Classically a cold abscess, usually in the neck. Ingested soil?
Overlying skin can become discoloured, and ultimately fistulation may occur. Child is usually systemically well.
Blood tests are normal. Mantoux testing can be positive due to cross reaction with BCG. Fine needle aspiration may be most appropriate.
Drug treatment needs to be prolonged and recurrence is common.
Surgery can be tricky.
Graves usually 10-20yrs at presentation. 6:1 female. Usually family history of thyroid or other autoimmune disease. Insidious else acute. Palpitations, diarrhoea, heat intolerance, agitation and deteriorating school performance, weight loss.
Tremor, fidgety, hypertension, goitre (diffuse, smooth), bruit, exophthalmos (rare in kids). Storm can be triggered by infection or non-compliance. Hyperpyrexia, tachycardia.
Neonates can get transient hyperthyroidism driven by maternal antibodies – improves after a few months.
Besides Grave disease, other causes of hyperthyroidism are solitary thyroid nodule (adenoma), multinodular goitre, TSH receptor abnormalities.
Besides TSH, do free T4 and T3. FT3 useful (T4 can be normal!) for showing T3 thyrotoxicosis (usually due to toxic nodular hyperthyroidism or early Grave).
Thyroid receptor antibodies usually positive. Do TPO also.
Carbimazole – Usually 24 months total, TFTs normalise within 12/52 and dose can then be reduced. Neutropenia as idiosyncratic side effect (so FBC monitoring not helpful!). If mild stop temporarily. Propylthiouracil second line (liver failure, ANCA vasculitis)
Radio-iodine – avoid <10yrs. Can have storm. Need long term thyroxine.
Surgery – total or near total excision. Risk of malignancy in remnant. Esp large gland. Hypoparathyroidism as transient side effect. Recurrent laryngeal nerve damage. Iodide used pre-operatively to help texture!
Propranolol short term e.g. 3-4 weeks
Block and replace strategy – where you add thyroxine rather than reduce carbimazole? But 2 drugs not 1!
Relapse common, 2/3 within 2yrs, in adults remission unlikely after 2 years but not true in kids.
Malignancy risk higher in Grave regardless of management…
=anal pain.
Rule out anal fissure (may be hard to see but bleeding or sentinel pile are clues, typically caused by constipation), thrombosed haemorrhoid, infection.
After that, functional (see Rome criteria)- often triggered by defaecation or sitting.
Classifed as acute (less than 20 mins – “fugax”) or chronic (greater than 20 mins episodes). Latter thought to be due to paradoxical pelvic floor contraction.
Biofeedback has best evidence but consider tricyclic antidepressants, Botox, and sacral nerve stimulation (!).
2 main groups – monoamine and GABA disorders.
Oculogyric crisis is characteristic! Can be mistaken for seizure.
So epilepsy with poor response to drugs and normal EEG?
Cerebral palsy with progression?
Should be only low levels until puberty kicks in.
Most of the research into testosterone and aggression comes from adults.
Some small studies have found a link between testosterone levels in children and aggression, particularly in boys, but not all. Similarly some studies have suggested low cortisol in association with aggression, but other studies have found links to high cortisol.
A small study of pre pubertal and pubertal children (boys and girls) found testosterone levels were associated with high moodiness and low attachment. Testosterone was also associated with low sociability, but only in the prepubertal group.
One study suggested that the influence of these hormones can modulate the balance of aggressive tendencies and empathy, with cortisol being relevant only to boys and testosterone only to girls.
All these studies at high risk of bias.
Serpiginous burrows between the fingers, in the flexures of the wrist, genitalia etc characteristic but rare. More usually papules, pustules – pruritus often on unaffected skin and esp at night. In infants, lesions on head, nappy area, occ palms and soles.
Caused by the mite sarcoptes scabiei, which does not fly or jump – direct skin contact, mostly. Infection by contact with fomites is very rare.
Rash is partly hypersensitivty so not related to number of mites, may take several weeks after inital infestation to appear – on reinfection just a few days. Cross reaction with related house dust mite.
Topical steroids will mask rash/itch. Superinfection common. Differential is contact dermatitis, animal scabies (do not form burrows, do not complete life cycle so self limited), lichen planus.
Rarely, nodular form (esp groin, axillae) – hypersensivity reaction.
