and diminish within a few years. Dantzer. 20% required adrenaline! Only some children assessed for QOL, with evidence of benefit – of the parents studied, no improvement in QOL! [Dantzer and Dunlop 2021]. Low desensitization rate for unheated milk means persisting concern about exposure in real life despite less frequent adverse reactions (8%–33%).
Other studies did not find this relationship, which is consistent with the meta-analysis results of Anagnostou et al. (41). Tolerance to heated or baked milk may be temporary and diminish within a few years. Dantzer et al. found that a protocol involving gradually increasing doses of baked milk was effective in promoting desensitization (73% achieved end dose of 4000mg cf 0% of controls). Mean age 11. “This suggests that the initial dose [and then building] may influence the efficacy of desensitization.”
[Yan Wang, China – Front. Immunol., 04 June 2025]4% rate of biopsy proven EOE – note EoE typically emerges approximately 2.8 years after initiating the maintenance phase so many studies will miss…
Longer duration better. None of the studies reported on sustained unresponsiveness.
Only Dantzer study reported quality of life!
Highlights “a dire need for a standardization in outcome assessment and reporting,” and that successful completion of OFC needs to be validated as a predictor of “real world” success. [Natasha trial will hopefully clarify further…]
Separate article on OIT recommendations – apart from balancing risks and benefits, recommends using omalizumab (monoclonal anti-IgE) in advance and in initial stages of oral immunotherapy with unheated cow’s milk. Inferring from limited evidence (use in other food allergies, mostly) that risk of anaphylaxis reduced (RR0.34 but not significant!). Not really any downside? (But costs at least £256 per dose, maybe double? Lasts a month?). Plus, does not recommend baked milk OIT as very low certainty of benefit. More evidence on effect, risks, QOL benefit obviously required.
Sublingual/epicutaneous immunotherapy (SLIT) for milk? Not much evidence – low rate of success and high rate of relapse.
[EGPHAN 2023, Frontiers in Pediatrics 2019; BMJ cmpa article sept 2013]
Rush study from Japan used microwaved milk – microwaved for 100s at 550W (!). Dosing was 2–4 times a day in hospital for several days (frequent adverse events) aiming for 200 mL dose (total daily, I assume). If not achieved, dose increases changed to 1ml per day. At 200ml, dosing changed to once a day. After 2 months of maintenance, length of time in the microwave gradually reduced.
Another Japanese study looked at using heated milk powder (3 mins at 125degC) vs unheated milk. Rush protocol (5 days in hospital) up to maintenance of just 3ml daily. At 1 year, 35% and 18% in the HM group and 50% and 31% in UM group passed the 3 and 25 mL OFCs, respectively, so not great efficacy. Rates of moderate or severe symptoms significantly lower (halved) in the heated milk group however.
Natasha Trial is looking at Peanut or cow’s milk OIT in UK – groups are Peanut age 6-23yrs, Peanut age 2-3yrs, Cow’s milk age 3-23yrs. Using everyday food products. Final results expected 2027.
Tics are recurrent, sudden, non-rhythmic twitches. Can be in 1 muscle or muscle group, but can also be a more complex semi-purposeful movement, or even present as a bizarre gait. Typically affect face (eg blinking, grimacing), neck, shoulder. Can be more complex sequences of movements. Characteristics are:
Differential includes stereotypy, spasms, chorea.
Although tics can wax and wane over time, there is a general tendency to improve, and they are very unusual in adulthood.
Tics occur most commonly in boys. Usually they are transient, lasting for between 4 weeks and 1 year. A chronic tic disorder does exist distinct from Tourettes.
Vocal tics (clearing throat, yelps, coughs, sniffs, grunts) can occur in isolation, but a combination of vocal and motor tics suggests Tourette’s syndrome.
Thought to affect 1% of children, so probably a lot subclinical! An inherited neuropsychiatric condition, it starts at a mean age of 7 but can be as young as 2yrs. Motor tics come first, about a year before vocal tics. Complex vocal tics may be seen but contrary to public understanding, most kids do not swear (coprolalia)!
