Webcam clinics for diabetes (Newham, all ages) – mean duration only 9 minutes for both consultants and nurses, cf 25/30 minutes for face to face! DNA rate 13% cf 28% for face to face.
Patients felt HCPs more focussed on them, other studies have confirmed that eye contact is better! But feels more impersonal, so prior relationship is important.
Or repetitive hair pulling. Previously classified as an impulse control disorder, ie a sense of tension that is only “satisfied” when hair is pulled out. However, many children do not get this tension and gratification so in DSM-V trichotillomania is included among obsessive-compulsive and related disorders.
Dutch cohort mostly girls, literature says no gender difference! Nail biting can co-exist, as can stereotypies. Many kids will also eat their hair once it is pulled out. Most common age of onset is in early adolescence (9-13 years), but frequently occurs in early childhood, even as early as 12 months of age. Triggering factors identified include concerns about physical appearance, family and school issues, and concurrent illness. Parents sometimes also pull their hair, so maybe (partly) learned.
Two distinct types of trichotillomania described: automatic and focused
Parents often miss the hair pulling and only present when hair clumps noticed on surfaces (esp bed – presumably due to pulling in sleep) or bald patches appear.
Exclamation mark hairs (thin proximally, at scalp, normal distally), usually thought of being evidence of alopecia areata, may be seen, so not very predictive. Pull test – gentle traction on about 20 hairs in 3 different locations. Positive if more than 5 hairs extracted – suggests active alopecia areata. You may miss dormant alopecia, but in that case hair regrowth should occur.
Reactions to local anaesthetics are often reported, but given how often they are used, most turn out not to be allergic but rather toxic (eg to parabens or sulphite preservative) or autonomic. Where allergy is confirmed, it is often of a delayed hypersensitivity type eg 24-72 hours after exposure. Beware latex allergy and C1 esterase inhibitor deficiency too. Local anaesthetics come in 2 main groups, the esters (procaine, benzocaine) and the amides (lidocaine, bupivocaine). Cross-reactivity is common among the esters but not among the amides or between the 2 groups. Neomycin sensitivity may contribute to a reaction.
Testing can be done with preservative containing products, although a higher rate of false positives may be found. Skin prick testing should be done to non-adrenaline containing products, else reaction is impaired. There can be discordance between patch testing and intradermal testing. The final step should be subcut testing, perhaps blinded (Contact Dermatitis. 59(2):69-78, 2008 PMID 18759873 ).
Suxamethonium sensitivity (where apnoea persists for half an hour or more) – is due to cholinesterase deficiency. Homozygotes will always be sensitive to suxamethonium. Heterozygotes may be sensitive, especially if pregnant, when cholinesterase levels drop further. Testing usually offered to 1st degree relatives of homozygotes (done in Bristol). Children tend to have higher levels so avoid testing unless procedure required (and you may have to retest after puberty).
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!).
6 of these is a confirmed case. But toxic shock criteria are there for research rather than clinical work – just treat if at all suspicious! For staph related TSS, blood culture usually (but not always) negative, although may be isolated from wound or trachea.
For streptococcal toxic shock syndrome, almost always associated with a healthy looking recent wound, or recent varicella. Criteria are looser but microbiological confirmation required:
1A plus 2 is a confirmed strep TSS case, 1B plus 2 is probable.
TSST-1 found in 75% of cases, the rest feature enterotoxins B or C. Recurrence is very rare. 90% of the adult population have antibodies against TSST1, not surprising since 20% of staphs are TSST-1 positive!!! Test is genotype based, not toxin based, so other factors must affect whether toxins are released, or how much disease is caused.
Females outnumber males 3:1.
Clindamycin has added benefit due to ability to reduce toxin production. IVIG has theoretical benefit but the only trial was stopped because of slow recruitment. Haemofiltration similarly has theoretical benefit.
Life threatening infective necrosis of superficial tissue fascia, often more extensive than would be suspected by appearance of overlying skin. Can start in previously normal skin, with an insignificant entry site!
Group A streptococcus mostly, but can be polymicrobial especially in immunocompromised.
The top three early presenting clinical features are swelling, pain and erythema but these are entirely non-specific, so initial misdiagnosis common (almost three-quarters of patients in 1 review). More specific features are:
Other possible characteristics described:
Early surgical exploration is the best approach in the uncertain case; and early surgical debridement is key to control. IVIG may be of benefit.
Notifiable in Scotland.
Various haemolytic groups, GAS is beta haemolytic. Other groups of beta haemolytic identified by Rebecca Lancefield.
M type proteins on GAS are the main virulence factors esp 1, 3. About 20 toxins, all superantigens. Antibodies to toxin are effective. Some HLA types appear more susceptible.
Culture from throat, skin etc.
ASO titre and DNAse B titres are not 100% sensitive, and high titres can persist after infection.
Group A streptococcus has never been resistant to penicillin! But doesn’t mean penicillin is the best treatment: Clindamycin shows superior killing (in animal models) – inhibits protein synthesis so works throughout cell cycle, cf penicillin where action only during replication. Will also inhibit toxins (in theory).
IVIG effective against toxins.
GAS vaccine? – danger of priming for rheumatic fever! New 26 valent, effective for sore throats and invasive disease, probably not long term effective or appropriate for preventing rheumatic fever.
Rare but well recognized allergic condition, about half related to a food trigger.
Anaphylaxis can occur with any degree of exercise, does not need to be extreme, but typically follows submaximal exercise pretty quickly. Deaths are fortunately rare.
Possible mechanisms:
All sound plausible but little evidence!
Co-factors play a role in many cases eg alcohol (but unpredictable), NSAIDs (85% will have reduced threshold, and severity increases too), infection, heat/cold – some evidence too for menstruation, anti-acids, stress, sleep deprivation (as in anaphylaxis). Co-factors also multiply risk of reaction.
Mostly wheat, including hidden sources eg soap, shampoo, cream.
SPT useful, also IgE omega-5-gliadin. But gold standard is provocation test (and still only 70% sensitive). No uniform protocol – use same as for exercise induced bronchoconstriction? Do 1 hour after meal with suspected trigger.
Prescribe adrenaline auto-injector. Avoid exercise 4-6 hours after food intake. Discuss unplanned exercise!
45XO but mosaics occur.
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: