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Psoas abscess

General paediatrics, Surgical

Insidious, no specific signs/symptoms so often delayed diagnosis. Pain in region of lower back or hip, fever. Often 10+ days later that becomes more obvious.

Usually caused by haematogenous spread, but may be due to local suppuration.

Blood tests are not very helpful!  WCC/CRP/ESR non-specifically high.  CK is rarely raised!  Blood cultures often positive.

MRI is investigation of choice as ultrasound is only 60% sensitive.

Rx IV antibiotics for min 5/7 then complete 3-6/52 oral.  Large abscesses will require surgical drainage (open or ultrasound guided).  No reported sequelae but can be complicated by iliac thrombophlebitis followed by pulmonary emboli (akin to Lemierre’s disease).

Appendicitis

General paediatrics, Surgical

Classic history in less than 60% of cases! Retrocaecal in 15% so hip pain (psoas irritation), flank or right upper quadrant pain/symptoms. A deep appendix tip can give rectal pain especially on defaecation, plus diarrhoea, dysuria!

Under 6 with 48+hr symptoms are likely to have appendicitis.

Periumbilical pain due to T10 innervation, then localises to RIF as serosa involved. But can be suprapubic if appendix lies medially, or flank pain if lateral.

Vomiting at start unusual except retrocaecal, tends to start later.

Fever low grade or absent.

Under 5 can just present with diffuse pain and peritonitis as omentum under developed, so fails to contain. Higher risk of delayed diagnosis, perforation.

To check for psoas irritation, hyperextend hip (lie on side). For obturator, flex hip and internally rotate.

Speed bump sign good positive predictive sign!

Investigations

WCC/CRP poor sens/spec especially in first 24hrs.

USS – hyperechoic mesenteric fat, fluid collection, local dilated loop suspicious if appendix cannot be seen. 90-95% sens/spec.

Management

2020 World Society of Emergency Surgery Jerusalem guidelines.

Alvarado score or paediatric appendicitis score can be used to stratify risk, in conjunction with white cell count and CRP.

Low risk can be discharged with safety net advice. Otherwise, ultrasound recommended.

If uncomplicated and no appendicolith, medical treatment with antibiotics recommended after discussion of risks.

Eosinophilic oesophagitis

Gastro, General paediatrics

=EOE, but in the US EE.

In Danish study, incidence tripled between 2011 and 2018…

Boys predominate!  Young kids non specific (aversion, FTT, vomiting), older may have pain, food bolus impaction. 

70% atopic. Besides eosinophils histologically (>15/hpf), “cat scratch furrowing”, exudates, strictures on endoscopy (“trachealization”).

High dose omeprazole 2-3mg/kg (max 80mg) in split doses (before scope, 8/52).  Then Budesonide syrup (nebules broken open, mixed with linctus), nil orally for 30 mins after.  Some reports of adrenal insufficiency with this regimen.

Elemental diet? Usually Milk free effective, else 2-6 food elimination (80% effective – milk, egg, wheat, soya, nuts, fish).  4 weeks at a time. Re-introduce 1 food per 2/52.  Use SPT to guide, as often positive even if not aware of type 1 reactions! 

Most experience in infants is with amino acid formulas, not clear if extensively hydrolysed would be ok or not.

Generally symptoms recur at 5-6/7, if they are going to.   Not practical to repeat endoscopy after each food but symptoms can settle without microscopic remission.  Egg allergy can get worse with exclusion so shorter time or ignore?

[Diana Flynn]

Orbital cellulitis

General paediatrics, Infectious disease, Surgical

Potentially serious infection of the eye.

Chandler classification describes the potential sequence of events:

  • Preseptal (periorbital) cellulitis, in other words, anterior to the eye. Usually caused by skin organisms entering via superficial trauma
  • Orbital cellulitis – surrounding the eye
  • Subperiosteal orbital abscess – penetration into bone of orbit
  • Orbital abscess
  • Cavernous sinus thrombosis

In older children, more likely to start with sinusitis, then eroding through into orbit. Differentiating between these types is difficult without imaging.

Different organisms cf skin commensals of preseptal cellulitis eg Haemophilus, streptococci including pneumococcus, anaerobes.

Often no organism is obtained, which adds to the difficulty of giving evidence based guidance. Multiple bugs not uncommon. Hence a variety of different guidelines, generally of poor quality.

In a large US review of 220 children and young adults, 98% were investigated by CT. High rate of steroid use – previous studies have suggested better outcomes, but no obvious benefit in terms of treatment success here. Various antibiotic regimens, various durations. More treatment failures if treated for more than 3 weeks but these will be the most severe/complex cases.

Management

Jointly managed by ophthalmology, ENT and paediatrics. Ophthalmology are best at performing eye movement assessment, but it is ENT who tend to do any surgery (usually endoscopic sinus surgery).

Red flags:

  • Severe proptosis,
  • worsening visual acuity,
  • elevated intraocular pressure,
  • colour indiscrimination,
  • intracranial involvement,
  • inability to perform a reliable serial ophthalmologic examination,
  • poor response to a trial of intravenous antibiotics for 24 to 48 hours

These are indications for surgery.

The size of any subperiosteal abscess on CT is a new prognostic factor: diameter >10mm and volumes ≥500mm3 (although volume measurements not routinely reported) are thought typically to require immediate surgical intervention, with the remainder going to surgery only in the event of clinical deterioration, lack of clinical improvement after 48 hours of antibiotics, or worsening abscess on imaging.

Treatment duration – most people would agree to IV treatment until clear improvement, followed by oral antibiotics for a total of 14 days.

Hereditary haemorrhagic telangiectasia

Dermatology, General paediatrics, Genetics, Surgical

=Osler-Weber-Rendu disease. Autosomal dominant with high penetrance. 

Not a problem in early life.  Usually presents with recurrent nose bleeds.  Red spots on lips, tongue and fingertips, not so obvious in young children. But potential for GI and pulmonary haemorrhage, pulmonary/liver/brain AVMs.  Migraine common.

Iron deficiency a problem, of course!

Life expectancy normal if assessed and screened for pulmonary AVMs (check sats!?).

No restrictions on physical activity unless pulmonary AVM (scuba diving)

No coagulation disorder but antiplatelet and anticoagulant medicines should only be prescribed after weighing risks and benefits.

For refractory bleeding, bevacizumab or thalidomide (anti-angiogenic drugs) can be considered.

Screening for AVMs done from age 16 (refer neurosurgery for brain AVM screening). Annual full blood count.

Beware nasogastric interventions! (Put alert on hospital records)

European guidance at www.doi.org/10.1016/j.ejmg.2021.104370


Faye Hawkins case

Clinical governance, Ethics, General paediatrics, Generic

A consultant paediatrician who received a formal warning from the GMC for missing a case of fatal appendicitis.

Found that she failed to consider possible underlying serious cause for fever, and that lethargy and mildly elevated heart rate are “red flags”. But actually, they are not – common and poorly predictive, and not in NICE Fever in under 5s table. Patient was 5 already, anyway. Did not flag on Sepsis tool.

Also found that she failed to examine again or look for other possible red flags when she discharged Elspeth from hospital; failed to adequately advise parents on how frequently they should monitor her temperature and pain symptoms; and failed to record the advice given in the notes.

British association for general paediatricians complained that the pressure of the acute unit were not taken into account, but GMC response was that tribunal (which is independent from GMC) took this into account, although they could not agree on what standards for a “reasonably competent clinician” could be applied!

Allergen families

Allergy, General paediatrics, Immunology

Hundreds of different allergens have been identified, and can be classified by similarities in structure/genetics, usually based on the plants being related to each other in evolutionary terms.

This is useful because cross reactivity is more common, the more closely different proteins are related. Not all are allergenic however, and not all cross react.

You can also predict how heat stable these proteins are by how cross linked their structure is. Linear proteins are more easily disrupted by heat, so the allergy is likely to only be an issue with raw (or frozen from raw).

Most allergens belong to one of a small number of groups:

