Asthma and Obesity

Obesity can mimic asthma, it affects respiratory symptoms and lung mechanics, but it can also overlap of course. Asthma is more often diagnosed in obese (misdiagnosed?). High birth weight is associated. , as is maternal obesity (and gestational weight gain) in pregnancy. Each BMI increase of 1kg/m2 increases risk by 2-3%!

Obesity is one of the factors associated with fatal asthma attacks (but note socioeconomic confounding).

Weight reduction leads to improved lung function, health status, symptoms and morbidity in adults. Not yet proven in adolescents.

Slightly increased risk of acute asthma attacks in obese adults and school age children.

Osteogenesis imperfecta

Recurrent fractures, often with minimal trauma, family history. Joint and bone pain can be an issue even without fractures.

No single test for osteogenesis imperfecta.  Clues might be deformities, short stature, hypermobility and poor dentition.

Type 1 is most mild, no deformities. Type 2 lethal in early life, antenatal scan may show chest wall abnormality and respiratory failure often at birth.

Type 3 is severe, with fractures in the womb or during birth. Short stature, deformities marked.

Type 4 variable, may only be diagnosed later in life. Type 5 associated with excessive callus formation.

Bisphosphonate infusions are used for the most severely affected. Otherwise, management revolves around:

  • Fracture and pain management
  • Aids eg wheelchairs
  • Physiotherapy, esp if immobile due to fractures

Epstein Barr virus

One of the Herpes virus family, and like other herpesviruses (herpes, varicella) becomes latent in the body after infection, in the case of EBV in B-lymphocytes. Immune system has developed specific strategies over the course of human evolution to control it – hence specific immunodeficiencies such as Duncan’s syndrome where EBV appears to be the only infection that becomes problematic (even catastrophic).

Associated with a number of tumours, including non-Hodgkin’s lymphoma, Burkitt Lymphoma (especially in Africa), nasopharyngeal carcinoma.

In most children, a mild febrile illness, with lymphadenopathy (“glandular fever” or infectious mononucleosis), sore throat (can be severe). Failure to improve with antibiotics is a clue! Peak age for severe presentations is teenagers – “kissing disease” (sexually transmitted!? Edinburgh students study found lower rates if routine barrier methods used). Prolonged incubation period of 30-50 days!

Classically rash triggered by amoxicillin (which is why amoxicillin isn’t recommended for sore throats, but rash can be seen with penicillin too) – maculopapular, sometimes petechial and/or urticarial, which is rather more suggestive.

On examination, hepatosplenomegaly can be seen.

Blood film characteristically shows atypical lymphocytosis. Monospot test (for heterophile antibodies) 70-90% sensitive so has false negatives as well as false positives so may need to proceed to PCR if important to know.

Mild hepatitis and cholestasis pretty common.

Rarer features are dacrocystitis, pneumonia, myocarditis, low platelets and neutrophils, interstitial nephritis, encephalitis. Haemophagocytic syndrome. 20x higher risk of Guillain Barre syndrome after EBV

Management

Supportive.

Splenic rupture after EBV has been reported but is very rare. Advice usually given to avoid contact sports. In ultrasound studies, peak spleen size is typically noted within the first 2 weeks of illness, but may extend to 3.5 weeks. The majority of spleen injuries occur within the first 21 days of illness and are exceedingly rare at >28 days, so one month avoidance probably sufficient.

A minority develop chronic fatigue type symptoms.

[Sports health 2014]

Anaemia

Like many things, low red cell count can be problem of production, loss or destruction.

So causes include:

  • Bone marrow failure or infiltration (leukaemia, Fanconi’s, Blackfan Diamond, erythrovirus/parvovirus)
  • Nose bleeds, gastrointestinal losses eg Meckel’s, gastritis, heavy periods
  • Haemolysis eg G6PD deficiency, hypersplenism, autoimmune
  • Iron, folate or B12 deficiency

In children, one of the most common causes is excessive milk consumption, which appears to lead to a low level colitis. Pica is often the presenting problem.

