Tag Archives: practical


Dipstick testing is highly sensitive and picks up tiny amounts of protein (and blood) that isn’t necessarily of any concern.

A significant proportion of well people will have one or 2 pluses of protein on dip testing at any one time. More common with intercurrent illness.

Can happen with urine infection. Can happen with exercise.

Large amounts of protein loss can indicate nephrotic syndrome. PCR (or ACR) would typically be above 200.

Rarely PCR can be extremely high, but turns out not to be albumin but Tam Horsfall protein – can be ignored!

Urine collection

Traditionally midstream urine, or at least clean catch.  Hard if not toilet trained.

New urine collection method –

  • Feed first!
  • Then hold the baby under their armpits with their legs
    dangling. Another person then starts bladder stimulation – gentle
    tapping in the suprapubic area at a frequency of 100 per minute for
    30 s.
  • The third step is stimulation of the lumbar paravertebral zone in
    the lower back with a light circular massage for 30 s.
    Repeat as necessary. 86% successful within 5 minutes, mean

[ [Madrid Infanta Sofia hospital, as reported in Arch Dis Child
2013;98:27-29 doi:10.1136/archdischild-2012-301872]]


Standard ECG settings are 25mm/s and 10mm/mV.  Beware small complexes, which may indicate someone has adjusted the Y-axis to 5mm/mV.

Axis @ birth 60-180, @ 1 yr 10-100, @ >1yr 30-90 (NB prems have LESS Rt dominance!)

RVH defined as:

  • Dominant RV1 +/- Q after 1 yr,
  • Upright TV1 over 1 week and under 7 yr,
  • SV6 over 15mm if under 1yr or over 5mm if over 1 yr.

Brugada syndrome – genetic arrhythmia. Persistent or intermittent right sided ST elevation and RBBB, leading to VF and sudden death.

QTc is normally under 0.490 up to 6 months, or 0.425 if over 6 months. Calculation = QT/SQR(RR), where QT is time from beginning of Q to end of T. Easiest way to calculate it is to count small squares: QTc is then QT/5 divided by SQR(RR) (where default is 25mm/sec).

PR 80-160ms, QRS less than 75ms, RV1 less than 20-26mm (trough at 1 year), SV6 less than 10mm at birth falling to 4 mm at 10 year.

LVH – deep Q waves in V6 are a clue (upper limit is 0.54mV, ie 5 small squares). The SV1+RV6 upper limit ranges from 3.1mV (newborns) through to 5.7 (older children), staying at around 5 for most children (ie 50 small squares, my calculations).

For adults, there are many different criteria for LVH eg:

  • Sokolow + Lyon (Am Heart J, 1949;37:161)
    • S V1+ R V5 or V6 > 35 mm
  • Cornell criteria (Circulation, 1987;3: 565-72)
    • SV3 + R avl > 28 mm in men
    • SV3 + R avl > 20 mm in women

But sensitivity of ECG criteria less than 20% at specificity levels of 88% to 92%. Obesity affects chest lead voltage, for example.  Better in patients with a specific cardiac disease. An elevated LVM (left ventricular mass) index is taken as the reference for LVH. In kids the SV3R + RV7 Sokolow-Lyon parameter performs best, but who does V7 routinely? (and still only 25.3% sensitivity).

So you can say voltage criteria for LVH met, but can’t say diagnostic of LVH.  More likely when other features such as left axis deviation, ST and T wave changes.  When clinical evidence is also taken into account, the sensitivity improves considerably (but still under 50%).

[Normal ranges – European Heart Journal (2001) 22, 702–711]

LVM (as estimated from echocardiographic measurements) is itself vulnerable to measurement error and may oversimplify the geometry of the left ventricle. Alternatively, a combination of increased LVM and clinical evidence of volume or pressure overload of the left ventricle may be a better reference standard.

Normal vitals

Respiratory rate = 40 under 1 yr, 30 between 2 – 5, and 20 over 12

Systolic Blood pressure = 70 – 90 under 1 year, 80-100 between 2 and 5, 90 – 110 between 5 and 12, and 100-120 over 12. [Arch Dis Child. 2007 Apr;92(4):298-303.]

In other words, range of 20 @ every age, increasing by 10 in each group, with a Max of 100 @ 2-5, and a minimum of 100 @ 12+.

Insensible losses

300 ml/m2/d – else:

  • > 1y –  12 ml/kg/24 h
  • term neonate – 15 ml/kg/d
  • preterm – 24 ml/kg/d

Increase if in hot climate or fever by around 50%.


