First decide if conjugated or unconjugated. Conjugated suggests a biliary problem, ie obstruction to bile flow, usually associated with raised gamma glucuronyl transferase (gamma GT). Unconjugated (as measured in split bilirubin) implies haemolysis or else hepatocellular damage (transaminases also go up ie AST, ALT). Unconjugated can also go up in conjugated disease, presumably competition for conjugation sites, or else because of secondary or mixed hepatocellular damage.
History – maternal if baby, immunisations, transfusions, outdoor activities, pets, holidays, drugs, tattoos. Family history (haemolytic conditions, in particular).
Look for signs of liver failure, lymphadenopathy, eyes (Wilsons – best with slit lamp), dysmorphic (Alagille’s).
Damage is from sodium hydroxide generated by electric current, not from leakage!
Should be recognised as a medical emergency, deaths have occurred.
Haematemesis, haemoptysis and respiratory difficulties can manifest up to 28 days after ingestion of the battery, so easy to miss or ignore. Given the age of the children involved, they are unlikely to tell you! Catastrophic aortooesophageal fistula possible, as in the case of Hugh McMahon in Lanarkshire. Earliest perforation has been at 12 hours – median is 5 days. [Am J Emerg Medicine 2019]
Removal of the battery alone may be insufficient action to prevent further damage, with further symptoms manifesting later; patients need expert input, and careful monitoring and follow-up. One further incident described the death of a child from late complications after they had been treated and sent home.
US Poisons centre recommends use of honey or sucralfate if ingestion within the last 12 hours.
Parental child-rearing attitudes (as assessed by the Amsterdam version of the Parental Attitude Research Instrument, A-PARI), are associated with constipation in children in Dutch study.
More specifically, both higher and lower scores on the autonomy attitude scale were associated with decreased defecation frequency and increased faecal incontinence. High scores on the overprotection and self-pity attitude scales were associated with increased faecal incontinence.
“Autonomy” reflects emphasis on encouraging independence. “Overprotection” refers to concern about child with respect to prevention of disappointment and problems for the child, and need to know what’s going on inside child. “Self pity” refers to irritability and frustration with respect to upbringing, which implies rejection.
More and stronger associations were found for children aged ≥6 years than for younger children.
Authors recommend addressing parenting issues during treatment and even referral to mental health services when parenting difficulties hinder treatment or when the parent–child relationship is at risk. [Arch Dis Child 2015;100:329-333 doi:10.1136/archdischild-2014-305941]]
Chromosome 15, fibrillin 1 gene (FBN1) locus but lots of different mutations. Variable penetrance, about a quarter de ovo.
Fibrillin is part of connective tissue, different from collagen, despite clinical overlap with Ehlers-Danlos etc.
Neonatal cases can occur, always severe, with cardiac abnormalities and contractures.
Clinical diagnosis – Beighton (he of benign hypermobility score fame) published Berlin criteria, later came Ghent criteria –
family history important, else
involvement of the skeleton, plus
at least 2 other systems, with a minimum of 1 major manifestation (ectopia lentis,aortic dilatation/dissection, or dural ectasia).
Skeletal – Tall, disproportionate arm span (>1.05x height – 8cm wider than tall at 160cm) and digits, anterior chest deformity, hypermobility (joint laxity), scoliosis/lordosis, high arched palate and crowded teeth.
Eyes – Myopia, corneal flatness, subluxation of lens (ectopia lentis).
Cardiac – MVP, MR, AR and aortic root dilatation (chart of normal measurements available). Cardiac examination is often normal despite abnormal echo findings! Aortic aneurysm and dissection can be life threatening.
Pulmonary blebs affect some people, recurrent pneumothorax. Dural ectasia (widening of lumbosacral spinal canal) on CT is very common, hence why a major manifestation, although symptoms unusual.
Life expectancy is reduced, particularly in males. [Omim]
ie bee/wasp. A common cause of anaphylaxis, and interestingly, not related to atopy. Reactions can be immunological (IgE or non IgE), or non-immunological (toxic).
Severe reactions related to allergy but also number of stings, insect type, cardiovascular/respiratory disease and also mastocytosis.
Whether it is bee or wasp or other is sort of important, from the point of view of cross reactivity and risk. Several major allergens eg hyaluronidase, phospholipase A2. Apid (bee) hyaluronidase is 50% identical to vespid, so good chance of being allergic just to one and not the other. Vespids subdivides into Vespa=hornets (found in UK, biggest, 35mm, reddish brown head); Vespula=wasps; and Dolichovespula (“short headed wasps” – harder to distinguish, “shorter distance between eyes and upper jaws”!). These 3 vespid types cross react strongly, so likely to be allergic to all. “Yellowjacket” is American name for wasps.