Investigations

  • Blood film – Howell Jolly bodies if hypersplenism. Leucoerythroblastic reaction (with immature red cells, as well as immature white cells) can be due to malignancy but can also be due to infection and haemolysis. Spherocytes or other abnormal forms may suggest a hereditary haemolytic condition. Sickle cells in sickle cell disease.
  • Low MCV suggests lack of iron, but may also be due to thalassaemia.
  • Reticulocyte count – indicates on going red cell production, may be high if recovering from low production
  • White cell count and platelets – if low too, suggests bone marrow failure but parvovirus can knock off all cell lines too.
  • Coagulation – deranged coagulation with low platelets suggests disseminated intravascular coagulation (DIC), usually due to sepsis, but can also reflect haemophagocytosis syndrome (due to sepsis or rheumatological disease)
  • Renal function – haemolytic uraemic syndrome (usually with diarrhoea and bloody stools, but not always)

Iron is found in red meat, pulses, green leafy vegetables, wholemeal bread, nuts, dried fruit, fortified breakfast cereals.

Polycythaemia

Polycythemia vera very rare in kids but described from age 7 months! More typically age 5-14yrs. 

Haemoglobin range of 15.5 to over 25, with haematocrits from 41-80%.  Yet high values often seen in asymptomatic teenagers.

Symptoms are headaches, pruritus, dizziness/syncope.  Serious complications not uncommon, often part of presentation eg Budd-Chiari syndrome, stroke, haemorrhage.  Leukocytosis appears to be associated with higher risk of complications.   Thrombocytosis often seen. 

Molecular studies available. [Ann Hem 2009 PMID PMID: 19468728]

Hypertension

In children under 10, high BP is usually secondary to an underlying disease or condition. Primary hypertension increasingly recognised in older, obese children.

Do repeated measurements, ideally automated home BP monitoring, before diagnosing hypertension. Check manually as well as with automated device. Beware “white coat effect”, even if not clearly anxious.

Use appropriate cuff size – cuff should cover at least 75% of the upper arm from the acromion to the olecranon (should be sufficient space at the antecubital fossa to apply stethoscope!) .  An inappropriately small cuff will overestimate BP.

Long list of causes, so follow the clues.

Family history important, of course.

Examination

So needs thorough history and examination, including:

  • Fundi
  • Bruits, radiofemoral delay
  • Neck for goitre

Complications

Consider then end organ effects –

  • Proteinuria, high creatinine
  • Retinopathy
  • Left ventricular hypertrophy, cardiac failure
  • Abnormal tone and reflexes, cranial nerve deficits if severe

Management

Depends on how high, whether other risk factors (diabetes, chronic kidney disease), symptoms and evidence of end organ damage.

Initially low salt diet, weight loss (if obese).  Remember other morbidities related to obesity.

Acute hypertension might need frusomide and/or nifedipine.

Long term treatment is only going to be started if no improvement with lifestyle measures. Target BP depends on risk factors, as above.

[2016 European Society for Hypertension guidelines]

Meningococcal disease

Gram negative diplococci, causing meningitis and septicaemia. Sometimes bone/joint infection. Neisseria (not meningitidis) responsible for ophthalmia neonatorum.

Main serogroups:

  • A – responsible for epidemics of meningitis across “Meningitis belt” of Sub-Saharan Africa, until Men A monovalent vaccine introduced in 2010 (still epidemics, but due to other serotypes). Hajj also triggers outbreaks.
  • B – 4 component vaccine introduced in 2015 to deal with B being the most common cause of invasive meningococcal disease since introduction of MenC vaccine. Based on vaccine developed for New Zealand epidemic.
  • C – used to be most common cause of invasive meningococcal disease in UK until vaccine introduced. So successful that early dose was dropped from routine schedule, although later resurgence in older children and young people, so teenage booster and university catch up programme introduced.

Clinically, notorious for rapidly evolving, often fatal septicaemia with non blanching rash and limb ischaemia. Curiously, meningococcal meningitis, on the other hand, is the most benign of the various causes of bacterial meningitis. Can be mixed picture, ranging from a few petechial spots only with an otherwise typical meningitis presentation, or else meningococcal septicaemia with neck stiffness, where presence of meningitis is actually a good prognostic sign.

Exquisitely sensitive to antibiotics. Meningitis epidemics in Africa treated with single IM dose ceftriaxone!!! Nasal carriage is the reason for spread, so prophylaxis for close contacts important.

History of Medical Failures

Where to start!? Leaches, blood letting, pretty much everything doctors did in the pre-modern period…

Thalidomide and birth defects, of course. But unforeseen.

X-rays for pregnancy monitoring. Took years before people paid attention to the alarms. X-rays were also used for tinea capitis – not just brain tumours, strokes and ischaemic heart disease about 30% higher too.

Ribavirin (via SPAG machines) for RSV. Not harmful, just useless and expensive.

Iron supplements for preterm babies – increased sepsis.

Allergy and mental health

Evidence that having a peanut allergy has worse quality of life for a family than having diabetes… Mostly due to fear of unexpected severe reaction, and restrictions on social activities particularly eating out, parties and holidays.

Allergic patients can feel embarrassed or even ridiculed for declaring their allergy. Allergy is often mocked in the media (Cobra Kai, the Box Trolls, Peter Rabbit).

School and nursery are a particular area of concern, whether the right foods will be served, whether teachers or other children might bring allergens into school (food is sometimes used in classes, for example making bird seed balls), whether reactions will be managed appropriately, school trips. Children have died in school (Nasar Ahmed, Mohammed Ismaeel Ashraf).

Mums tend to be more concerned by limitations in the child’s own social life, dads seem to care more about limitations in the whole family’s social life. [Stensgaard, Clin Exp Allergy 2017]. Mums are the ones most studied. There probably are significant differences between mums and dads. In some studies, parents overrate their child’s quality of life, but in others (particularly with teenagers) parents can be seen as over anxious. Teenagers tend to take on the perspective of the parent of the same sex.

How bad previous reactions have been, interestingly, does not in itself contribute significantly to quality of life – in some cases, not having ever had a reaction can make families more anxious, because they don’t know what to expect! In one study, having multiple allergies and having an adrenaline pen was associated with worse quality of life. [Protudger, Clin Transl Allergy 2016]

Parents can feel guilty if their child has a reaction, a failure of their duty to protect. Mums can feel guilty about having “caused” their child’s allergy, either through their own medical history or what they ate or didn’t eat in pregnancy (even there is no good evidence for this being a factor).

Better quality of life is seen in allergic families with greater self efficacy for food allergy management, and lower perceived likelihood of a severe reaction [Knibb, Pediatric Allergy & Immunology. 27(5):459-464, August 2016].

APPEAL-1 study

8 European countries, questionnaire study of adults and children with peanut allergy

Only a minority remembered getting any training in future emergencies or use of medication, after their initial reaction. There was a low rate of satisfaction with AAI training! 

43% reported bullying, and a third of these described it as severe. 

65% confident in ability to recognize a reaction, but only 45% confident about knowing when to use an AAI and 59% how.  62% say the carry AAI all the time.

25-30% said it was not easy (or rarely easy) to talk to friends or family about their allergy, although most felt confident talking to new people about their allergy. Friends and family were generally seen as “believing there is too much concern over allergy” even though overall they were seen as having a good awareness and understanding of allergy (cf other people, where this was seen as the opposite).

Dutch respondents had lowest rates of uncertainty and stress around activities, and for feeling anxious.  At same time, they had the highest rates of confidence around knowing when and how to use AAI.  France had highest rate of being made to feel different in a negative way, and feelings of isolation.

NB – likely to be the most affected families who participated.

[Dunngalvin, Allergy 2020]