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Consent

Ethics, Generic

Neuberger criteria: competence, information, understanding, voluntariness. All dubious!

GMC guidance on consent (2008) – places it in context of process of discussion and decision-making. There is no “once size fits all” method. Starts with information being provided, in different formats. References advocacy services. Does not set threshold values for discussing risks: sensible, given how complex the communication of risk can be!

Acknowledges that some patients do not wish to go into detail about their condition. While doctors must respect their patients’ wishes, there is a minimum level of information that a patient is likely to need in order to give valid consent.

Adults with Incapacity Act (Scotland 2000) and Mental Capacity Act (England 2005) establish mechanisms for incapacitated adults. Provides practical advice on assessing capacity.

In Scotland, legal age of consent is clearly defined as 16yrs (Age of Legal Capacity (Scotland) Act 1991).  In England, Family Law Reform Act 1969 defines “child” as under 18yrs!  This leads to some issues when it comes to competency.

Written consent – the law only requires written consent for a very few things, eg IVF, organ donation! But you must record the fact that you have gained consent in medical records. And it may just make everything easier to get it written anyway.

For research

Proxy consent by parents can create conflict of interest eg handicapped child. Authorization a better concept (presumes right of child to take part in research)? Non-therapeutic research is not strictly legal, but usually accepted if minimal risk ie not significantly increased risk compared with standard care. Right of research enshrined in possibility of benefit outweighing possible risks. Alternative is therapeutic orphans, treated without good evidence of benefit. Failure to conduct research led to prophylactic sulphonamide disaster in 1950s (increased kernicterus). Research without consent not strictly legal but possibly acceptable for emergency situations, but retrospective consent should be sought (not really consent at all, of course) else assent (simplified consent) with later ratification, in stages if necessary.

Reasons for refusal in EURICON study: perceived risks/distress; distrust of research/researchers; dislike of the tone of approach of the doctor; shock and inability to decide; inconvenience of follow up. Hence communication skills essential. Information sheet should be given but should not be relied upon. As a minimum, parents must know that the treatment is being given as part of a trial, that their child may be receiving an experimental or unproven treatment, that they are free to say no and to opt for standard treatment. Check list should be provided. Involvement of independent committee should be highlighted. Feedback to parents should be encouraged.

Inability to give consent eg children, unconscious, learning difficulties does not mean research should not be done – indeed that would deprive patients and others of potential benefit. But should only be done if unable to do same study with patients who can give consent; risks should be minimal (for non-therapeutic research that means equivalent to everyday life or minimally invasive therapeutic interventions; assent should be sought from appropriate advocates eg relatives, who should be provided with the same information which would have been given to a competent patient; research should be explained after its completion to participants who have regained their competence subsequently (NOT retrospective consent, mind you).

Use of medical records without consent is a moral wrong – should be balanced against potential benefit. Patients should be informed of this potential use of their records and reassured about confidentiality. Only do if consent not praticable; research is of sufficient merit and has potential benefit; identifiers should be removed where possible; contact with patients is not anticipated; permission should be gained from responsible clinician.

How to get consent

  • Parents should feel they are being cared for, as well as their child. They should feel that they are being involved in the discussion of care. They should feel that they are being asked for their permission to enter the baby into a trial, not to defend the best interests of the baby.
  • Parents hate the idea of their baby being a guinea pig, so emphasize background to study: importance, plausibility, etc.
  • Acknowledge the pressure being put on parents to absorb and understand all the information. Invite questions and interruptions, reiterate key points.
  • Accept that research has negative connotations. Randomization is difficult to understand (and if they do, computer allocation is seen as more appropriate than tossing a coin or drawing from a hat!)!
  • Don’t say what you would do.
  • Beware strange comments/questions – suggest misunderstanding.
  • Reinforce that whatever the decision, the best proven care will be given.
  • Don’t rush.

Parental Rights and Responsibilities (PRRs)

Ethics, Generic

For births registered in Scotland, a father acquires parental responsibility if he was married to the mother at the time of the child’s conception or
subsequently. An unmarried father will acquire parental responsibility if he is recorded on the child’s birth certificate and the child was born on or after 4 May 2006 (Scotland), December 2003 (England).

If not on the birth certificate, an unmarried father must obtain a court registered parental responsibility agreement or order.  Birth certificates can be updated with new information.

Parental responsibility is not lost automatically with divorce, loss of custody rights, or if a parent makes no financial contribution! Young people under the age of 16 who bear children still get rights, although usually additional support will be necessary.

Foster parents usually do not have parental responsibility – that remains with the local authority and the birth parents. The parental rights of a child born under a surrogacy arrangement remain with the surrogate until the new parents complete adoption procedures or else obtain a court order (under the HFE Act).

Parents are allowed to authorize 3rd parties eg child minders, Grandparents to take over particular responsibilities. In terms of the Childrens Act, what is reasonable to safeguard/promote the child’s welfare is permitted to such carers (in loco parentis). If however the parent is thought likely to
object to a treatment decision, only emergency actions are acceptable pending contact with the parents directly.  Competence of child themselves obviously relevant too.

Up to 6 people can have PRRs for the same child.  But becomes unmanageable!

Decisions regarding the following should involve consultation between all with PRRs:

  • schooling,
  • serious medical problems,
  • changing surname,
  • leaving country for more than 1 month
  • Etc (not exhaustive)

But PRRs are not a weapon for interfering with day to day life!  Gillick ruling made it clear that parental rights exist only for the benefit of the child! Less serious decisions may simply require other party to be informed.

Stepfathers are in a funny position.  Marrying the mother gives rights, but does not remove rights from biological father.  Not being married leaves only the option of adoption, or else applying for court order if later separation after being an important part of a child’s life.

Non-consensual adoption under close judicial scrutiny – the consent of the parent with capacity can only be dispensed with if “nothing else will do”, and not because providing requisite support is difficult.[https://ukhumanrightsblog.com/2013/10/01/when-adoption-without-consent-breaches-human-rights/]

Civil Partners – biological parents remain the legal parents.  Civil partnership confers equivalent step-parent status as married non-biological parent. Parental responsibility can therefore be obtained either by consent of biological parents, court order or adoption.

Residence Order confers PRRs too. Contact Order does not.

It should be noted that parents who do not have parental responsibility may also play an essential role in determining best interests and may have a right, under the Human Rights Act (rights, as individuals, to respect for private and family life – Article 8), to participate in treatment decisions  [BMA toolkit].

 

 

Thyroid

Endocrinology, General paediatrics

Thyroid issues can be congenital, neonatal, autoimmune, or related to syndromes eg Downs, Digeorge.

Note that thyroid function tests can be affected by intercurrent illness, there is also viral thyroiditis where you might get transient (usually mild) abnormalities.  So borderline results (especially if asymptomatic or other medical issues) usually just need repeated.  If results confusing, do T3.  If normal then abnormal T4 likely to be transient.  If suspicion of evolving problem, do autoantibodies (TPO antibody, Thyroid Receptor Ab (TRab)).  If progressive decline then likely to be emerging autoimmune condition.

All kinds of unusual clinical presentations in thyroid disease, for example:

  • Effusions in hypothyroidism, including pericardial effusions – capillary dysfunction!? Impaired lymphatic drainage?
  • Body pain
  • Precocious puberty (although delayed more typical)

Congenital Hypothyroidism

Endocrinology, General paediatrics

Isolated TSH elevation >20 is usually treated.

True congenital hypothyroidism mostly dysgenesis, ie poorly formed gland, of which <2% have identified mutations (mostly thyroid peroxidise, thyroglobulin and TSH receptor proteins – EDTA sample, Dr Therese Bradley at SGH Genetics).  May be due to dyshormonogenesis (10%, autosomal dominant, gland looks normal on scan), TSH Receptor defect. Do a Family History.

Mostly found on newborn screening now.  Life long.

Placental thyroxine important, iodine too, on neonatal thyroid function.  In the first 14/7 of life, high TSH/T4/T3 seen.  Transient neonatal hypothyroidism seen, 25% of +ve guthrie tests!

Symptoms

If missed or untreated, classic signs are umbilical hernia, goitre, hoarse cry, coarse facies, Developmental Dysplasia of Hip!

Imaging

SPEG recommend that all families should be given the opportunity for imaging, subject to availability, because more informative than blood tests alone, will aid in genetic counselling, likelihood of lifelong treatment if proven permanent CH, provides a useful guide as to thyroxine dose.

Combined isotope and ultrasound imaging (dual scanning) is preferred. Isotope scans should be performed by day 5 of start of treatment to ensure avoidance of false negatives due to TSH suppression (advisable to take thyroid function sample on day of scans to confirm reliability of results). Ultrasound may show an abnormal gland (dyshormonogenesis) or else agenesis (no gland).   But in agenesis may be remnants of embryonic structural elements which can be mistaken for a gland – can persist into teenage years but max 5mm x 5mm! Hence importance of supporting radio-isotope imaging.  Experience of ultrasonographer important.

Management

Some concern that thyroxine liquid not as consistent levels?  Automatic script request from pharmacy, patient then notified when ready.

Repeat TGTs at 10-12 weeks.  Aim to keep TSH in lower half of reference range (room to spare as child grows).

Follow up

  1. Scottish guideline suggests typical doses at different ages, up to age 3, to encourage dose changes with growth rather than waiting till dose insufficient and hypothyroidism emerges (see table).  Use TFTs to confirm compliance.
  2. Assess growth: weight, length until 2 years, then height, head circumference until 3 years
  3. Assess development – consider pre-school audiology (for subtle hearing impairment due to CH)
  4. Transition – patient education. Boys to GP (unless problems with control), girls – to adult endocrinology (for pre-pregnancy counselling).

Aim for fT4 > 15 pmol/l and TSH <5.0 mU/l

Age LT4 dose (ug daily) LT4 dose (ug/kg/day)
Female Male Female Male
3 months 41.3 43.3 7.2 6.9
6 months 45.8 50.0 6.1 6.2
9 months 47.9 53.1 5.6 5.7
12 months 55.0 53.1 5.8 5.2
18 months 62.5 61.1 5.8 5.3
24 months 70.3 58.3 5.9 4.6
36 months 75.0 62.5 5.3 4.25

Haemophilia

General paediatrics, Haem/Oncology

The clinical severity of a patient’s hemophilia is gauged by the baseline clotting factor level, a value that remains fairly constant throughout that person’s life, and is pretty consistent through a family. Around 5% of normal is moderate.

Intramuscular injections should be avoided if at all possible. If they must be given, factor replacement therapy should precede the injection. Parenteral agents should be given intravenously or subcutaneously. Immunizations are administered subcutaneously.

Aspirin is contraindicated due to antiplatelet effect. Avoid NSAIDs if possible, and contraindicated if actively bleeding or being treated for a recent bleeding problem.

Indications for Factor Replacement Therapy

  1. Suspected bleeding into a joint or muscle.
  2. Any significant injury to the head, neck, mouth or eyes or evidence of bleeding in those areas.
  3. Any new or unusual headache, particularly one following trauma.
  4. Severe pain or swelling at any site.
  5. All open wounds requiring surgical closure, wound adhesive, or steri-strips.
  6. History of an accident or trauma that might result in internal bleeding.
  7. Necessity of a surgical or invasive procedure.
  8. Heavy or persistent bleeding from any site.
  9. Gastrointestinal bleeding.
  10. Acute fractures, dislocations and sprains.

Treatment

Hemophilia A

The treatment of choice for individuals with factor VIII deficiency is recombinant factor VIII. There are different brands, with different combinations of additives which may or may not be antigenic. Cryoprecipate and fresh frozen plasma are used only if factor cannot be obtained.

  • When bleeding is severe, or for a head injury, the appropriate dose of factor VIII is 50 units/kg. This should result in a factor VIII level of 80-100%. Half life is 8-10 hrs so repeat if necessary.
  • Mild Hemophilia A (factor VIII greater than 5%) with Non-Life/ Limb Threatening Bleeding may respond to desmopressin (some don’t) – 0.3mcg/kg IV over 30 minutes, else as nasal spray (Stimate, 1 spray in one nostril for individuals <50 kg and 1 spray in each nostril for individuals >50 kg). Otherwise, treatment dose is 15-25u/kg.

Hemophilia B

For individuals with Christmas disease (factor IX deficiency), recombinant factor IX is the treatment of choice. Fresh frozen plasma is only used if factor is unavailable.

  • When bleeding is severe, or head injury, the appropriate dose of factor IX is 100-120 units/kg. This should result in a factor IX level of 80-100%, but in Hemophilia B the response is variable so check the level and adjust as necessary.
  • Mild – 25-35u/kg, check level

Ideally let patients/parents reconstitute and administer their own factor. Families should have an emergency dose of factor concentrate or DDAVP in their home and to take it with them when they travel, esp if they do not live close to a hospital. Factor replacement should be offered within 1 hour of the patient’s arrival: it should be readily available, the patient should not be left waiting, and treatment should not be deferred pending x-rays or other results. The most experienced IV therapist or phlebotomist available should perform venipuncture – misses and tourniquets may cause painful hematomas which then limit further IV access – use the smallest needle possible unless volume replacement is needed..

Factor replacement must be administered intravenously by IV push over 1-2 minutes. Round the dose up to the closest full vial ie don’t throw away any left overs (excess factor does not create a hypercoaguable state but will prolong the therapeutic half-life of the product administered).

For individuals with inhibitors (antibodies to factor VIII or IX), treatment decisions may be more complicated. The care of inhibitor patients should be urgently discussed with the patient’s hematologist. If an individual with an inhibitor presents in a life- or limb-threatening scenario, the safest immediate action is to prescribe recombinant factor VIIa (rFVIIa, Novoseven) at a dose of 90 mcg/kg or activated prothrombin complex concentrates (FEIBA, Autoplex) at 75-100 units/kg (contraindicated in factor IX patients with a history of inhibitors and anaphylaxis). Hopefully the patient/family can provide information on response to second line therapeutic agents.

[Medical and Scientific Advisory Council (MASAC) of the US National Hemophilia Foundation 2003]

Haematuria

Common, General paediatrics, OPD, Renal

In a study of 342 kids with asymptomatic microscopic haematuria, no cause was found in the large majority of patients. The most common cause discovered was hypercalciuria (16% of patients) followed by post–streptococcal glomerulonephritis (1%). No evidence for value of early detection of hypercalciuria (may be at long-term risk for nephrolithiasis and bone demineralization).  The children with asymptomatic post–streptococcal glomerulonephritis all improved spontaneously and without complication.  None had evidence of urinary tract infection! Clinically insignificant abnormalities in the upper urinary tracts of 5 children and grade 3 reflux in 1  [Arch Pediatr Adolesc Med. 2005;159(4):353-355. doi:10.1001/archpedi.159.4.353]

Asympt recurrent can be monitored for 5yr!

Beware:

  • frank blood,
  • protein,
  • hypertension,
  • other features (joints, rash, wt loss)

Haematuria defined as persistent dipstick positive on at least 3 occasions for at least 3 months. Else as >2rbc per HPF (not same as flow cytometry). Then consider:

  • Red cells or not?
    • myoglobinuria = haemolysis
    • beetroot!
    • Porphyrins, other unusual pigments
  • Proteinuria or not?

If spot urine abnormal, repeat on early morning urine and then proceed to 12-14hr collection. Urine calcium/creatinine has age specific normals, high at birth (up to 1.5 in toddlers) falling to adult max of 0.7 at age 7. High levels especially significant in the presence of a normal plasma calcium

Investigations – only do bloods if macroscopic or nephritis suspected:

  • Do urine culture and microscopy.
  • Do PCR if proteinuria.
  • If macroscopic, do FBC, U&Es, LFTs, Coag.
  • Renal USS
  • Screen family members with urinalysis
  • Spot urine calcium/creatinine
  • If acute nephritis, do C3/4, ASOT, immunoglobulins, ANCA, anti GBM as below.
  • If stones suspected, do 2 sets of spot urine Ca/creat, Oxalate/creat, Urate, amino & organic acids, pH, KUB.

Differential is:

  • Tumour – bladder (colour changes during voiding, dysuria with sterile culture) or kidney
  • IgA nephropathy – persistent, progressive in 30%, diagnosis on biopsy
  • Alports – usually X dominant, deafness in minority, cataracts in 10%
  • Sickle cell – 1% macroscopic, 16% microscopic. Papillary necrosis, usually painless, episodic. May progress to sickle nephropathy.
  • Venous thrombosis – esp neonates, nephrotics.
  • Vascular – AVM, Nutcracker syndrome (compression of the left renal vein between the abdominal aorta and SMA)
  • Nail-patella syndrome (BM disorder, like Alports)
  • Polycystic Kidney Disease

Biopsy if persistent high grade microscopic, or microscopic with proteinuria (>150 mg/24 hr)/hypertension/impaired renal function, or 2 episodes of gross haematuria. Cystoscopy for bladder problem.

Health anxiety

General paediatrics, Medical, Patients, Psychology

DSM-5 has “illness anxiety disorder”, defined as preoccupation with the idea that you’re seriously ill, based on normal body sensations (such as a noisy stomach) or minor symptoms (such as a minor rash), to the degree that it gets in the way of normal life. Other features are persistence of such ideas over 6 months, finding little or no reassurance from negative test results or a doctor’s reassurance, repeatedly checking body, avoiding people, places or activities for fear of health risks.

In other words, hypochondriasis. Which gets its name from the idea that such feelings came from liver/spleen/gall bladder (“melancholy” – black bile).  William Cullen, in Edinburgh in the 1790s, appeared to take a particular interest in this.

For the sake of diagnosis, this disorder requires the absence of symptoms, which excludes the large group of people who have similar preoccupation and fears about non-specific or unexplained signs and symptoms.

Health anxiety is therefore a broader concept, and can include anyone who is more desperate for relief from worry, than for relief from actual symptoms.

Cyberchondria = combination of increased pathologisation of society, and ability to browse the internet.  Because provides the opportunity to find very serious, extremely unlikely explanation for problems.

Diagnosis of health anxiety is well accepted by patients if explained respectfully!

[BMJ 2016;353:i2250]

Mastocytosis

Dermatology, General paediatrics

Proliferation of mast cells.  Can be restricted to skin or be systemic, with infiltration of bone marrow, spleen, liver and lymph nodes.  Systemic involvement not always obvious in the skin! Messy though, since mast cell mediators might act systemically even if mast cells themselves not widespread.

Systemic mastocytosis can present with episodic symptoms of dyspnoea, collapse (hypotension), reflux, diarrhoea.  Rather non-specific, so easily missed.  May also have hepatosplenomegaly, lymphadenopathy, osteoporosis, bone abnormalities.

Skin lesions may be present but not always dramatic (might just look like freckles).  May be history of dermatographism, recurrent itching, flushing and/or urticaria.  Different skin patterns seen, but overlapping:

  • mastocytoma – slightly raised, can be slightly pigmented.  Physical irritation eg scratching causes flare and weal (Darier’s sign).  Can be present at birth, tend to be a good size eg 2-4cm nodule, may be blistering (in first 2 years of life only), else appear in first year of life.
  • Urticaria Pigmentosa – usually presents in first 2 years of life, freckles or larger nodules/papules/plaques.  Can be blistering.  Resolves if not improves at puberty.
  • Diffuse cutaneous mastocytosis (DCM) – no distinct lesions visible! Serious.
  • Telangiectasia macularis eruptiva perstans (TMEP) –  brownish small macules with telangiectasia, generally in adults.  Can be systemic.