Bumblebee PLA2 is 53% identical to honeybee PLA2, so not necessarily cross reactive!
Polistes=”paper wasps”, distinct from other vespids, Southern Europe only (so far) – large, long legs, not esp colourful. Limited cross reactivity to wasps/hornets, thankfully.
Ants are also hymenoptera!
Clinical
“Normal” local
“large” local = >10cm swelling, plus >24hrs. Blisters sometimes present). Mech prob toxic, but sometimes evidence of IgE mediated mechanism,
systemic toxic (haemolysis, nephropathy, coagulopathy – rare, usually from multiple stings)
systemic +/- anaphylaxis [usually igE, rarely short term IgG, or complement activation by IgG-venom complexes]
(plus “unusual”).
Wasps and hornets not as fuzzy as bees. Was a barb left behind? Bees, not wasps. Multiple stings at the same location? Wasp, not bee.
Systemic reactions should be assessed by allergy specialist, including skin prick tests, total IgE and baseline tryptase tests.
Hypotension is the dominant feature and may occur alone.
Risk factors for outcome of anaphylactic reaction:
age,
CVS disease/drugs,
insect type,
time interval between stings (short interval increases risk of systemic reaction to second sting),
number of stings,
severity of previous reaction,
elevated mast cell tryptase, else known mastocytosis.
Bee allergic at higher risk of systemic reaction than vespid allergic. Hornets risk seems to be esp high.
Frequent stings can induce tolerance (but probably needs more than 200 per year!).
Venom IgE >1 had 12x risk of anaphylaxis (beekeepers, regardless of previous history). Pos skin test (adults without history of anaphylaxis) had 17% risk, cf 0% of neg skin test [so negative test v reassuring, but risk still low even if you are pos, which would be unusual in most kids]
Majority of fatalities have significant cardioresp co-morbidity. 40-85% of fatal reactions had no documented history of previous anaphylactic reactions.
Mild systemic reaction previously gives 18% risk of subsequent systemic reaction (kids). Compare after large local – 5-15%, so sl higher but not much. Children tend to have mild systemic reactions, cf most adults get resp or CVS symptoms.
Several case reports of severe reactions in mastocytosis; even without mastocytosis, high basal tryptase seems to increase risk of anaphylaxis.
Testing
Even when SPT pos, 25-84% of subjects do not react to subsequent sting!
Similarly, up to 22% of those with neg tests will have systemic reaction in future. [Allergy 2005: 60: 1339–1349]
Test all with systemic reaction, not recommended otherwise. If not witnessed? Only really useful to distinguish bees vs wasps (says the Anaphylaxis Campaign)!? Unless you’re a bee keeper, wasps are the one you are most likely to be stung by.
Skin prick testing more sensitive/specific. Probably sensible to leave a month or two between the event and testing else false negative due to “refractory period”. This period can sometimes be longer so consider repeating if good history. If negative, try IgE; then intradermal ( with 0.001-1mcg/mL solution -seems to have higher sensitivity).
Stepwise skin testing with 0.01-100mcg/ml solutions incrementally recommended.
Some people will be persistently negative on testing, probably due to being allergic to an unusual protein. Consider systemic mastocytosis as a differential.
Family history of venom anaphylaxis is a common cause of concern. Unfortunately, there is no point testing other family members – you are unlikely to test positive if you have never been stung.
Specific IgE levels (if you do test positive) only vaguely correlate with anaphylaxis risk (not statistically significant) [Allergy 62(8): 884-889, August 2007]. However, having low total IgE (<50kU/l) predicts anaphylaxis (not v sensitive, only explains 25%), whereas high total IgE (>250) protects (very specific)!
Serum IgE appears within a few days of sting, begins to decline at a variable time – wait long enough, and no IgE may be detectable. Double positivity to bee/vespid could be genuine cross sensitivity but might be cross reactivity of IgE to epitopes of unknown clinical significance.
Baseline serum tryptase over 11 has high positive predictive value for anaphylaxis but is not very sensitive. Good for picking up mastocytosis though!
So you may be able to find the occasional person who seems to be at particular risk (high tryptase, low total IgE), or relatively protected (high total IgE) but you will still miss most cases of anaphylaxis.