  • PR-10 eg Bet v 1, Ara h 8, Cor a 1, Pru p 1, Mal d 1. Heat labile, homologous. Most pollen food syndrome cases (birch pollen).
  • Profilin eg Bet v 2, Cor a 2. About 20% of pollen food syndrome cases. More common in Southern Europe – birch and oak too, but also olive tree, London plane, grasses (eg Phl p12), ragweed. More common in high grass pollen intensity areas? Citrus, tomato, banana, melon/watermelon (but different from latex-fruit syndrome). Can be associated with severe food reactions (not citrus so much but the others).
  • Prolamin – includes nonspecific lipid transfer proteins (nsLTP) which are heat stable but very cross reactive, and are found in fruit, vegetables, nuts, legumes, seeds and cereals. Best known is Pru p 3, which is a good surrogate marker for any nsLTP sensitisation, even if peach (prunus persica) isn’t a known issue. Ara h 9, Cor a 8, Jug r3, Mal d 3. Mugwort related pollen food syndrome is usually due to an LTP (Art v 4 with Api g 4 of celery and Dau c 4 of carrot, else Foe v 5 (fennel), Sin a 3/4 of mustard). Severe reactions possible.
  • Cupin – includes legumins. Heat stable. Ara h 1 and 3, lentil, cor a 9/11 (hazelnut), some soya.
  • Thaumatin – named after W African shrub! Various fruit including apple, kiwi, plus cedar pollen.
  • 2S albumin eg Ara h 6.

Glasgow lab offers only hz, peanut, peach/cherry, egg (Gal d 1), alpha galactose and bee/wasp. Dundee offers those plus milk and cashew.

Private testing available for Bos d 8 (milk casein) and soya.

Pubertal staging

Clinical, Common, Endocrinology, General paediatrics

Tanner stages – verbal descriptions but images helpful esp for self assessment.

Pubic Hair Scale (both males and females)

  • Stage 1: No hair
  • Stage 2: Downy hair
  • Stage 3: Scant terminal hair
  • Stage 4: Terminal hair that fills the entire triangle overlying the pubic region
  • Stage 5: Terminal hair that extends beyond the inguinal crease onto the thigh

Female Breast Development Scale

  • Stage 1: No glandular breast tissue palpable 
  • Stage 2: Breast bud palpable under the areola (1st pubertal sign in females)
  • Stage 3: Breast tissue palpable outside areola; no areolar development
  • Stage 4: Areola elevated above the contour of the breast, forming a “double scoop” appearance
  • Stage 5: Areolar mound recedes into single breast contour with areolar hyperpigmentation, papillae development, and nipple protrusion

For males you then have testicular volume, measured by orchidometer (between £26 and £208):

  • 4 ml (1.8cm long by formula below) is first pubertal sign
  • Adult is >20 ml (or >3 cm long)

Cadbury’s Teasers and Truffles (from Celebrations box) are 8ml, equivalent to 50th centile at age 13.

If you only have a ruler, use maximum width in millimetres and the formula: (W-1.5)3 x 0.88, where ss is double scrotal skin thickness (for Tanner stages 1, 2, and 3).

Medically unexplained symptoms

Clinical, Common, General paediatrics, Mental health, OPD, Psychology

“Persistent physical symptoms” preferred term? Chronic pain overlaps.

“Functional disorder” is used for various gastro and neurological problems, preferred by some adults, but needs explained!

Chronic fatigue syndrome and PANDAS are health disorders that appear to have a physical/scientific cause but disputed.

Health anxiety, malingering, or factitious illness, different from a psychological point of view.

Bleed the symptoms dry! [John Stone, Glasgow].

In a 1965 paper by Eliot Slater, more than half of patients diagnosed as having “hysteria” later turned out to have “organic” disease – but John Stone’s study of adult neurology referrals found very few who turned out to have an occult disease.

Louise Stone in Australia has done a lot of work in primary care. She identifies negative feelings and a lack of diagnostic language and frameworks as barriers to managing these patients effectively. The negative feelings (such as frustration, shame and helplessness), are shared between doctors and patients…

Managing your own feelings and frustrations, and finding ways of understanding and managing the therapeutic relationship important.

Let family feel validated for all concerns – at least in the first instance. Helps develop a therapeutic alliance.

Commit to the patient, which includes advocacy and support.

Family response to symptoms?

Explore beliefs, specific worries (eg cancer). May then allow broadening out to more general worries. 

Manage uncertainty – including managing the need for a disease name! Not having a predictable outcome is hard.

Harm minimisation. Shift from diagnosis to coping with ongoing symptoms.

Good to offer a tentative preamble to difficult conversations! “This is something we as doctors have to deal with every day – signs and symptoms that are very real, with a real impact on a child/family, but where physical examination and investigations do not offer any clues to what the underlying problem might be…”

Paed psychology if issues mostly seem related to child and this is a new problem; CAMHS if new problem adding to existing child/parent issues.  

Can be rewarding in the long term!

[Louise Stone, Aust Fam Physician 2013 Jul;42(7):501-2]