Norwegian or crusted scabies esp immunosuppressed (but not necessarily) – psoriaform, not always itchy, very infectious.
Treat with Permethrin 5% (=Lyclear) dermal cream [Permethrin 1% rinse cream ineffective in scabies cf head lice]. Safe in infants (rarely CNS side effects). An alternative treatment is Malathion (safe in pregnancy). All household members should be treated simultaneously. After treatment the itching from scabies can take weeks to settle. Treatment should be extended to the scalp, neck, face and ears in children up to the age of 2 years. All skin surfaces should have the agent applied for 24 hours for malathion and for 8-12 hours for Permethrin 5% and have treatment repeated at 7 days.
Oral ivermectin in single dose is effective in over 70%, given twice 2 weeks apart 95% effective. Use for crusted (along with keratolytics), epidemics. Lancet Infectious Diseases Volume 6, Number 12, December 2006
Group of similar gram negative, low pathogenicity organisms – not actually related to each other, but cause similar infections:
Commensals of the mouth – usually just cause dental infections but can cause endocarditis (gram positives are the usual cause) and osteomyelitis (esp Kingella – named after Elizabeth King – can be spread by respiratory route, so outbreaks of septic arthritis!).
May grow on chocolate agar but not the McConkey you usually use for gram negatives. Some beta-lactamase but most susceptible to cefalosporins.
Autosomal dominant, PTEN gene (10q23). See OMIM.
Clinically –
In some cases intestinal polyps, papilloedema, immunodeficiency.
Lipid transfer protein. One of the allergen families. Cross reactions therefore seen with fruit (stoned fruit but also raspberry), nuts, seeds (eg linseed/flaxseed), pulses, even cereals, tomatoes, vegetables (lettuce! Cabbage!). You may also see reactions only to composite foods eg pizza, curry, due to multiple allergens being present, but only producing reaction due to co-factors.
A less common cause of Pollen food syndrome than PR10 allergy. Thought of as a Mediterranean thing but increasing reports from Northern and Western Europe. Plane tree and mugwort have LTP but not thought to be the usual cause for sensitisation (except maybe in China). In N/W Europe, often birch sensitised too but not to be confused with PR10 type PFS!
Important to identify because heat stable (so not affected by heat, processing, digestion etc in the way PR10 allergens are) and potential for severe reactions.
So do component testing if atypical (eg unusually severe) reactions to fruit.
LTP allergy also seems to be more likely to cause reactions of varying severity, compared with primary food allergy, with co-factors perhaps more important. Eating multiple different plant foods at the same time seems to be the most likely cause of co-factor associated severe reactions. Of course, co-factors can co-exist too (alcohol and dancing, for example). So some would advise:
Danger that with LTP allergy you show sensitisation to multiple foods, and then you end up on a restricted diet without knowing whether there is allergy or not.
Peach allergen Pru p 3 is a good surrogate for LTP allergy, even if peach hasn’t been a problem! If not available, you could test with SPT reagent for peach that is rich in pru p 3 (but might be false positive due to other components being present. London plane and mugwort allergy would also support.
Wheat is a bit tricky – the wheat LTP Tri a 14 is only 45% homologous with Pru p 3 so may get missed. Given the co-factor issue, probably good to do Tri a 19 (omega 5 gliadin, as in exercise induced anaphylaxis) as well.
Where hay fever and atypical reactions to nuts, do the LTPs Ara h 9 (peanut), Cor a 8 (hazelnut), Jug r 3 (walnut). You would do the other components to exclude primary food allergy which can co-exist with LTP sensitisation.
Food challenges have limited use in this situation – if positive, unclear whether LTP is the cause, and if negative, perhaps because of co-factor issue! Exercise challenge?? May just need a bigger dose!
Individualize, to balance risk of reaction against dietary restriction.
Safest fruit/veg appear to be potato, carrot/root vegetables, beans, peas, melon, cashew and pistachio. Avoid pips and skin. Banana is hit and miss.
Good results with Pru p 3 sublingual and oral peach juice immunotherapy in Spain and Portugal.
Julie McCabe died in 2011 as a result of anaphylaxis to Para-Phenylenediamine (PPD) in hair dye. Black henna is known to contain PPD, so may sensitise.