Immunoblotting, basophil activation tests etc sometimes used if others tests negative. But sens/spec generally not known.
High basal tryptase may increase risk of reactions with VIT but still indicated.
Give allergy plan and prescribe Adrenaline if severe systemic reaction, consider if moderate.
If successful VIT, still get adrenaline if further symptoms, continued exposure, high tryptase.
Reported, in most cases appears to be due to pollens contained in the honey, or at least allergens highly cross reacting with pollens. But in a minority, does appear to be due to bee derived components. Type of honey will determine what pollens are contained in it; commercial honey often contains v low amounts due to production techniques.
Prevention
Risk of sting related to zone, climate, temperature, outdoor activities etc. Some repellents marketed as effective against wasp/bee (IR3535 (Ethyl butylacetylaminopropionate) eg Jungle Formula “outdoor & camping”) but most creams/sprays (DEET, Citronella oils etc) are for biting insects (midges, mosquitoes etc), not stinging. Bees/wasps generally not interested on landing on your skin anyway! Sting because they are threatened!
Differential of eye allergy includes tear film dysfunction, infection, autoimmune/inflammatory conditions, blepharitis, dry eye.
Severe -2 of vision disturbance, impairment of daily activities (leisure, sport, school, work); troublesome symptoms.
Perennial conjunctivitis usually related to house dust mite (HDM), animal dander, moulds else multiple. Itch characteristic, as per seasonal conjunctivitis, findings non-specific eg tearing, redness, eyelid swelling, small papillary hypertrophy of tarsal conjunctiva. Neither has corneal involvement.
Beware pain, photophobia, visual disturbance, grittiness or foreign body sensation. These can indicated Vernal keratoconjunctivitis, which does affect the cornea (warm climates eg Mediterranean/Africa): typically boys aged 4-12yrs, T cell and IgE combined, improves after puberty. Severe itching, exacerbated by nonspecific stimuli eg wind, dust, sun. Cobblestone appearance of tarsal plate (ie inside upper eyelid) else limbic thickened and opacified +/- white/yellow gelatinous deposits (more typical of tropical form). Can get corneal ulcers.
Atopic keratoconjunctivits is also rare, the eye can be the only affected area cf atopic dermatitis. Hall mark is fissured eyelid. Staph colonization contributes. Limbus and cornea can be affected.
Giant papillary – associated with contact lenses.
Contact blepharoconjunctivitis is eyelid itching, oedema, eczema with less in the way of conj redness.
Conjunctival provocationtest can be done with standardized allergens – defer if on local or systemic antihistamines or anti-inflammatories, contra-indicated if uncontrolled asthma. Ideally when asymptomatic and eye not inflamed! Dilute extract to obtain several lower concentration solutions (last up to 6 hours at room temp). Administer 20microl dose at 30 min intervals at infero-external quadrant of right eye. Left eye is control! Have local antihistamine and steroids available, in addition to usual systemic medicines. Only 1 reported case of anaphylaxis!
Patch test for non-IgE. Else Conjunctival cytodiagnosis eg eosinophil infiltrates.
Treatment and prevention –
Avoid allergens, protect eye with sunglasses.
Lubricants and cold compresses are good.
Topical antihistamines eg azelastine, olapatadine but also Lodoxamide, ketotifen.
Mast cell stabilizer (ie cromoglycate) needs 2/52 preloading and multiple doses per day, plus stings! So poor compliance.
Systemic antihistamines if other symptoms else may be excessively drying.
Topical steroids should be avoided except where cornea involved, ie VKC, AKC, and then only in short pulses. Twice daily steroids for a month or more raises concern about glaucoma, cataracts.
Ciclosporin drops oily, supply probs – veterinary products used! Tacrolimus not available in drops; cream burns a little but gets better.
Nasal steroids work well for eye symptoms and appear to be safe.
For blepharitis, eyelid hygiene, emollients, 1% hydrocortisone.
Rome III classification (now Rome IV?) of functional GI disorders – has child section. Colic, rumination, cyclical vomiting, diarrhoea, dyspepsia, abdo migraine, IBS, abdominal pain, constipation.
