Category Archives: General paediatrics

Vitamin D

General paediatrics, Nutrition, OPD, Orthopaedic

=colecalciferol.  Essential for bone health.

Obtained from sun exposure to the skin.  Only a few dietary sources – oily fish, cheese, egg yolk, fortified cereals. Diet more important for calcium, of course. Once you apply sun screen, you don’t make vitamin D any more so there is a conflict with the potential for skin solar damage including cancer.

Children under 5 considered a high risk group, along with pregnant, pigmented skin, northern latitudes, wearing concealing clothing, being housebound etc.

2021 Scottish government advice is that everyone consider taking a Vitamin D supplement, particularly between October and March, but that all year round supplementation should be taken by:

  • all pregnant and breastfeeding women
  • all infants and children under 5 years old
  • people who have low or no exposure to the sun, for example those who cover their skin for cultural reasons, are housebound, confined indoors for long periods or live in an institution
  • people from minority ethnic groups with dark skin such as those of African, African-Caribbean and south Asian origin, who require more sun exposure to make as much vitamin D

2017 chief medical officer (CMO) advice – all babies from birth up to one-year-of-age should be given a daily supplement of 8.5 to 10μg vitamin D with Healthy Start vitamin drops being the recommended choice of vitamin, other than babies who are formula fed getting at least 500ml per day, as infant formula already has added vitamin D.

Nonetheless, breastfeeding is preferred – supplementation needed for breastfed infants given lack of sunlight in the UK (probably only useful sun exposure in Scotland between April and September, and between 11 and 3pm).

Children aged 1-4 years old should be given a daily supplement containing 10mcg of vitamin D.

“Healthy Start” vitamins preferred – made for  NHS,  available free to those on income support,  contains recommended dose (approx 300 units) .

Standard prevention dose is 300-400u (10mcg) (neonates), between 400u and 1000u (over 1/12) per day.  Over the counter multivitamins often contain surprisingly little Vitamin D.  Drops, tablets, sprays all available.

Many vitamin D preparations around this dose contain calcium, which may improve efficacy in fracture prevention, but some people won’t like.  Fultium D3 capsules have 800u (20μg) vit D and no calcium.

Symptoms

Aches and pains, delayed walking, seizures and tetany, genu valgum/varum, muscle weakness (incl cardiomyopathy).  The classic features of rickets are bowed legs, rachitic rosary (expanded costochondral junctions), pectus carinatum, curvature of the spine, expansion of the metaphyses at the wrist/ankle, poor dentition.

Testing

Historically deficiency defined as 25hydroxyVitaminD below 25nmol/L. But debated what is optimal.  NICE CKS uses this figure, and defines ‘insufficiency’ as between 25 and 50 nmol/L.

Treatment

Vitamin D3 preferred – D2 sometimes used.

If rapid correction needed eg deficiency with symptoms, fixed loading dose used for 8-12 weeks:

  • 1-5 months: 3000 IU
  • 6 months -11 years: 6000 IU
  • 12yr+: 10 000IU. Single/divided oral dose totalling 300 000IU can be considered if compliance issues.
  • After that, standard prevention dose as above unless significant lifestyle changes to improve Vitamin D status.

Otherwise 400-600IU daily from age 1 month to 18 years. Buy over the counter unless for chronic condition that leads to deficiency.

Assess need for calcium supplementation eg milk allergy. Online calcium calculators available.

Colecaciferol liquid available (3000u/ml), tablets come in 1000u doses and higher.  The combined VitD/Cal tablets tend to have lower Vit D doses and may not be tolerated.

Weekly doses, or single megadoses (30x daily dose) have been recommended where compliance a concern. Intramuscular ergocalciferol 7.5mg (300,000 units, 1ml) can be given in special situations.

Alfacalcidol is used in chronic kidney disease, needs specialist advice and careful monitoring.

Monitoring

Repeat measurement of serum 25 OH vitamin D is not usually necessary, and certainly not within 3 months of starting treatment unless agreed with the duty biochemist.  Check compliance eg empty bottles?

Continue supplementation until child has stopped growing.

Vitamin D deficiency in children | Health topics A to Z | CKS | NICE

Bell’s palsy

General paediatrics, Neurology

bells palsyDiverse causes, some of which are extremely serious (mostly infiltrative):

  • Zoster sine herpete ie zoster reactivation without vesicles – probably responsible for a third of otherwise unexplained facial palsies
  • EBV- the most commonly found cause (20%)
  • Ramsay Hunt – look out for soft palate, tongue as well as external auditory meatus lesions
  • Mycoplasma
  • Cat scratch disease, HIV, Lyme disease (erythema chronicum migrans, travel history)
  • Acute otitis media (historically the most common cause!  Reactivation of virus?  Toxin induced demyelination?  But beware mastoiditis!)
  • Trauma
  • Malignancy – leukaemia, cerebellar astrocytoma, rhabdomyosarcoma
  • Histiocytosis
  • Haemophilia
  • Hypertension!

Bell’s Palsy is what you would call it if idiopathic, but perhaps you just haven’t looked hard enough? Often otalgia, facial or retroauricular pain. Typically mild except in Zoster, where it is severe. Pain may precede palsy.

Warning signs (for a serious underlying cause) are:

  • otitis media (in case direct inflammation, ie osteomyelitis),
  • hearing loss,
  • lymphadenopathy, tonsillar enlargement (parotid tumour),
  • mastoid enlargement,
  • frontal sparing, motor function of tongue/fingers (adjacent cortical representation) (UMN lesion)
  • or duration longer than 1 month.

Assess using House-Brackmann scale:

House Brackman criteria

Management

Do hearing test, blood pressure, check frontal sparing/tongue/finger function. FBC if any suspicion of leukaemia. Check blink reflex (prognostic).

Treatment

Apply lubricating drops hourly during day, and an ointment overnight. Patching seems to be frowned upon now.

Treat underlying cause!

For Bell’s, still controversial.  Cochrane review (2016) found that steroids reduce chance of permanent facial weakness (NNT=10), involuntary movements (motor synkinesis) and crocodile tears.  Adding antivirals may improve rate of recovery but low quality evidence – certainly less good than steroids, in fact not much different from placebo when used alone! Even without treatment most make a full recovery within 9 months. (Dundee study in adults, NEJM 2007; 357:1598 PMID 17942873)(Adour, Ann Otol Rhino 1996)(Hato Otol Neurotol 2003, PMID 14600480)

Only 2 studies in children from what I can see.

IV aciclovir in Ramsay Hunt since poor prognosis. Valciclovir would in theory be better, 96% recovery in Hato study (5 day course with steroids cf steroids alone) but unblinded (Otol Neurotol 2007;28:408-13)

Some evidence for methylcobalamin and hyperbaric oxygen.

Recovery usually within 3 weeks, else nerve regeneration takes 4-6 months. Beyond 6 months improvement is unlikely. For long term palsy, feedback training, surgical techniques may result in functional as well as cosmetic improvements. Synkinesis and facial spasm are complications, treat with botulinum. (BMJ 329:553)

Antibiotic classes

Microbiology

Protein synthesis inhibitors

Act on ribosome.  In theory, reduce toxin production as well as growth.

  • Macrolides
  • Aminoglycosides
  • Clindamycin
  • Chloramphenicol
  • Tetracyclines
  • Linezolid

Aminoglycosides

Eg Gentamicin.  Broad spectrum but poor CSF penetration (but still used for Listeria meningitis!).

Some important bacteria are usually resistant to the aminoglycosides, including gentamicin:

  • most streptococcal species (including Streptococcus pneumoniae and the Group D streptococci),
  • most enterococcal species (including Enterococcus faecalis, E. faecium,  and E. durans),
  • anaerobic organisms, such as Bacteroides species and Clostridium species.
  • Salmonella and Shigella
  • Pseudomonas unless you use ones with antipseudomonal activity eg tobramicin

Hearing damage is an important side effect, known genetic marker for this but usually not done ahead of treatment.