Definition requires that motor and vocal/phonic tics are present (at some point) for at least a year, on a daily basis, with onset prior to 18yrs, in absence of substance misuse, medical condition or medication. The characteristic features of Tourette’s are:
Tics wax and wane, evolve over months. Can be self harming eg scratching, rubbing, head banging, punching, poking, stabbing oneself (see also obsessive compulsive co-morbidity below).
In some patients, there is a non-obscene compulsion to shout socially inappropriate things (NOSI). Often worsens around puberty. 50% abate after puberty, but mostly just better self-management?
Differential is basal ganglia or cerebellar abnormality eg post-encephalitis, Huntingtons. Investigations only necessary where unusual deterioration or progression of symptoms.
Pure tic disorder is unusual in Tourettes. 85% have comorbidity, most commonly:
The comorbidities are often more significant on school performance than the tics. Comorbidities are common in relatives, even if tics are not.
Counselling is useful for self-esteem, anger management, and social functioning. Habit Reversal Training is effective but not widely available – officially 12 weekly hour sessions, need to recognize premonitory urges and then replace tic with controlled movement, or position self to prevent tic (eg chin on chest to prevent shouting).
Drug treatment may be considered eg self harming, but not much evidence for effectiveness. Traditional or atypical neuroleptics, or clonidine (esp where behaviour or sleep problems) used.
Deep brain stimulation being researched.
Tic frequency and severity decline with age in a large proportion of patients (59–85%).
Predictors of NOT improving include higher childhood tic severity, smaller caudate volumes and poorer fine motor control.
The presence of untreated comorbid psychopathology, such as ADHD and OCD, can adversely affect the long-term outcome of patients with TS.[Funct Neurol. 2012 Jan-Mar; 27(1): 23–27. ]
Tourettes Action parent support group.
[Stern, Curr Peds 2006:16:459]
Five possible causes for discrepancy between reported and observed symptoms/signs suggested in the RCPCH guidelines:
It is important to keep an open mind and to carefully plan appropriate assessments for both medical causes and evidence of maltreatment, without putting the child at further risk of harm.
RCPCH National guidance supports the clinician and team in withholding concerns about FII from the parents at early stage of investiagion. This highlights the main difference in dealing with suspected FII compared to other forms of abuse. Documentation and information sharing need to be handled carefully, as alerting the parents to your concerns may put the child at greater risk of harm – concerns should not be recorded in case notes, parents should not be informed. Important that team is united.
Gather information about the parents’ background and any known health problems, including some assessment of parenting capacity and risk factors such as domestic violence, mental health issues or drug abuse. This is essential not optional.
Chronology – given multiple attendances for multiple children with different services, helps see overall picture for a family. Should also include significant events eg moves, bereavements etc.
It is important to feed back your findings to the parents that there appear to be no medical problems and that this is good news. How family responds to initial assessments and management plans is key to making the diagnosis.
In-patient: clarify nursing ability to supervise 24hrs a day. Can child leave ward with/without nurse escort? Who gives medication/food/drink? Where should notes be kept?
If parents demand a new consultant, you can agree to involve another consultant for a specific medical issue eg asthma/epilepsy. You should definitely discuss with named doctor. CAMHS could also be useful for discussing case (and supporting staff, esp if conflicting views)
Disclose to parents – if decision is made to disclose concerns, keep it positive (health of child, etc). Bring in dad, gran etc if potentially useful. Don’t confront or challenge, acknowledge how parents and professionals can have different perceptions and responses to a child’s problems. Present united front, and unambiguous plan.
Scaly skin condition in babies, particularly affecting scalp. Red/orange scales, oily, flaky. Not terribly itchy.
Affects sebaceous (greasy) zones – face, scalp, centre of chest, skin folds (neck, groin). Often nappy rash. V common (includes dandruff!). Inside, outside and around ears can be affected. Eyelids can be affected (blepharitis).
Babies get transient type – cradle cap (scalp) and nappy area, clears after a few months. In adults, affects face (esp around nose and ears) and can affect chest and upper back. Can lead to hair loss but more usually cosmetic concerns.
Thought to be caused by overgrowth of Malassezia yeast. Can be severe in HIV.
Differential is psoriasis. Scales in psoriasis are thicker and whiter – unusual for face to be affected.