Functional abdominal pain (FAP) must include all of the following:
Episodic or continuous abdominal pain
Insufficient criteria for other functional GI disorders
No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’s symptoms
Criteria fulfilled at least once per week for at least 2 months before diagnosis
Childhood Functional Abdominal Pain Syndrome
Must include childhood functional abdominal pain, and at least 25% of the time have 1 or more of the following:
Some loss of daily functioning
Additional somatic symptoms such as headache, limb pain, or difficulty sleeping
Criteria fulfilled at least once per week for at least 2 months before diagnosis
That loss of daily function is an optional criterion is because it would exclude motivated children who continued activity despite the pain and children whose parents insisted that they continue activities. However, it is recognized that there is a subgroup of children in whom loss of daily functioning and/or accompanying somatic symptoms form an important component of their symptom complex. This group is now referred to as having FAPS.
It is still debatable whether H pylori can cause symptoms in the absence of peptic ulcer disease. Young children may of course not give a typical ulcer history, but clues would be epigastric, pain before meals or helped by eating or antacids. Not helpful when functional abdominal pain or reflux disease.
A meta-analysis of 45 studies concluded that H pylori infection is not associated with abdominal pain. In a German study of 1221 children social and familial factors (single-parent household, family history of PUD, or functional pain) were significantly associated with abdominal pain, but not with the H pylori status of the child, as assessed by the 13C-Urea Breath Test.
In a study of 695 schoolchildren between 10 and 12 years old there was no association between H pylori and recurrent abdominal pain, in fact there was an inverse relationship after adjustment for selected possible confounders!
Although there have been studies that seem to show that symptoms improve with treatment, these have been of poor quality and the natural course of illness is to improve anyway.
Now that a link has been established between helicobacter and cancer (esp stomach, via chronic gastritis, also non-Hodgkins lymphoma) in adults, benefits and risks of treatment when it has been discovered should be discussed.
Refractory iron-deficiency anaemia is not considered a good reason for testing anymore.
Gold standard is Gastric biopsies (antrum and corpus) for histopathology during endoscopy. Initial diagnosis of H. pylori infection can be based on either positive histopathology + positive rapid urease test, or a positive culture.
Stool antigen test is pretty reliable. Could simply indicate asymptomatic carriage though. Once you know about it, of course, you need to consider eradication given cancer risk.
You should wait at least 2 weeks after stopping proton pump inhibitor (PPI) therapy and 4 weeks after stopping antibiotics before doing any of these tests.
Detection of antibodies against H. pylori (whether in blood, urine, saliva) are not reliable for use in the clinical setting.
Who needs one? Anyone at risk of anaphylaxis, is the simple answer. But there are no reliable ways of identifying who is at risk of anaphylaxis!
There is also a big problem with them not being used even when they are available.
Who needs one?
EAACI position paper – see Anaphylaxis management. Only a couple of absolute indications, otherwise a risk assessment.
Prescribing a pen is only part of the overall management: nothing worse than prescribing a pen and not properly discussing avoidance, or having a pen that does not get used when it should be, because it’s left at home or because no-one remembers how to use it or they are too scared to use it.
In various studies, prescribed AAIs were only used in a third of recurrent episodes, despite being available and in date in two-thirds of episodes. The reason(s) for non-use requires further study: parental questionnaires indicate that parents have a poor recall of anaphylactic symptoms and how to use the AAI despite training.
2021 Expert working group – MHRA set up after further coroner’s inquests into anaphylaxis deaths, following European safety review in 2015. Recommendations are:
Early adrenaline. Which means teaching families/children recognition of signs.
Need for 2 pens emphasized.
Brand specific training
Key messages on packaging eg “don’t delay”, “use second pen if necessary”
Posture detailed – “lie down with legs up”, “sit up if breathing difficult but don’t change position suddenly”, “stay lying down [regardless of whether you feel better or what people tell you to do]”
Wider availability of AAIs in public places likely to be beneficial but this would require legislative amendment as well as public training, and concerns about storage conditions and supply would need to be addressed.
Dosing errors in hospital common, but given pressure on AAI supply may not be great solution. Other solutions would be labelled kits, pre-filled syringes, different system of labelling adrenaline (!).
Reporting of device related adverse events, and anaphylaxis events (including re-establishment of fatal anaphylaxis registry).
Technique
Patient should lie down (but if respiratory symptoms then may be more comfortable sitting). Video available at Epipen and Jext websites. 3 minute training video with more explanation on Youtube. Or scan this:
Remove safety cap (Blue for Epipen, Yellow for Jext).
Jab orange (Epipen) or black (Jext) tip firmly into upper outer thigh, through clothing if necessary but avoid seams and pocket contents eg coins, mobiles – clicks as it activates.
Hold for 3 secs (Epipen), 10 secs (Jext).
Previous advice was to rub area (probably now white) vigorously for 10 seconds. Adrenaline causes vasoconstriction in skin, but vasodilatation in muscle so should be absorbed as long as IM. Not specified now.
Phone 999.
Dispose of device safely (device is self sheathing). Note that some drug left behind, which is normal, and that pen cannot be reused!).
Repeat after 5 minutes if necessary. Use a different leg!
Training checklist (from GOS):
When to use it
How to use it
When to carry it ie at all times!
Storage/disposal – should be protected from heat and light
Expiry date – reminder service available from support website (link above)
They come in two different doses – standard strength is 0.3 mg, there is a 0.15 mg strength prescribed for younger children (15-30kg). Emerade (not currently available) gcomes in a 0.5mg strength for adults and children over 12, which is a more appropriate dose for bigger people viz over 60kg.
If patient is under 15kg, CYANS guidance is that over 7.5kg, the potential benefit outweighs the risk. For those under 7.5kg, need to balance risk of anaphylaxis with risk of drug error from drawing up adrenaline from vial with syringe and needle.
Epipen has 18 month shelf life, self sheaths, and has a window to show ready to use. Blue safety cap, orange needle end. JEXT pen similarly self sheathing, coloured window to show whether it is live or not, 24 months shelf life. Yellow safety cap, black needle end. Same needle length.
Anapen has been discontinued. Had a shorter needle, different technique – remove caps from both ends, hold against leg, put your thumb over the end and press red button.
Emerade pen has safety cap over needle end – this is different from the other types but is logically simpler. Needle is 25mm long cf 15mm Epipen/Jext. Currently off market due to reliability of activation concerns.
Number of Pens
2018 MHRA review recommends 2 pens available at all times, and made the recommendation directly to families so they can demand them from their doctor! BSACI (2016) suggested children should in most cases just get 2 pens, 1 for home and 1 for school, but this was contradicted by later European Medicines Agency (EMA) and previous NICE guidance. Still not clear why they should ever by prescribed in single rather than twin packs…
due to uncertainties about the site of drug delivery and the speed of adrenaline action within the body, it is recommended that healthcare professionals prescribe 2 auto-injectors, which patients should carry at all times
the needle length of the device is now stated in the product information because this may be an important factor for the prescriber to consider when choosing a suitable auto-injector
the training of patients and their carers in the correct use of the product is important and manufacturers were required to update their educational materials
manufacturers should carry out studies in humans to more fully understand when and how much adrenaline reaches the blood stream, and how quickly and effectively it acts on body tissues when given through an auto-injector
EAACI guideline says number of pens should be guided by individual assessment, and BSACI also allow that 2 pens may be more appropriate in some cases, eg obesity, previous need for 2 doses, remoteness etc. There has been good evidence published indicating that one-third of children with anaphylaxis require a second dose of epinephrine (Kornblat P, et al Allergy Asthma Proc. 1999; 20: 383–6), and deaths have occurred despite a single injection, but most of these reports describe subcutaneous adrenaline use, rather than intramuscular use. Dose is more likely to be an issue with big teenagers (eg over 45kg).
If you carry your pen, know how and when to use it, then you are doing to do significantly better if you have a bad reaction than most other people, so don’t get too hung up on how many pens!
Spare pens in school
New legislation (2017) allows schools to obtain without prescription spare pens. These can be used if the pupil’s own pen is not immediately available or already given. Note that children with food allergies are not always prescribed adrenaline auto injectors but may still be at risk of anaphylaxis. The spare pen can be used in such children if:
The child’s care plan confirms child is at risk of anaphylaxis
A health care professional has authorised use of the spare pen in an emergency
The child’s parent/guardian has provided consent for a spare pen to be administered
Note that advice on using pens can be given over the phone by emergency services, if it is made clear pens are available.
Further information about spare adrenaline pens, and advice on reducing the risk of reaction sin school, treating reactions in school, staff training etc can be found at https://www.sparepensinschools.uk/
Needle length
Doing ultrasounds of thighs shows that in a significant proportion of people, including children under 5 with high BMI, the distance to muscle is more than 15mm (and not including any clothing). 82% of the obese children studied had skin surface to muscle depth greater than needle length. This was only true for 25% of the non-obese children. 3/4 the way down the thigh, only 17% of obese children and 2% of those not obese. Arkwright, Royal Manchester Children’s Hospital – 2013 Annual AAAAI meeting.
Some suggestion from injection models that “jet” of adrenaline penetrates significantly deeper than needle alone, that the angle, force used, whether the device is spring loaded or not, all potentially affect depth. So concerning, especially given the cases where multiple injections have failed to prevent death (eg Natasha Ednan-Laperouse).
Emerade had longer needle (25mm) but not currently available. So inject in lower lateral thigh?
2015 European medicine agency review discussed above concluded that training remains the paramount issue, although further research into needle length should be done.
2021 Review found that blood adrenaline levels actually higher after Epipen and Jext cf
Failure to use
In a prospective UK study of children prescribed AAI for at least a year, the most common reasons given by patients for not using their AAI (245 episodes of anaphylaxis, AAI used in only 16.7%) were ‘thought adrenaline unnecessary’ (54.4%) and ‘unsure adrenaline necessary’ (19.1%). Device not being available only mentioned in 5%.
In 2002 Australian retrospective study of patients with previous anaphylaxis, shortness of breath usually recognised as anaphylaxis symptom but less commonly upper airway or cardiovascular symptoms/signs. Half forgot the need to remove safety cap and hold for 10 seconds in scenario. 71% of anaphylactic reactions were not treated with AAI, even though AAI was available in most cases. About half of those needed adrenaline treatment in hospital (which was rare in AAI treated cases).
In a 3 year Canadian study of 1500 ED episodes, almost 50% of adults were not treated with epinephrine in or outside of the hospital. Slightly better for kids, 28.7%. Almost all of these children had been prescribed auto-injectors. The need for multiple doses in ED was less in those who received epinephrine outside ED. [Allergy, Asthma & Clinical Immunology 2014, 10(Suppl 2):A3]
In a Canadian email survey of 1885 anaphylaxis survivors (adults and kids, food and insect etc), 73% did not give epipen. Most common reason for not giving, was that an antihistamine had been given first. Only 28% gave reason as being that they did not have epipen! 13% judged reaction as mild. 41% of epipens were given by someone other than patient, mostly family of children. 53% of epipen users had previously used one before. [simons, clark, camargo – JACI 2009:124;301 doi:10.1016/j.jaci.2009.03.050]
Failure to prescribe
In an online survey presenting 10 paediatric allergy case histories to paediatricians (all were severe, although only 1 case specifically mentioned anaphylaxis). There was significant variability in prescribing practices. Although all allergists and generalists prescribed an autoinjector (94.4% and 92.6%, respectively) or would offer the patient a choice about autoinjectors (5.6% and 7.4%, respectively) in the case specifically mentioning anaphylaxis, many cases had almost no consensus on prescription of adrenaline autoinjector. The prescribing patterns of allergists and generalists showed no significant differences for 9 of the cases. For the remaining case, which described a child with oral allergy syndrome, all specialists (n=54, 100%) reported that they would not prescribe an autoinjector (in line with guidelines) compared with only 20 (74.1%) of generalists (p<0.001). [Johnson MJ, Foote KD, Moyses HE et al. (2012) Practices in the prescription of adrenaline autoinjectors. Pediatric Allergy and Immunology 23: 124-7]
In a survey of all GPs in Scotland, 90% of the 613 respondents had prescribed adrenaline autoinjectors. However, only 49% of prescribers were confident in use of these devices, and only 17% had access to a trainer pen for demonstration to patients. If called upon in an anaphylactic emergency (experienced by 36% of respondents), only 50% of respondents would use the appropriate dose and 14% would use an inappropriate route of administration (subcutaneous or intravenous). [Lowe G, Kirkwood E, Harkness S (2010) Survey of anaphylaxis management by general practitioners in Scotland. Scottish Medical Journal 55:11-4]
Failure to Use – Doctors
When scenarios presented to junior doctors (same questions posed 10 years earlier) – all recognized need for adrenaline in anaphylaxis scenario but dose often wrong and 25% gave adrenaline IV. For non-anaphylactic scenarios, adrenaline frequently recommended eg inhaled peanut. Not much improvement over decade. [Postgrad Med J 2015;91:3-7 doi:10.1136/postgradmedj-2013-132181 ]
Editorial discusses how doctors know that adrenaline is required in anaphylaxis, but that this knowledge is often not translated into practice. Many of these doctors had had ALS training; most had not worked in an emergency department. Simulation? Australian experience. Booster sessions?