Renal excretion.

Quinolones

Block DNA synthesis.  Broad spectrum but not great gram positive, excellent absorption, penetration and intracellular too.  See quinolones.

Vasculitis

General paediatrics, Immunology

Inflammation of blood vessels, clinical manifestation depends on which part of the body (often widespread) and what size vessel affected.

Classic presentations are:

  • rash esp purpuric, pernio (swelling of subcutaneous tissue),
  • ischaemia eg infarction (brain, gut, digits),
  • nephritis,
  • asthma.

The Chapel Hill system provides definitions for 10 different forms of adult vasculitis but is of debatable utility.  EULAR consensus criteria look pretty good [Annals of the Rheumatic Diseases. 65(7):936-41, 2006. PMID 16322081].

Differential: hyperlipidaemia esp severe familial, coagulopathy, fibromuscular dysplasia (familial).

Primary vasculitis

Classified by size of vessel affected (although a degree of overlap often exists):

  • Large vessel ie aorta- Takayasu. May be preceding inflammatory-type illness. ?headache/dizziness, ?inflamm eg Raynauds, episcleritis etc.  Claudication, absent pulses, subclavian bruit.
  • Medium vessel – Kawasaki disease, Wegener’s (C-ANCA pos, nasal/oral lesions, pulmonary lesions, GN, granulomata), Polyarteritis Nodosa (PAN: livedo, neuropathy, aneurysms), Churg Strauss (ANCA pos, asthma, eosiniophilia, neuropathy)
  • Small vessel vasculitis – Henoch Schonlein Purpura (HSP) is the classic one, but also cryoglobulinaemia (?hyperviscosity, assoc with malignancy and chronic viral infection)

Secondary vasculitis

eg SLE, mixed CT, infective esp streptococcus.

Investigations

Characterized by one or more anti-neutrophil cytoplasm auto-antibodies.  These are screened for by immunofluorescence (IF) that can reveal specific patterns of staining, viz pANCA (peripheral staining), cANCA (cytosol staining).  cANCA is predominantly due to Peroxidase 3 antibodies, and is seen in Granulomatosis with polyangiitis (previously Wegener’s granulomatosis, so should be Wanca?!), pANCA is mainly due to Myeloperoxidase antibodies and bacterial permeability increasing factor (BPI), and is seen in 50% of microscopic polyangiitis.

These patterns and antibodies are also associated with rheumatoid arthritis, CF, IBD, drug induced vasculitis, Churg Strauss syndrome, autoimmune liver disease etc.

But in children these are not very sensitive and in any case no evidence that distinction influences treatment or prognosis. The type of ANCA seems to be related to the population rather than the disease! Probably has direct toxic effect.

Imaging is the second modality of investigation, esp MR angiography.

Untreated, these diseases have 90% 2 yr mortality…

Diabetes

Endocrinology, General paediatrics, OPD

Updated NICE guidance 2016.  Characteristics:

  • random glucose >11,
  • polyuria, polydipsia,
  • excessive tiredness,
  • weight loss.

WHO 1999 criteria – fasting normally <5.6, >7 diagnostic.  Random >11 diagnostic (assuming there’s nothing sticky on the finger tested!!!).  Glucose tolerance test (starts with fasting level) 2hr level >11.1 diagnostic, 7.8-11.1 is impaired glucose tolerance.

False positives – infection, recent surgery, uncontrolled thyroid disorder, starvation.

Epidemiology

Increasing rates in Europe. Scotland rate second only to Scandinavia.  Marked increase in under 5s. Aiming for routine pump therapy within a few months.