So look at skin, try Darier’s sign (not v sensitive).  Feel for liver and spleen.  Check Tryptase level (rarely normal even in systemic – compare baseline to peak, rather than just absolute level). Consider bone marrow biopsy to look for mast cells. Consider bone scan to look for abnormalities.  PCR for the D816V mutation in KIT gene?

Management

Control triggers (very individual):

  • Stress (emotional/physical), sleep deprivation, pain
  • Physical stimuation eg heat/cold, exercise/sex, sunlight, skin/scalp friction or trauma (tickling!)
  • Bee/wasp stings
  • Drugs esp aspirin/NSAIDs, opiates
  • Alcohol

60% of kids resolve during puberty!

In later life there is a slightly higher risk of haematological disorders including cancer. There is also an increased risk of osteoporosis.

Stabilize mast cells:

  • Anti-histamines, including H2 blockers.  Titrate dose to effect.
  • Cromoglycate
  • PUVA offers some temporary relief

Emergency treatment: Adrenaline auto-injectors for –

  • systemic
  • previous systemic reactions
  • Extensive blistering lesions?

UK support group at www.ukmasto.org [Jess Hobart]

[Am Fam Physician. 1999 Jun 1;59(11):3047-3054.]

Colic = Cry-Fuss Behaviour

Common, General paediatrics, Nutrition, OPD

Cry-fuss behaviour (=colic etc), mean is just short of 2hrs per day for first 6 weeks, reduces to 72 minutes by 10-12 weeks.

“Colic” suggests that there is a bowel issue, usually suspected due to drawing legs up, passing wind – but these could be considered normal for crying and distress, of any cause.  Reflux (GORD) is often blamed, yet international consensus states there is no evidence to support an empiric trial of acid suppression as a diagnostic test in infants and young children, even though symptoms tend to be less specific [Vandenplas, J Pediatr Gastroenterol Nutr. 2009 Oct;49(4):498-547. doi: 10.1097/MPG.0b013e3181b7f563]!

Cause

Mums with an anxiety disorder prior to pregnancy are at higher risk of having a child with excessive crying at 2, 4 or 16 months postpartum compared with mothers without an anxiety disorder.  Risk increased further for mothers who developed an anxiety disorder during pregnancy.

So does maternal anxiety lead to “intrusive” parenting, in turn increasing infant crying ?[Arch Dis Child 2014;99:800–6]. Else fetal programming?  Genetics?

What’s the influence of fathers!?

Surprisingly, maternal depressive disorders, cf anxiety, experienced before or during pregnancy, did not predict maternal report of excessive infant crying.  Is the difference withdrawal, rather than intrusiveness?

Reflux

Consider 2 week trial of anti-secretory eg ranitidine (but NOT PPI – increase risk of infection esp respiratory and GI, associated with parietal cell hyperplasia, and possibly food allergy!).  But don’t assume improvement due to response!  Or investigate with pH monitoring.  Or stick to supporting parents!   Even if arching and refusing to feed, no evidence of effectiveness.

Infection

5% have UTI retrospectively, but in absence of other signs, investigations not routinely required.

Associations

Crying that lasts more than 3 h per day, for more than 3 days per week and for more than 3 weeks in a row—is associated with child abuse and maternal depression!  Higher scores on PND scale persists at 6/12 even if crying resolves…

6% of parents retrospectively admit physically abusive behaviours towards baby when crying.

Predicts shorter duration of breast feeding.

Persistent problems with cry-fuss behaviour at 5/12 associated with later behavioural problems (metanalysis, but confounded by psychosocial risk factors).

Management

Reassure the parents/carers that infantile colic is a common problem that should resolve by 6 months of age.

