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Sickle cell disease

General paediatrics, Genetics, Haem/Oncology

Autosomal recessive genetic disorder caused by a single nucleotide mutation of the haemoglobin ß-unit, from glutamic acid to valine. The resulting mutant haemoglobin S (HbS) is prone to distortion in cooler or hypoxic conditions, turning into a sickle shape. This damages the erythrocyte causing haemolysis.

The gene is more common among Africans and is occasionally seen in races from the Middle East and South Asia. Its existence is due to protection from malaria seen in sickle cell trait (the heterozygote form), due to shortened red cell lifespan.

You can of course get combinations of sickle cell with other genetic haemoglobin disorders.

Triggers for sickling include cold environment, acidosis, hypoxia and hyperviscosity eg dehydration. Blood flow in capillaries is impaired by the damaged red cells, which leads to a vicious cycle of increased tissue acidosis and hypoxia. Infarction may occur.

Diagnosis

Can be diagnosed even in newborns. Sickle test followed by haemoglobin electrophoresis.

Screening programmes exist in some countries, so that prophylactic oral penicillin can get started early, preventing sepsis.

Clinical

Presents in infancy or early childhood, often with episodes of painful, swollen hands or feet (hand-foot syndrome). The neonate with its high proportion of Haemoglobin F does not get symptoms until there is enough abnormal haemoglobin A produced for red cells to start to sickle.

Acute Crisis

  • Pain
  • Chest syndrome
  • Aplastic crisis
  • Gut crisis
  • Stroke
  • Priapism
  • Sepsis (may precipitate crisis or complicate it)

Pain

Pain can be widespread, but particularly involves bones, the spine, the chest.

Acute Chest syndrome

Can mimic pneumonia, with unilateral or bilateral signs of consolidation, pleuritic pain, and hypoxia. Pain is in chest wall, thoracic spine and upper abdomen. Leads to hypoventilation, causing vicious cycle of atelectasis and subsequently worse sickling. High mortality, so low threshold of suspicion.

  • Hypoxia should be managed aggressively, with respiratory support if necessary.
  • Antibiotics in infection contributing.
  • Avoid diuretics – signs may suggest pulmonary oedema, but likely to exacerbate hyperviscosity.

Aplastic Crisis

Usually secondary to Erythrovirus B19 (formerly known as parvovirus B19) infection, which can trigger transient bone marrow arrest. So sudden drop in haemoglobin with an absence of reticulocytes. Classic “slapped cheek” appearance may never become apparent. Can affect multiple members of a family simultaneously. Differential is spleen sequestration.

Abdominal crisis

Manifest as anorexia, abdominal pain, distension. Usually not diarrhoea or vomiting. Usually not rebound. Bowel sounds usually quiet.

  • Girdle or Mesenteric syndrome – ileus with vomiting. Associated with liver enlargement and bilateral basal consolidation.
  • Differential includes appendicitis, biliary colic or cholecystitis, ischaemic colitis.

Stroke

Typically affects middle cerebral artery territory but may affect any region of the brain; may be transient or permanent. Seizures may occur. Predictive factors are:

  • Previous TIA/stroke
  • Chest syndrome
  • Hypertension
  • Family history of SCD related stroke
  • Low HbF and/or low total haemoglobin
  • Doppler velocities >200cm/sec in children

Differential is meningitis, subarachnoid haemorrhage (associated with multiple intracranial aneurysms).

Sequestration syndromes

  • Splenic sequestration – Seen in infants and young children. Precipitated by fever or dehydration. Symptoms are:
    • Abdominal pain/distension
    • Rapidly expanding spleen (may or may not be painful)
    • Shock, pallor due to drop in haemoglobin (but high reticulocytes cf aplastic crisis)
  • Management is by fluid resuscitation with blood (type specific/O negative if necessary).
  • Hepatic sequestration: similar to splenic, although less shock, and possibly jaundice along with enlarging liver.
  • Priapism: =sustained painful erection. Potentially leads to peripheral gangrene, else cavernosal fibrosis and hence impotence. A urological emergency. Management:
    1. Warm bath, hydration, analgesia
    2. Catheterize if unable to urinate
    3. Sedation eg diazepam
    4. Aspiration + irrigation – ideally within 4-6hrs of onset. Else shunt.
    5. Top-up transfusion may be considered if unstable with other sickle related problems (aiming for Hb 10-12g/dl).
  • Sepsis. Children are relatively immunocompromised due to functional hyposplenism from recurrent spleen infarction. This increases susceptibility to capsulated organisms eg pneumococcus, salmonella, haemophilus.
    • Yersinia is a particular risk in children on desferrioxamine. Causes diarrhoea.

Management

  • Analgesia, aiming to get rapid symptom control with IV bolus doses of opiates eg morphine, diamorphine ideally within 30 minutes of admission, followed by infusion or regular oral doses. Paracetamol and non-steroidal anti-inflammatories may be synnergistic.
  • Oxygen, esp for acute chest syndrome. Debatable if effective for other problems.
  • Hydration, even hyperhydration eg 150% normal daily requirements, IV if necessary. Impairment of renal concentrating power may contribute to dehydration.
  • Warm environment
  • Identification and treatment of infection. Give treatment doses of penicillin (else erythromycin) even if no specific agent identified.
    • Treat with IV antibiotics if severe symptoms/signs
    • Add macrolide eg clarithromycin if chest symptoms
    • Treat empirically for Yersinia with ciprofloxacin if diarrhoea on desferrioxamine.
  • Folic acid (should be on already)

Transfusion

Although anaemia is common in SCD, repeated transfusions lead to the possible complications of:

  • Allo-immunization
  • Iron overload

Hence top up transfusion is only used for acute symptomatic anaemia eg cardiac failure, severe sequestration or pre-operatively. Do not transfuse above Hb 11g/dl. Regular transfusions have a prophylactic role – see on-going treatment below.

Hyperhaemolysis is a life threatening complication of red cell transfusion in sickle cell disease. Can be acute (within 7 days of transfusion) or delayed. Affects not just transfused but autologous cells so Hb can drop below previous level. Fever, haemogobinuria as usual; negative DAT, reticulocytopenia seen (cf parvo). Cover subsequent transfusion with IVIG and steroids; use erythropoietin to maintain. For elective surgery, prophylactic postop CPAP has been used without transfusion. Risk factors poorly defined.

Exchange transfusion

Undertaken to rapidly reduce the percentage of sickle cells in the circulation where life-threatening eg severe chest syndrome, stroke, multi-organ failure. The aim is to reduce %HbS to <20%. Complications are common eg fluid overload, transfusion reaction.

Other Treatments

  1. Pneumococcal prophylaxis is essential for all children. Polysaccharide vaccine should be offered with repeat doses as per Green book.
  2. Folic acid
  3. Hepatitis B immunization
  4. Splenectomy for recurrent splenic sequestration.

On-going treatment

Consider for:

  • Recurrent or stuttering priapism (etilefrine orally is another option here)
  • Stroke/TIA
  • Chronic organ damage eg renal failure
  • Failure to thrive
  • Intractable crises

Options:

  • Regular transfusions. The aim is to keep %HbS <25%. Compared with exchange transfusion, regular transfusions are just as good at reducing complications, are less challenging in terms of vascular access, involve less donor exposure, but cause more iron accumulation.
  • Hydroxyurea. Reduces frequency of crises and transfusion requirements, improves growth. Trials ongoing. Long term risks need to be clarified (toxicity, mutagenicity, teratogenicity).
  • Bone marrow transplant

Iron overload and chelation therapy

Iron overload can be monitored by means of Ferritin levels. Chelation therapy should commence at ferritin levels of 1000mcg/l, with desferrioxamine (desferal) the chelator of choice. Treatment should include vitamin C. Ophthalmological, audiological and cardiological review is necessary.

Eczema management

Dermatology, General paediatrics

Scoring systems available – eg Eczema Area and Severity Index (EASI – clinician rated), Patient Oriented Eczema Measure (POEM – lived experience). Clearly needs to be both – visible eczema may bother some more than invisible but itchy lesions.

Remember house temperature, clothing.  14-16 degrees in bedrooms, max 18 in house. 

Stepwise approach, with early recognition of eczema flares. Use lots of emollient frequently, even if skin clear. Management can then be stepped up or down, according to the severity of symptoms, with the addition of the other treatments as listed below.

Mild atopic eczemaModerate atopic eczemaSevere atopic eczema
EmollientsEmollientsEmollients
Mild potency topical corticosteroids Moderate potency topical corticosteroids Potent topical corticosteroids
 Topical calcineurin inhibitorsTopical calcineurin inhibitors
 BandagesBandages
  Phototherapy
  Systemic therapy

Emollients

Mostly underused.  Should always be used, even when the skin is clear (see immunology of eczema).  250-500g per week for most (10g per day for a baby)! 1FTU (finger tip unit) covers 2x area of hand with fingers closed.   Apply in downwards motion, in direction of hair rather than rubbing (which might increase irritation).  Allow to soak in as much as possible.

Should be easily available to use at nursery, pre-school or school.  

Aqueous cream not recommended as “leave on” (ok as soap substitute) says NICE – higher risk of skin reactions. Not much evidence to say one better than another, so whichever suits family best, be it a combination of products or one product for all purposes!  Only risk is is flammability, and slipping when washing!

Offer a choice of unperfumed emollients to use every day for moisturising, washing and bathing.  Offer an alternative if a particular emollient causes irritation. Spray on emollients are also available, if skin is really sore.  Ideally allow several minutes between different creams where practical.  Pump dispensers preferred (and don’t share!) as bacterial contamination possible, which may make skin worse. Folliculitis another risk with emollients.  

Quickest is steroid first, but ideal is emollient first, steroid 20 mins later!  But family preference.

Ointments are greasier, so messy, and leaves you looking shiny.  Tend to only come in tubs, not pump dispensers. Relatively free from additives so perhaps less likely to lead to irritation, but can occlude, leading to heat rash.  Good for fissured skin.  50:50 white/soft paraffin good for lichenification. Emulsifying ointment is difficult to use. Cream applies better to moist, weeping areas.  Lotion good for scalp (most soluble). Epaderm and Doublebase are cream/ointment mixes. Sprays involve less rubbing, which some children appreciate.

Adding urea can be good for dry, scaly or lichenified skin eg Balneum Plus, Hydromol intensive, Eucerin Urea Repair.

Stinging may just be under treated eczema, which will only improve with regular topical steroids. Some people find paraffin containing products makes things worse, but not many alternatives – bee’s wax? Doublebase cream, diprobase ointment perhaps less likely to sensitise?

[BMJ 2019]

Combined antibacterial products available, good for flexures eg Dermol 500 lotion, Dermol 600 bath emollient, Fucidin H (hydrocortisone) and Daktacort (hydrocortisone with miconazole) are mild potency, Trimovate (clobetasone with nystatin and oxytetracycline) are moderate potency, Fucibet (betamethasone), Synalar C and Betnovate C (both clioquinol) are potent.

Bathing

Baths should be short (max 20 minutes), not too hot, towel dry by patting not rubbing. Oats in muslin bag or sock can be squeezed under tap and as sponge. Use a bath additive eg Oilatum NOT bubble bath (beware how slippery the bath gets) and a soap substitute – or just apply your usual emollient before hand, rinse off, and re-apply. Cleans just as well as soap!

For scalp eczema, if inflamed then use your usual topical steroid, applied directly to scalp rather than hair.  For scale, you can just use emollients and/or emollient wash products instead of shampoo, usually all you need for babies. Shampoo for older children should be unperfumed and ideally labelled as being suitable for eczema; washing the hair in bath water should be avoided.  Coal tar shampoo eg Capasal available.  Otherwise, apply emollient at night (use old pillowcase), wash out in morning [itchybaby.co.uk].

  • Soap substitutes – cetraben wash, doublebase wash, E45 wash, oilatum soap bar, ultrabase etc.
  • Shower additives – doublebase shower, E45 shower, oilatum shower etc. Sanex Zero shower gel (limited ingredients)?

Topical Steroids

It is important to remember that undertreatment can be just as damaging as overtreatment.

Topical steroid withdrawal panic really kicked in 2024-2025.

Strengths of steroid:

  • Mild eg hydrocortisone (any strength, incl 2.5%), Synalar 1 in 10. Mild combinations include Fucidin H, Daktacort, Timodine
  • Moderate eg Eumovate, Betnovate RD (betametasone valerate 0.025%, so 1in 4), Synalar 1 in 4. Moderate combinations include Trimovate, Hydromol HC intensive (hydrocortisone, but additional urea)
  • Potent eg Betnovate (valerate 0.1%), Mometasone (Elocon), Hydrocortisone butyrate (Locoid). Combinations include Fucibet (£5, cream only, cf Betnovate C (clioquinol) – comes as cream or ointment but £50 a tube!).
  • Very potent eg Dermovate (NN is with nystatin/neomycin)

Note that Fucibet is potent steroid, don’t confuse with Fucidin H (mild)!

  • Use mild potency only for the face and neck, except for short-term (3–5 days) use of moderate potency for severe flares.
  • Use moderate or potent preparations for short periods only (7–14 days) for flares in vulnerable sites such as axillae and groin.
  • Do not use very potent preparations in children without specialist dermatological advice, or potent topical corticosteroids in children aged under 12 months [ie you can/should prescribe everything else!]
  • Only apply topical corticosteroids to areas of active atopic eczema (or eczema that has been active within the past 48 hours), which may include areas of broken skin.
  • Exclude secondary bacterial or viral infection if a mild or moderately potent topical corticosteroid has not controlled the atopic eczema within 7–14 days.
  • In children aged 12 months or over, potent topical corticosteroids should then be used for as short a time as possible and in any case for no longer than 14 days. They should not be used on the face or neck. If this treatment does not control the atopic eczema, the diagnosis should be reviewed and the child referred for specialist dermatological advice.
  • Consider pulse treatment of problem areas of atopic eczema with topical corticosteroids for two consecutive days per week to prevent flares, instead of treating flares as they arise, in children with frequent flares (two or three per month), once the eczema has been controlled. This strategy should be reviewed within 3 to 6 months to assess effectiveness.

Lichenification reduces penetration so needs more intense and longer treatment (but lower risk of toxicity too!). 

Flares

Teach how to recognise flares: increased dryness, itching, redness, swelling and general irritability. Give clear instructions on how to manage flares according to the stepped-care plan

Treat flares as soon as signs and symptoms appear and continue for approximately 48 hours after symptoms subside.

Eczematous skin is predisposed to staph aureus infection, and this may result in acute flares. Topical steroid is not contra-indicated in infection, but consider a steroid-antibiotic combination e.g. Fucibet, tailing down to steroid only over a week as things improve. If severe, topical corticosteroids with oral flucloxacillin would be a good option.

Eczema herpeticum can spread rapidly, forming extensive sheets of monomorphic eroded or umbilicated vesicles. Risk factors include early onset, clinical severity, high total serum Ige. Clinically, lymphopenia and fever are hallmarks of disease.  Treatment is with aciclovir 200mg 5x a day for 5 days. Parents of children with eczema who have cold sores should be warned not to kiss their children until the sore has healed.

IgE antibodies to Malassezia furfur (a fungus) are found more commonly in eczema patients. Use of antifungals is under investigation.

Bandages and Garments

Cotton gloves help hand eczema eg pompholyx, but also reduce scratching.  Nail care similarly important.  Tubular bandages (Comfi-easy) keep cream in place, less scratch (but too hot?).  Protects clothes too.  Garments available, tubular or silk, which are looser, look less medical.

Wet wrap technique is 2 layers: wet 1st layer and wring out, 2nd layer dry.  Should only be recommended by experts as higher absorption of steroids.

Ichthammol bandages soothing but messy – pleat, don’t wrap round.  Or Zinc.

Duoderm hydrocolloid wound dressing good for putting on top of steroid in poorly healing areas (1-2/7) eg discoid.

Haelan topical steroid tape – for cracks, sticky, can be cut into shape eg T for wrapping around finger.  Apply for 12 hrs.  See youtube videos.

Cavilon spray or foam applicator is a no-sting barrier film esp hands.  Lasts up to 72 hours.

Other treatment options

Tacrolimus 0.03% ointment (Protopic) is a topical calcineurin inhibitor (TCI) – licensed for use in children 2yr+. Particularly good for face/neck? Application is twice a day for up to 3 weeks (discontinue if no benefit after 2 weeks), reducing to once daily after three weeks until the atopic dermatitis is clear. Tacrolimus needs time to work, don’t stop too soon after flares (2-4 weeks!). 

Can also be used 2x a week to prevent flares – if a flare occurs you can then go back to twice a day, or if necessary once a day with once a day topical steroids (or stop and just use steroids). According to BAD, some people like to alternate calcineurin inhibitors with steroids.

More effective than mild topical steroid but not more than potent. No skin atrophy was observed when patients used it daily for up to 2 years. Irritation in first week of use can settle. Do not apply if infected skin; use sunblock (or avoid using in morning). Do not apply under bandages/wraps? Avoid if macrolide allergy!?

National Eczema Society talks about combination treatment with topical steroids – with a flare, only topical steroids are used, as it improves, TCIs are added once a day (e.g. in the evening) alongside topical steroids (e.g. in the morning). Then you can wean steroids in the usual way while still using TCIs twice a day. In large clinical trials, this approach has been shown to reduce the chances of a flare recurring.

Pimecrolimus (Elidel, 0.01%, also age 2+) is a cream, not ointment – probably not as strong as Protopic but never directly compared!? Only tested in mild to moderate disease and has not been compared to mild topical steroids. It is not as effective as potent steroids. Discontinue if not effect after 6 weeks. BAD lumps together with Protopic, talks about preventive twice weekly use but not in BNFC. Tacrolimus and pimecrolimus are approximately 10 times more expensive than topical steroid preparations. (Arch 2004; 89)

For unresponsive patients, referral to a dermatologist for wet-wrap bandaging, ultra-violet treatment, in-patient care. Methotrexate/ciclosporin were traditionally next line, now dupilumab (anti IL4/13 – shared receptor – Dupixent).

Acupuncture reduces itch in placebo controlled cross over study vs cetirizine – flare size less too!

Immunosuppression and Biologics

Cyclosporin usually only used in short term. Methotrexate can be used in the long term but needs blood monitoring for liver/marrow toxicity. Azathioprine and MMF only really where the others not tolerated.

Dupilumab is anti IL4/13 (Th2 pathway). Twice weekly. Less side effects, in theory. Also benefit for co-morbid atopic conditions. Risk of respiratory infections.

JAK inhibitors need more monitoring, and risk of TB. [Carsten Flohr, KCL]

Lanolin allergy

Allergy, General paediatrics

Prob less common than suspected or talked about in eczema circles. Allergy to medical grade lanolin particularly uncommon, cf raw wool.

Patch testing pretty non reproducible! Not all lanolin the same?! Presence of alcohol important?!

So some v vocal critics of allergy “panic”!

Lanolin in cosmetics tends not to cause any problems, presence of damaged skin may be important for reactions.

For moisturisers, the following are lanolin free:

  • Aveeno
  • QV
  • Hydromol ok too?
  • [Not E45]

For bath additives, the following are lanolin free:

  • Cetraben
  • Diprobath
  • Balneum
  • Doublebase
  • Hydromol
  • Dermol 600
  • [Not Oilatum]

Steroid creams seem to be ok, at least Eumovate, Betnovate, Fucibet.

Eosinophilia

Allergy, General paediatrics, Immunology, Infectious disease

Usually just a marker of atopy, so common with asthma, hay fever, eczema. Mild generally accepted as 0.5–1.5×109/L, moderate 1.5–5, and severe >5. Persistent would be over 2 weeks.

But beware rare things eg HyperIgE syndrome. Any evidence of organ impairment? Also seen with malignancy, PFAPA, Familial Mediterranean Fever. With the rheumatological conditions, eosinophilia is often severe (>5) but with malignancy, usually mild…

And helminth infection, viz

  • Fever and hepatosplenomegaly
  • Liver/lung/brain cysts
  • Uveitis/macular oedema
  • Anaemia with abdominal pain or wheeze
[Turkish study and protocol, not v useful European Journal of Pediatrics (2023); from Florence – https://doi.org/10.1111/apa.17266]

Cysticercosis

General paediatrics, Infectious disease

Infection with T solium can be asymptomatic, or lead to subcutaneous lumps, or enter the central nervous system.

In tissues, can cause muscle pseudohypertrophy, can enter the eye, can cause conduction defects.

In the brain, acute encephalitis, pseudotumour with raised intracranial pressure, dementia/psychosis, chronic meningitis and neuropathies, spinal cord compression.

Finding T solium in the stool has low sensitivity/specificity. CSF may show eosinophils but may be normal. Imaging shows rings or blobs, can look like TB. Can be calcified, doesn’t necessarily mean dead!

Treat with albendazole or praziquantel. Immune reactions to treatment can be severe (raised ICP).

Helminths

General paediatrics, Infectious disease

So nematodes (round worms), cestodes (tapeworms), trematodes (flukes). Do not multiply in human hosts cf parasitic protozoa. Multiply through reinfection though! Most have life cycle in other hosts.

Cestodes

Mostly intestinal tapeworms, not that important, but Taenia solium eggs cause cysticercosis.

Hydatid cysts (larval stage of Echinococcus granulosus) are life threatening. Adult stage found only in dogs.

Trematodes

Complex life cycles involving snails. Cysts are ingested, with exception of schistosomiasis, where larvae (cercariae) penetrate skin. Migration within the body is a feature, where they end up causes problems even if it’s a dead end for the organism.

Cushing’s disease

Endocrinology, General paediatrics

Excessive cortisol due to an ACTH secreting tumour. In children, Cushing’s syndrome usually due to steroid treatment.

Manifests as dramatic weight gain, usually with angry striae, growth arrest (in terms of height), change in facial appearance, buffalo hump, hypertension.

These findings are hard to spot given that obesity with striae (and hypertension) in children common. Main clue is height centile below mean (and below MPH). Delayed bone age also a clue, as both of these things tend to be above normal in obese children.

Investigation is tricky as pituitary adenomas are not always seen on MRI and petrosal sinus sampling for cortisol is sometimes required! Even exclusion is tricky, requiring 24hr urinary cortisol collection over 3 days, low dose dexamethasone suppression testing.

CRH test done as part of work up, to see if ACTH is ectopic, which is exceptionally rare. Increased response to CRH test is almost diagnostic for Cushing’s though! High dose dexamethasone suppression rarely done.

Alpha-gal allergy

Allergy, General paediatrics, Immunology

Described in 2015, revolutionary in that allergy is to an oligosaccharide (ie a sugar, not a protein), specifically galactose-alpha-1,3-galactose.

Accounts for anaphylaxis to cetuximab, a cancer drug, but even more bizarrely, allergy to red meat (beef and pork). The latter appears to follow sensitization through a tick bite, so is really only an issue in endemic areas eg parts of United States and Europe, Australia.

Anaphylaxis to red meat can be immediate or delayed, with or without exercise induction!

In a small series of beef allergic patients reported in 2003 (strong family history), skin prick and labial contact tests only positive in minority.  All positive on IgE.  In another series, most beef allergic were also gelatine allergic. Risk from gelatine is mostly from intravenous products, but big dose of jelly sweets as risk??? Interestingly, a proportion of “idiopathic” anaphylaxis turned out SPT positive for gelatine. 

Bovine specific albumin (Bos d6) is another possible allergen for beef allergy – a minor cow’s milk allergen, so you would probably react to both – heat labile.

In Asia allergy described to galacto-oligosaccharides in milk formula, also a carbohydrate!

Thought to be T cell independent!

IgE test available. Levels appear to fall over time unless continued tick exposure.

Emerging? Changes in land use (less sheep, more deer)? About 50 cases in Scotland (2025) – certainly not all rural so prob recreational exposure. Youngest 4yrs (Argyll). Mostly strongly co-factor modified; cf America (big steaks?)

Some seem to have associated milk allergy.

Adrenal insufficiency

Endocrinology, General paediatrics

Cortisol over 800 excludes a problem, normal response to Syncathen test (ACTH) at 1 hr should be over 470nmol/l (over 6yrs), 650 (under 6yrs).

Primary adrenal insufficiency – congenital adrenal hyperplasia (mostly 21OH deficiency), else autoimmune, genetic, infiltrative, adrenleukodystrophy (and exogenous steroid suppression).

Classic Addisonion picture – low sodium, high potassium, hyperpigmentation (can look slim and tanned, so misleadingly healthy!).

Physiological hydrocortisone replacement =10mg/m2/d in 3-4 divided doses.  Medication alert bracelet recommended, in case of crisis.  Monitor growth, BP.

If unwell, double HC dose (if varying doses, double highest dose) and give it three times daily. IM if necessary, +/- infusion.

Screen time

Child protection, Community, General paediatrics, Mental health, OPD, Psychology, Sociology

Sedentary time spent in front of screens programs metabolism and brain neurochem.  Similar to addiction.

But it’s complicated! Partly because there are so many different kinds of activity that can now be done with mobile phones and tablets, and because it’s difficult to control or randomize.

How people interact with screens is changing too. In the mid-2000s in the US, children over 8 spent an average of 6.43 hours a day on electronic media, but this was mainly watching TV.  Evidence of stress response (reduced cortisol increase) on waking after using screens for average 3 hours a day.

But now mobile devices are the centre piece of young people’s social lives.  Boys tend to spend more time gaming, girls more time on social networking.

UK government advice 2026 is 1hr a day but pref less under 5 years, and under 2 only if joint watching/activity with adult.

Effect of high levels of screen time does not seem to be attenuated by equivalent exercise.

High levels of screen time (over 4 hours daily) is associated with poorer school performance. Social skills are poorer. These children tend to form cliques with shared interest, that create further social isolation.

Violent games and media are associated with aggression in children as young as pre-school. Aggression in children can be manifest physically, or verbally, or relationally (ignoring, excluding, spreading rumours). There is also significantly more hostile attribution bias, where you interpret behaviour (such as not being invited to a party) as hostile, even when it is not, or at least ambiguous.

Parental involvement matters – how frequently parents watch TV with their children, discuss content with them, and set limits on time spent playing video games.

Exposure to media violence must also be seen within a risks/resilience approach. [Gentile and Coyne, Aggressive Behaviour 2010] ]

Some evidence that some “social” games themed around cooperation and construction eg Animal crossing have benefits. Similarly, links between media and relational violence pretty weak, but that could be because relational violence content isn’t really examined! Actual content probably more important than time spent playing. Note that in that study of Animal Crossing, background mental health problems seemed to reduce benefit.