Subtypes

Type 2 more often in S Asian, Hispanic, Afro-Caribbean.  Clue is raised c-peptide – as this is co-produced with insulin, it means there is still endogenous insulin being produced (and cleared at more consistent rate than insulin, so more reliable, esp if on exogenous insulin).  C-peptide also used to look for insulinoma or factitious hypoglycaemia.  May also predict glycaemia control, complications and response to hypoglycaemic agents.

LADY – latent autoimmune diabetes of the young. More common? Different HLA type. Antibody positive but insulin sensitive and slow progress.

MODY – inability to produce insulin but normal beta cells.  Eg KIR 6.2 mutations, within months of birth.

Management

Reduced ideal HbA1c target – 48mmol/l (6.5%).  

No DAPHNE for kids.

Multiple daily injections from diagnosis, with level 3 carbohydrate (CHO) counting education, blood ketone testing strips.  Other regimens eg BD, TDS only for where problems with compliance.  See also pumps.

NICE guidance now includes Type 2 – suspect if strong FH, obesity, black/Asian origin, minimal insulin requirements (<0.5u/kg after “partial remission phase”), evidence of insulin resistance (viz acanthosis nigricans).

BMJ NICE diabetes infographic

Optimal blood glucose range is 4-7 on waking and between meals; 5-9 after meals; 5+ when driving.  At least 5 tests per day recommended, more frequently during physical activity and illness.But take into account:

  • risk of hypoglycaemia;
  • competitive sports;
  • need to lose weight;
  • life goals (careers, exams, foreign travel);
  • any relevant co-morbidity.

Monitoring

Annual thyroid, hypertension, albuminuria checks from diagnosis; retinopathy testing from age 12.  Type 2 don’t need thyroid but do need dyslipidaemia.

School

Most schools happy to give insulin. But no legal requirement. Lancets for school retract into cartridge.

Self-Efficacy

Encourage ownership of meters etc, downloading at home. Over 14 to get access to SCI-DC, as adults.

Cerebral oedema

Clinical, Emergency medicine, General paediatrics, Neurology

Cytotoxic vs vasogenic (resistant to steroids) vs interstitial (obstruction eg meningitis – not steroids, ?osmotic) vs osmotic (CSF, ECF low osmo) vs hypertensive.

In DKA, there is a 25% mortality from cerebral oedema, 34% long term neurodisability. 

Presents with headache, irritability, agitation (which can be difficult when child is unwell with something else).  Then altered consciousness, posturing, focal neurology (check eye movements, pupils).  Classically Cushing’s triad: hypertension, bradycardia, irregular breathing pattern.

Clinical diagnosis really.  CT can show (better than MRI!).

Hypertonic saline (2.7 or 3%, 2.5-5ml/kg over 10-15 mins) or mannitol (20%, 0.5-1g/kg over 15 mins), some people prefer hypertonic saline but whatever is closest to hand!  Frusemide adjunctive.   

Consider Aciclovir if diagnosis unclear (in case herpes encephalitis – CT not great, LP can be non specific).

Brain protection = 30deg head up, midline position. Avoid hypotension. Avoid hypocapnia (intubate and ventilate if in doubt).

Hyponatraemia common – typically due to SIADH but treat any underlying cause, esp hypovolaemia.

Constipation

Common, Gastro, General paediatrics, OPD, Psychology

Consider constipation if:

  • episodes of faecal incontinence (stains or smears in pants, potentially larger accidents),
  • retentive posturing (standing or sitting with their legs straight and stiff or crossed legs, some will sit on their own heel),
  • occasional massive but soft stools that virtually obstruct toilet.

Not just hard painful infrequent stools! Beware also dyschezia, where baby appears to strain at stool but not actually hard/large.

In a population-based prospective birth cohort, where dietary types were extracted from questionnaire, adherence to a ‘Western-like’ dietary pattern was associated with a higher prevalence of constipation up to 48 months [aOR 1.39; 1.02-1.87], which was not mediated by overweight or sedentary behaviour. Adherence to a ‘Health Conscious’ dietary pattern was only associated at short term, with a lower prevalence of constipation at 24 months (aOR; 0.65; 0.44-0.96). This suggests that specific dietary patterns in early childhood could be associated with higher or lower risks for constipation, but these effects are time-dependent. [Maternal & Child Nutrition. 9(4):511-23, 2013 PMID: 22288911]

Straining is not a criteria, in NICE, interestingly, although it is in Rome III criteria!

Red flags:

  • multiple anal fissures,
  • gross abdo distension,
  • tenderness with guarding,
  • abnormal lumbosacral or lower limb findings,
  • failure to thrive
  • ribbon like stools (?anal stenosis)
  • etc

“Do not use dietary interventions alone as first-line treatment for idiopathic constipation” – because no evidence that it helps! But yes, adequate hydration and fibre important (whole grains, fruit/veg, pulses).

NICE recommends Movicol/Laxido (macrogol) as first line, combining with a stimulant (picosulfate, biscodyl, senna) as second line. If macrogol not tolerated, use stimulant +/- softener (lactulose, docusate).

Warn that pain and soiling gets worse before getting better!

Review of adherence and dose important.

Toilet training eg diary, reward system, regular post prandial sitting 5 mins +/- feet on hard surface eg stool.

“Poo should be as soft as toothpaste and should come out like a snake” (Snakes and ladders booklet, Kidney Kids Scotland). Tell your teacher if no toilet paper/soap or broken seat/locks etc.

Soiling

Typically, episodes of soiling (large and small) are due to overflow of liquid stool past a large impacted stool in the rectum.  The child is unable to control, due to the distortion of the rectum.

However, children often try to deny being aware of soiling, despite the obvious smell or discomfort – this is simply a coping method, and normal sensation is usually easy to demonstrate.

The diagnosis is easier in the presence of a large suprapubic mass, or a rectal mass on digital examination.  Some children however soil for attention, without any bowel or rectal disorder.

The presence or implication of a large rectal mass requires disimpaction – an escalating regimen of a paediatric formulation of macrogol (Laxido or Cosmocol are cheaper than Movicol) as per NICE guideline 99 (doses and licensing may differ from product literature):

  • Child under 1 year: ½-1 sachet daily (non-BNFC recommended dose)
  • Child 1-5 years: 2 sachets on 1st day, then 4 sachets daily for 2 days, then 6 sachets daily for 2 days, then 8 sachets daily (non-BNFC recommended dose)
  • Child 5-12 years: 4 sachets on 1st day, then increased in steps of 2 sachets daily to maximum of 12 sachets daily (non-BNFC recommended dose)
  • If macrogol not tolerated, use stimulant laxative eg picosulfate +/- lactulose

If no progress after 2 weeks add stimulant laxative eg senna, picosulfate, bisacodyl, docusate.

Enemas eg citrate can prevent megarectum where prolonged medical treatment fails.

Polyethylene glycol licensed for distal intestinal obstruction!?

Maintenance

I suggest half disimpaction dose for maintenance.

Preferred treatment is paediatric formulation of macrogol (Laxido or Cosmocol are cheaper than Movicol) as per NICE guideline 99 (doses and licensing may differ from product literature).

  • Child under 1 year: ½–1 sachet daily (non-BNFC recommended dose)
  • Child 1–6 years: 1 sachet daily; adjust dose to produce regular soft stools (maximum 4 sachets daily) (for children under 2, non-BNFC recommended dose)
  • Child 6–12 years: 2 sachets daily; adjust dose to produce regular soft stools (maximum 4 sachets daily)
  • If macrogol not tolerated, use a stimulant laxative eg sodium picosulfate (5mg/5ml, NICE recommended doses):
    • Child 1 month to 4 years: 2.5–10 mg once a day
    • Child/young person 4–18 years: 2.5–20 mg once a day
    • Add lactulose or docusate if stools hard

For babies, Senna and lactulose from age 1/12.

At least 3/12 of maintenance before weaning if disimpaction required initially.

I always highlight that laxative use does not induce dependency, rather, that chronic constipation is unlikely to improve without adequate treatment.

Review regularly – symptoms, toileting, taking medication.

Continue maintenance treatment until regular bowel habit established for at least a few weeks or until toilet trained. Do not stop dose abruptly.

General advice re balanced diet including fruit, vegetables, high-fibre bread/breakfast cereals, baked beans, regular toileting, exercise, sufficient fluid intake (1000-1400ml age 4-8yrs, 1200–2100ml age 9–13yrs).

Involve Health Visitor in pre-school group.

Consider trial of milk exclusion (to rule out cow’s milk protein allergy if intractable (ESPGHAN 2023).   Coeliac disease, hypothyroidism, cystic fibrosis, Hirschsprung’s disease and hypercalcaemia also come into the differential.

Surgery

Rectal biopsy indicated if delayed meconium at birth (ie >48hrs), Downs, enterocolitic episodes.

Anal fissures have high spontaneous healing rate with medical treatment.

Manual evacuation under GA may be required if resistant. No benefit on RCT for anal dilatation. Small RCT found botox as good as internal sphincter myectomy for refractory constipation.

Appendicostomy or caecostomy antegrade colonic enema (where bowel irrigated using catheter) has a role in refractory cases after age 6yrs. QOL, continence improve but appreciable morbidity.

Relapses more common in boys, under age 4, background of psychosocial or behavioural probs, encopresis. 1/3 of post pubertal children continue to have severe problems.  See also parenting and constipation.

Parent information

ERIC website – www.eric.org.uk

[NICE clinical guideline 99 – constipation in children and young people (Published 2010)]

[BMJ 2012]

Chronic fatigue syndrome

General paediatrics, Mental health, Neurology, OPD, Psychology, Rheumatology

NICE update 2021 a bit depressing:

  • Therapy based on physical exercise should NOT be offered “as a cure”, nor should graded exercise programmes (which by definition use fixed increments in exercise) be used!
  • Instead, self management, flexible and tailored
  • CBT should only be offered to manage symptoms, improve functioning and reduce distress.
  • Talks about “energy management” – includes emotional, social, cognitive.
  • “Care and support plan” – physical activity including mobility but also activities of daily living.  Plan periods of rest and activity, and incorporate the need for pre-emptive rest.  Management of relapses and flares.

Main thrust of update is that CFS/ME is a complex, chronic medical condition affecting multiple body systems and its pathophysiology is still being investigated. It affects everyone differently and its impact varies widely – for some people symptoms still allow them to carry out some activities, whereas for others they cause substantial incapacity.  It is a fluctuating condition in which a person’s symptoms can change unpredictably in nature and severity over a day, week or longer.

Often it profoundly affects different aspects of the lives of both people with ME/CFS and their families/carers including social life, emotional wellbeing and education.

Another big theme is prejudice, disbelief and stigma experienced by patients.

US IOM expert panel have rejected the name “chronic fatigue syndrome”, as patients hate it!  Myalgic encephalitis (ME) also rejected on basis of insufficient evidence that this is the pathological process.  They suggest “Systemic exertion intolerance”, which is probably even more rubbish, in my opinion.

Diagnostic criteria: all of the following 3 [BMJ 2015; 350]

  1. Substantial reduction/impairment in pre-illness levels of activity, that persists for more than six months [NICE 2007 says 3/12 for children], and accompanied by fatigue (often profound, new or definite onset, not the result of ongoing excessive exertion and not substantially alleviated by rest)

  2. Worsening of symptoms after any type of exertion (including cognitive and emotional stress) – “post-exertional malaise“

  3. Unrefreshing sleep, and/or sleep disturbance.

In addition, should have at least one of:

  • Cognitive impairment

  • Orthostatic intolerance.

Doesn’t mention chronic pain?! NICE says reconsider diagnosis in absence of cognitive difficulties or chronic pain.

Causes

Evidence (reproducible) implicating certain infections as a trigger. Co-existing mood disorder in substantial proportion of patients, sometimes sleep-wake disorder – likely to perpetuate/exacerbate.

Brain imaging has identified alternations suggesting that it is a brain problem.

Investigations

[NICE 2007]

  • Urinalysis
  • FBC, LFTs
  • TFTs
  • Coeliac disease screening
  • CK
  • ESR/CRP
  • Glucose
  • Ferritin

NOT microbiology unless indicated: borrelia, HIV, Hepatitis viruses, EBV, CMV, toxoplasmosis

Management

Exercise

Cochrane review of graded exercise therapy – may benefit sleep, physical function, self-perceived general health, and no evidence that it worsens outcomes. Curiously, no evidence for loss of aerobic fitness! Perhaps graded exercise tackles a hyper-reactive CNS response to exercise-related physiological signals. Note that fear of physical activity becomes conditioned when it commonly exacerbates symptoms.

Warn that exercise programmes can make things worse rather than better. Exercise should only be done as part of supervised programme, with physiotherapist – don’t just tell them to go the gym more! Start below baseline activity level.

Other

Relaxation techniques recommended by NICE.

CBT – should only be offered to manage symptoms, improve functioning and reduce distress.  Again, not a “cure”. Analysis of both CBT and graded exercise suggests that benefit comes from reducing inactivity.

Sleep hygiene important.  Include rest periods in plan but avoid day time naps, especially since sleep doesn’t usually help anyway!

Many people find exclusion diets useful, esp bowel symptoms, not recommended but involve dietician if attempted anyway.

Equipment to maintain independence can improve quality of life and should be part of overall management.

Beware boom-bust! Many patients over do it when they have a period of relative wellness. Flares and relapses are to be expected.  Trigger? New medical problem? Adjust plan as necessary.

Pain and orthostatic intolerance are big issues for some people.

Severe CFS can increase risk of pressure ulcers, DVT, vitamin D deficiency and contractures.

Prognosis

Important to be honest at time of diagnosis.  More optimistic in young people.  Most adults improve, some are able to return to usual activities but others experience long term symptoms or relapse.

PACE trial aimed for less than full restoration of health as “recovery”, future trials should use clinically relevant improvement and patient self-perception.

[bmj 2015;350:h2087]

[NICE 2021] 

2010 Scottish Good Practice statement needs update.

National Review of asthma deaths

Common, General paediatrics, Respiratory

2014 Report (adults and kids) finds that routine asthma care, management of previous and final attacks is generally poor, but particularly for children cf adults.

Almost half did not seek medical help before death. 10% deaths within 1 month of discharge from hospital for asthma. Many being treated for mild/mod asthma, but review suggested prob poorly controlled severe asthma. Widespread over reliance on reliever inhalers and underuse of preventers. Overall 39% had used more than 12 blue inhalers in the year before death. 80% of deaths did not get 12 preventer inhalers in the previous year. Nearly half had not had an asthma review in previous year.

Poor follow up of previous severe attacks (but only about 20% had been in A&E in the previous year).

Delays in primary and secondary care in about a 1/3 of final attacks.

In 93% children and young people, one or more avoidable factors relating to patients, their families and their environment: eg exposed to smoke or smoked,  allergy,
Poor recognition of risk of adverse outcome from asthma.

Recommendations

Any patient prescribed more than 12 relievers in a year should have urgent review. Follow up should be made after every ED attendance for asthma. Every hospital discharge should have hospital outpatient follow up.

Should have personal asthma action plan (PAAP).

Better education on when to use asthma medication, recognise poor control, how/when to seek emergency advice.

For parents/patients

Triple A online test!

See GP within 48hrs of discharge.

Associations with depression and anxiety. Obesity mentioned.