RCTs of behavioural sleep intervention under 3/12 did not decrease crying.  So encourage parent-infant reciprocity (ie responding to crying) until old enough to suit Gina Ford type regimented sleep regimes.

Encourage the parents to try relaxed cue based care, sleeping in the same room as the baby (not the same bed – beware SUDI) , offering physical contact esp skin to skin contact, and ensuring the baby gets lots of rich sensory experiences during the day.  This,  combined with average 10 hours of physical contact per 24hr (even if asleep), associated with 50% less crying and fussing. Only 37% of 3/12 babies sleep 8hrs straight at night.

Night waking is associated with co-sleeping and breast feeding, but breast feeding does not equate with less total sleep for parents over the whole 24hr period (quality, however, may be inferior).

Over sensitive babies may benefit from OT/Physio, but beware removing sensory stimulus as associated with neurodevelopmental problems.  Massage, wrapping may help, little evidence for chiropractic, craniosacral, nutritional.  Offer diverse sensory stimulation (through parents’ own social life and activities).

If symptoms are severe (subjective, of course) or persist after 4 months, consider an alternative underlying cause for symptoms.

NICE says seek specialist advice from a paediatrician if infant is not thriving, or symptoms are not starting to improve or are worsening after 4 months of age.

Caveat for GPs is “Seek specialist advice if Parents/carers feel unable to cope with the infant’s symptoms despite reassurance and advice in primary care.”

 

Feeding

Feed refusal is often linked, often impaired mutual regulation of feeding that result in entrenched patterns of difficult feeding esp breast feeding issues.

The following suggest a feeding problem –

  • 4 heavy disposable nappies per day minimum
  • 3-4 yellow curdy stools if breast fed minimum
  • Nipple/breast pain, attachment problems
  • falling asleep within 10 minutes, feeding longer than 30 minutes (active feeding ie not including dozing, interacting) regularly
  • clicking sound, gurgly sounds, absence of swallowing sounds
  • Increased resp effort

Expect 125g per week growth average in first 3 months.  Tongue tie only really relevant to breast feeding babies.

Babies who have infrequent large feeds are not necessarily abnormal, and cue based feeding rather than scheduled 3-4hrly feeds often works better.

So offer feed calmly, unless already full blown crying, in which case calm holding eg skin to skin until more settled.  Cochrane review concluded that pacifier use does not interfere with breast feeding in mothers who are motivated.

Some evidence for trial of hydrolysed formula. RCT of 107 breast fed babies with colic excluded dairy, soy, wheat, nuts, fish and shortened duration of crying, but only CMPI really substantiated.  Probiotic has helped in RCT but roles of feed management, lactose overload etc need to be elucidated first?

Functional lactose overload? – as feed progresses, fat level usually increases so transit time slows.  If insufficient fat, rapid transit leads to lactose fermentation in colon (lower cholecystokinin levels seen).

Parent Support

The self-help support group Cry-sis for families with excessively crying or sleepless children, has a website and runs a national telephone helpline (0845 122 8669).

There’s also parent info including a video at http://www.nhs.uk/Conditions/Colic/Pages/Introduction.aspx

 

[https://cks.nice.org.uk/colic-infantile#!scenario]

[Clinical review BMJ 2011;343:d7772  doi: http://dx.doi.org/10.1136/bmj.d7772]

Capillary refill time (CRT)

Clinical, General paediatrics

In children over 7 days of age, the upper limit of normal CRT is approximately 2 s when measured on a finger, and 4 s when measured on the chest or foot, irrespective of whether the child is feverish or not. Longer pressing times and ambient temperature outside 20°C–25°C are associated with longer CRT.

Evidence suggests that the use of stopwatches reduces variability between observers.

Recommend following standardised CRT method: press on the finger for 5 s using moderate pressure at an ambient temperature of 20°C–25°C. A capillary refill time of 3 s or more should be considered abnormal.  Other timings apply to other sites.

[Systematic review – 21 studies on 1915 children.  Arch Dis Child doi:10.1136/archdischild-2014-307079]