Category Archives: General paediatrics

Laryngomalacia

Intermittent squeaky inspiratory noise from collapsing larynx during respiration. Usually from birth.

Often worse when lying on back, or with colds, or with reflux (vomits).  Worse if hypognathia eg Pierre-Robin sequence.

Clinical diagnosis usually. Settles in first few months of life.

Will need intervention if significantly increased work of breathing, cyanosis or apnoeas, or growth failure.

Juvenile xanthogranuloma

Well circumscribed, raised yellow/brown firm papule or nodule, typically solitary. Can be congenital but otherwise typically very young boys, head and neck area, asymptomatic.

Can affect the iris – presents with a red eye…

Can ulcerate, otherwise they tend to atrophy and disappear after 3-6 years.

Seen in 10% of Neurofibromatosis type 1.

Can rarely be multiple and internal (liver, bone marrow etc). Screening of asymptomatic cases probably only justified if multiple.

Differential – mastocytoma, Langerhans histiocytosis, molluscum.

Variceal bleeding

Due to portal hypertension from chronic liver disease.

Potential for large losses – may need local major haemorrhage protocol (FFP, platelets etc) – typically if blood loss >150mls/min, or else 20% blood volume loss in <1 hour (normal blood volume is 80ml/kg).

In adults, they try not to transfuse above 80 – thought that excessive transfusion may increase bleeding.

Terlipressin preferred to octreotide – from age 12. IV injection every 4 hours. No evidence for Tranexamic acid!

NG tube may cause more trauma…

In adults, Glasgow-Blatchford score used. Authors are Oliver and Mary Blatchford (couple?) – he was actually in Paisley at the time…

Social determinants of health

David Gordon of International Poverty Research centre at Bristol has parody of Chief Medical Officer’s top ten tips for health – Number 1 is “don’t be poor”.

1Don’t smoke. If you can, stop. If you can’t, cut down.Don’t be poor. If you are poor, try not to be poor for too long.
2Follow a balanced diet with plenty of fruit and vegetables.Don’t live in a deprived area. If you do, move.
3Keep physically activeDon’t be disabled or have a disabled child.
4Manage stress by, for example, talking things through and making time to relax.Don’t work in a stressful low-paid manual job.
5If you drink alcohol, do so in moderation.Don’t live in damp, low quality housing or be homeless.
6Cover up in the sun, and protect children from sunburn.Be able to afford to pay for social activities and annual holidays.
7Practise safer sex.Don’t be a lone parent.
8Take up cancer screening opportunities.Claim all benefits to which you are entitled.
9Be safe on the roads: follow the Highway Code.Be able to afford to own a car.
10Learn the First Aid ABC: airways, breathing and circulation.Use education as an opportunity to improve your socio-economic position.

Pyrexia of Unknown Origin

A technical term, not just a fever without obvious source! Essentially presence of confirmed fever for 8 days or more in a child in whom a careful thorough history and physical examination, and preliminary laboratory data fail to reveal a probable cause.

Long list of possible causes, long lists of possible tests – do thorough history and repeated examinations, then follow the clues!

In kids, infection is the commonest cause. But can be connective tissue disorder, or malignancy.

Beware factitious fever – admission sensible.

If possible, stop all drugs. Antipyretics may obscure the pattern of fever, and can occasionally be its cause (drug fever is one cause).

Unless the child is critically ill, try not to give antibiotics. If the diagnosis remains obscure, go back and take the history again, examine the child (fully) again, send the specimens again!

Special points in history/examination

  • Travel – malaria can present 6-12 months later. Typhoid.
  • Ethnicity – tuberculosis
  • Outdoor activities – rats/ticks as vectors of infectious diseases
  • Animal contact – cows/sheep (brucellosis), cats (cat scratch)
  • Mouth ulcers (IBD, Behcets, PFAPA)
  • Periodicity – see Periodic fever
  • Sinus tenderness, nasal congestion (sinusitis)
  • Bone/spine tenderness – discitis, vertebral osteomyelitis

Tests

  • 3 sets of blood cultures, different sites, different times (at least a few hours apart), off antibiotics – standard for endocarditis
  • ASOT
  • EBV, CMV
  • LDH, CK
  • ANA/RF
  • Urine/stool culture
  • Swab everything!

Stroke in children

Rare but happens.

Differential:

Can be due to arterial or venous occlusion.  50:50 in kids cf adults (80% infarct). Haemorrhagic can be due to rupture into infarct.

Presents with focal signs, headache, seizures most commonly. Else dysphasia, vomiting!, confusion. Fever! Acute signs often lacking or fluctuant cf history!  FAST criteria only 78% sensitive. 