NICE (CG57, 2007) diagnostic criteria:  itchy skin plus 3+ :

  • visible flexural dermatitis (or visible dermatitis on the cheeks and/or extensor areas in children <18/12) – can look like dirt where darkened esp neck
  • personal history of flexural dermatitis (or dermatitis on the cheeks and/or extensor areas in children  <18/12)
  • personal history of dry skin (xerosis) in the last 12 months
  • personal history of asthma or allergic rhinitis (or history of atopic disease in a first-degree relative of children aged <4yr)
  • onset of signs and symptoms under the age of 2 years (do not use this criterion in children under 4 years).

On examination, may also see lichenification (increased skin markings due to chronic rubbing), excoriations caused by scratching, and hyperlinear palms (look at thenar eminence).

Risk factors

Eczema (or atopic dermatitis, same thing) associated with parental allergies (OR 1.94), parent-reported infection after birth (OR 1.45), parent-reported jaundice (OR 1.27). Being a migrant (OR 0.63) and keeping a dog (OR 0.78) are protective. Prenatal probiotics did not reduce risk (Lactobacillus rhamnosus GG, LGG).  Respiratory viral infections in pregnancy associated with wheezing illness in infants (mothers with asthma) and eczema.  [Australia, Ped All Imm 2014:25:151].  Febrile and gynae infections in pregnancy associated with eczema in child (Italy, Ped All Imm 2014:25:159].  Children of Japanese mothers with higher anxiety scores during pregnancy were more likely to be affected by eczema!


Many roads lead to Rome!  Can be seen as combination of impaired innate and distorted adaptive immunity, interacting in framework of cutaneous immune system with suboptimal barrier function.  Epidermal barrier can be genetically disturbed, but gene expression (eg of filaggrin) is also influenced by microenvironment eg Th2 cells.  Some genetic structural abnormalities can be seen to induce nonspecific inflammatory reaction (eg SPINK5 defects).  And almost certainly, epigenetic regulation will affect gene expression in both keratinocytes and immune cells.

Facilitated antigen presentation mediated by IgE bound to high affinity IgE receptor FcEpsilonRI, on dendritic cells, is an important part of it.  Vitamin D plays a key roll, stimulates Toll like receptors, increasing pro-inflammatory cytokines but studies equivocal whether low (or indeed high) levels increase risk.

Eczema can exist without IgE against aeroallergens and food allergens, so is primarily a non IgE mediated disease, although both IgE and non-IgE hypersensitivity can co-exist, particularly in babies.

Still not understood how eczema and Staph aureus interact.  Colonization appears to amplify local inflammatory reaction, but also increases IgE against a large spectrum of other things (possibly including self proteins).  It is as if there is something specifically different about how immune cells handle Staph.  Toll like receptors esp TLR-2 recognize Staph aureus cell wall. Overgrowth of staph during flares is associated (preceded?) by loss of diversity of skin microbiome.

Unmasking of the HSV entry receptor Nectin-1 in adherence junctions, among other things, contribute to eczema herpeticum.  See Flares, below.

Atopy patch test (using intact protein allergens) can prove type IV reactions. Correlates with oral food challenge. Hyper IgE syndromes are important differential for AD, STAT3 mutations, skin (and other) abscesses, recurrent pneumonia (and pneumatocoele), connective tissue and skeletal abnormalities, mucocutaneous candidiasis. DOCK8 type Hyper IgE syndrome show sensitization predominantly against food allergens, which is a clue (STAT3 and AD show predominantly sensitization to aeroallergens).

Normal looking  skin is not immunobiologically normal!  Invisible inflammation, hence still needs treatment. Pimecrolimus and betamethasone both normalize expression of filaggrin, the later is perhaps a better anti-inflammatory but steroids reduce expression of enzymes for lipid and protein synthesis, so may impair skin barrier restoration.


Stress, humidity, extremes of temperature can cause flares of atopic eczema. But what causes a flare in some can apparently help in others! Any factors causing flares should be avoided where possible.

UVB causes sunburn.  UVA (longer wavelength) more relevant to photosensitivity reactions.  Both cause long term skin damage.  EU commission recommends UVA protection making up at least 1/3 of total suncream SPF.  A few available on prescription for photodermatosis (incl vitiligo) but not for eczema per se.  Lipscreen (Uvistat) available for chronic/rec HSV labialis.  Sunsense is lotion.

Avoid wool in contact with skin.  No evidence that bio detergent or fabric softener a major problem.  Avoiding excessive product and not overloading machine (so disperses fully) prob more important.


See eczema management.

Parental support

National eczema society, British Association of Dermatologists, Eczema Outreach Scotland.