For cradle cap in babies, usually enough just to use daily mild shampoo and gentle brushing. Shampoo may make it worse if the diagnosis is actually atopic dermatitis! Failing that, coconut oil (NOT olive oil, which has potential to damage skin, apparently) or other moisturizer left in overnight or applied just before bath.
For scalp, Zinc pyrithione, selenium or ketoconazole shampoo (but only licensed for older children). Leave 5-10 mins before rinsing. Descaling treatment available – coconut oil and salicylic acid, needs hours.
For body, moisturizer, topical steroids+antifungal eg Canesten HC, Trimovate.
For blepharitis, use baby shampoo to lift flakes.
In adults, anti -androgens.
Follow-up from LEAP study, after both groups (eating and avoiding) told to avoid peanuts for 12 months. The rate of adherence to avoidance in the follow-up study was high (90.4% in the peanut-avoidance group and 69.3% in the peanut-consumption group). Peanut allergy at 72 months was significantly more prevalent among participants in the peanut-avoidance group than among those in the peanut-consumption group (18.6% [52 of 280 participants] vs. 4.8% [13 of 270].
[George du Toit, Gideon Lack in London, DOI: 10.1056/NEJMoa1514209]
Mild: fever +/- rash, hand/foot/mouth, herpangina, pleurodynia, pharyngitis, conjunctivitis, croup.
Serious: meningitis, encephalitis, acute paralysis, neonatal sepsis, myo/pericarditis, hepatitis, chronic infection (immunocompromised).
Meningo-encephalitis in neonates usually associated with other organ involvement. In adolescents headache can be severe and symptoms last several weeks! Early CSF can show around 1000 neutrophils! Prognosis good, although some subtypes with encephalitis highly aggressive eg EV-71 outbreak in Taiwan in assoc with hand/foot/mouth (78 deaths).
Acute flaccid paralysis can occur cf polio. Particularly Enterovirus EV-D68 (also associated with respiratory disease), some clusters. Increased incidence across Europe including Wales since April 2016.
Neonatal disease can be severe, mimicking bacterial sepsis or HSV. Maternal history is often elusive.
Virus is shed in throat and stool (rectal swab quicker than stool!), can also be detected in CSF, blood and urine.
Role of IVIG is unproven but antibody plays an important role in immune response to EV. Pleconaril in enteroviral meningitis RCT, 38% to 50% improvement in symptoms in the drug-treated group with improvement noted as early as 24 hours after initiation of therapy – no longer available.
[Current Opinion in Pediatrics. 13(1):65-9, 2001]
Human Parechovirus has been described in Japan, Canada and now the Netherlands, causing neonatal sepsis or encephalitis in about 10% of cases where culture suggests enterovirus but PCR is negative. [Clin Infect Dis. 2006 Jan 15;42(2):204-10]
Only 3-5% of cases of MS have symptoms before the age of 16. Most have a relapsing-remitting course, particularly in the beginning, typically with one to two relapses per year. The frequency of attacks does seem to predict disease severity and earlier evolution to secondary progressive phase.
Although it takes longer in kids to develop persistent disability, they still develop it at a relatively young age, for example the third or fourth decade of life. That is of course going to have significant effects on life course, including work and family life.
Even at onset, cognitive function is often reduced, which will also affect education and socialisation. So clearly there is interest in disease modifying treatments.
Presentation in younger children often follows an infectious illness. Cognitive impairment is more common relative to older kids.
MRI of brain and spine, looking for demyelinating lesions.
Monoclonal bands in CSF.
Steroids 10-30mg/kg for 3-5 days effective. No good evidence for IVIG. Where acute life threatening symptoms, plasmapheresis may be effective where steroids fail.
In adults good evidence for interferon Beta in relapsing-remitting disease, IM or SC depending on product, reduces relapse rate and probably slows progression of disability. Glatiramer is a synthetic product with similar effects.
Second line treatments in adults include Natalizumab, mitoxantrone and cyclophosphamide.
Since these are genetic conditions, essential for management and genetic counselling.
J Weisfeld-Adams http://brain.oxfordjournals.org/content/138/3/517