NIH stroke severity scale has paeds version. 

Risk factors

Black/Asian

Cardiac (esp surgery, right to left shunt)

Sickle cell – esp anaemia, acute chest syndrome, HbS or HbS/Beta thal

Thrombophilia

Liver/kidney disease (secondary prothrombotic tendency)

VZV within 1yr, enteroviruses, HIV.

Vasculitis – Moya Moya (peaks at 5-9yr else adulthood), SLE, other

Cocaine, glue.

Marfans, homocysteinuria, Fabry’s disease, Neurofibromatosis

Cancer, radiotherapy

Hypoglycaemia. 

Management

High flow O2, 10ml/kg saline 

Imaging within 1hr. 

BP – avoid high and low? Cf adults

Monitor for RICP

Treat with aspirin.

Tests

  • CTA/MRA at time of CT/MRI
  • Echo
  • (Transcranial doppler in sickle cell- via temporal bony window)
  • Hbopathy screen
  • Cholesterol
  • Lupus anticoagulant, Anti cardiolipin ab (ACLA), consider beta 2GP1
  • Homocysteine
  • Alpha galactosidase
  • Lipoprotein A – marker for CVS disease, genetic. 
[RCPCH guideline May 2017]

Allergy testing

Gold standard is double blind challenge, but who has time for that?

Mostly based on history – combination of characteristic features without other, more likely, explanation.

NICE has list of type 1 vs non type 1 allergy signs/symptoms – some overlap, eg vomiting, diarrhoea, itch.

EAACI guidance 2023 says where type 1 allergy suspected (signs/symptoms but also timing and consistency of reaction):

  • Do skin prick testing and/or specific IgE testing as first line
  • For peanut, hazelnut or cashew, if in doubt do component tests Ara h 2, Cor a 14, Ana o 3 respectively as well (if available) – otherwise do skin prick or IgE if not done already.
  • Where peanut or sesame allergy still in doubt, do basophil activation test (BAT – if available)
  • “Reassessment of food allergic children, at regular intervals, depending on age, food and patient’s history, is suggested for possible development of spontaneous tolerance”

Ara h 2 (cut off 0.44) has 82% sensitivity and 92% specificity cf 84 and 86% for SPT of 4mm. Cor a 14 (cut off 0.64%) has 73 and 95%, Ana o 3 (cut off 0.4) 96 and 94%.

Common hidden allergens (!): celery, mustard, cochineal, lupin, soy, fenugreek, other legumes such as pea/bean/lentil protein, insects/mealworm, pink peppercorns).

Bartter’s syndrome

Abnormal renal excretion, leading to low potassium.

Presents in early childhood with failure to thrive. Could also be constipation, muscle cramps and weakness (potassium needed for membrane potential, so these are all neuromuscular) and non-specific dizziness and fatigue.

Characteristic hypokalemic, hypochloremic metabolic alkalosis. High plasma renin activity and high aldosterone concentration seen.

Gitelman syndrome is similar, less severe (distal tubule, rather than ascending limb of loop of Henle) – less failure to thrive, in fact often asymptomatic detected incidentally. Might present with nocturia/polyuria.

Urinary calcium excretion distinguishes the two syndromes. Bartter’s waste calcium (more severe, after all), Gitelman retain.

Treatment is with supplementation.

Decompensation can be precipitated by diarrhoea or vomiting. Acute treatment can include potassium-sparing diuretics (spironolactone), cyclo-oxygenase inhibitors and renin-angiotensin blockers.

Pseudo-Bartter’s is due to CF.

Hypokalaemia

Could be reduced intake but usually excessive losses –

RenalNon-renal
Renal tubular acidosis (type 1 or 2)Vomiting eg pyloric stenosis
Bartters or Gitelmans syndromeDiarrhoea
DiureticsLaxative overuse
Hyperaldosteronism (CAH, tumour)Thyrotoxicosis
Salbutamol
Familial periodic paralysis
Pseudo-Bartter’s
Trauma
Diabetic ketoacidosis

Symptoms depend on severity and how rapidly decrease has happened. Chronic low levels are better tolerated. Since potassium important for membrane potentials, effects are mostly neuromuscular.

  • Cramps, weakness, paralysis
  • Ileus
  • Metabolic acidosis (although underlying cause often produces alkalosis)
  • Arrhythmia, heart failure
  • Rhabdomyolysis

ECG classically shows U waves, T wave flattening, and ST-segment changes. Can be tall wide P waves, can look like long QT if T and U waves merge.

Do urine and blood electrolytes to look at fractional excretion.

[Endocrine connections 2018][Current Treatment Options in Peds 2022]