Gastroenteritis

Cite this article as:
Angharad Griffiths. Gastroenteritis, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.28790

Conor is a 10 kg, 13 month-old boy who’s presented to the ED with a 24-hour history of diarrhoea and vomiting.  He has had 5 episodes of non-bloody, non-bilious vomits. Since waking up this morning has two episodes of loose/watery non-bloody malodorous stools. They have not ‘flooded’ the nappy but were quite large.  He is taking sips of fluid (mixtures of water, milk, and juice being offered) and has only eaten half a digestive biscuit so far today.  He has had a fairly large wet nappy last night, but not since, though it’s now difficult to tell as his last nappy was dirty.  He is alert and looking around while being carried but is upset on leaving his mother’s arms.  He cries with tears, has a normal heart rate but his mother is worried about his dry lips.  She was told by a healthcare worker neighbour that he will “need a drip”. CRT, HR, and BP are normal.  His temperature is 37.8.  His nappy is dry and has been on for 3 hours now.  His capillary glucose measurement is 3.2.  You decide he’s probably mildly dehydrated.

Introduction

Gastroenteritis (GE) is the presence or diarrhoea or vomiting (or both) that may or may not be accompanied by fever, abdominal pain and anorexia.  Diarrhoea is the passage of excessively liquidy or frequent stools with liquid high water content.  Although often felt to be a common minor illness presentation, it is a major cause of childhood mortality and morbidity, causing millions of deaths worldwide in children in low and middle-income countries; of all child deaths from gastroenteritis 78% occur in Africa and South-East Asia. 

Gastroenteritis accounts for a huge proportion of GP and ED presentations. In Europe, acute gastroenteritis the third commonest cause of hospital admission, accounting for between 4-17% of admissions.  In Australia, gastroenteritis caused by rotavirus alone accounts for 115,000 GP visits, 22,000 ED visits and 10,000 hospital admissions a year, with an estimated cost of 30m Australian Dollars (£12m, €18m).  In the UK, 20% of GP consultations in the under 5’s are for GE.

It is imperative that the child with gastroenteritis is differentiated from more sinister causes of vomiting.  The presence of diarrhoea is reassuring but doesn’t exclude other intra-abdominal causes.  The same can be said for pain out of proportion with gastroenteritis, distension, peritoneal signs or localised tenderness.

Most cases are not associated with complications but when complications do occur, the commonest are electrolyte disturbance and metabolic acidosis.  Supplementary fluids through oral or intravenous routes are the most effective way to avoid these complications.

Gastroenteritis in low and middle-income countries can present differently, has different aetiologies, is often managed differently, and is a larger burden to healthcare systems in general than in high-income countries.  This post will focus on gastroenteritis in high-income countries. For more information about comparisons of guidelines across the world; Vecchio et al (2016) is an interesting read.

This is not meant to provide a clinical practice guideline; rather an overview of the illness.  Many (if not all!) paediatric emergency departments or general paediatric units have their own guidelines.

Pathophysiology

Worldwide, the commonest causes are viral pathogens, most commonly rotaviruses and noroviruses.  Viral infections cause damage to the small bowel enterocytes with resultant low-grade fevers and watery diarrhoea – classically without blood.  Rotavirus strains are seasonal and vary within different geographical areas.  The peak age for these infections is between 6 months and 2 years.  Children with poor nutrition are at higher risk of acquiring gastroenteritis and developing dehydration and complications.

Children with bacterial gastroenteritis are more likely to have bloody stool.
Escherichia coli and Shigella dysenteriae can be complicated by haemolytic uraemic syndrome (HUS).  This is an acute onset, microangiopathic haemolytic anaemia, thrombocytopaenia, acute renal impairment and multisystem involvement.  (Just to confuse things, HUS can present in the absence of bloody diarrhoea.)

Pathogens can be generalised into four groups:

  • Viral (70% of cases): Rotavirus, Norovirus, Adenovirus, Enterovirus
  • Bacterial (10-20% of cases): Campylobacter jejuni, Salmonella spp, Escherichia coli, Shigella spp, Yersinia enterocolitica.
  • Protozoa (unusual, accounting for <10%): Cryptosporidium, Giardia lamblia, Entamoeba histolytica
  • Helminths (very unusual): Strongyloides stercoralis

Transmission

Pathogens are spread mainly via the faeco-oral route, acquired by ingesting contaminated food or drink.  Water may be contaminated with bacteria, viruses, or protozoa. Undercooked (or inappropriately stored/cooked) meats and seafood are common culprits of bacterial pathogens.  Bacterial contaminants can produce toxins (e.g. Bacillus cereus in re-warmed rice or Staphylococcus aureus in ice-cream).

Pathogens causing gastroenteritis can also be transmitted without the patient being symptomatic.

Assessment

Gastroenteritis is a clinical diagnosis.  Enquire about sick/infectious contacts and potential sources (recent travel, food).  Enquire about the frequency of symptoms and intake of fluids.  Note the frequency of urination.  Note other things that may cause diarrhoea e.g. recent use of enteral antibiotics or chronic constipation with overflow diarrhoea the presenting feature. 

In the presence of signs such as high fever, long duration of symptoms, severe abdominal pain or bilious vomiting; review the diagnosis and do not immediately label as gastroenteritis.

Oral hydration fluids

Most children are not dehydrated and can tolerate oral fluids and so can be managed at home.  Take a look at Nikki Abela’s DFTB19 talk on top tips for a high yield dehydration assessment.

When children are only mildly to moderately dehydrated, as a general rule they can be treated with oral / enteral rehydration with low osmolality oral rehydration solution (ORS).  Worldwide, ORS is recognised as first line therapy and treating mild to moderate dehydration with enteral rehydration is supported by the WHO, European Society for Paediatric Gastroenterology and the American Academy of Paediatrics. The WHO recommends a low osmolality (hypo-osmolar) solution, usually containing sodium, potassium, chloride, carbohydrate (glucose) and a base.  Low osmolarity solutions reduce the need for IV fluids, reduce stool output and reduce vomiting frequency.

But… a major limitation to the use of ORS is its taste – and this is where apple juice comes in. For minimally dehydrated patients, half-strength apple juice is associated with fewer treatment failures compared to ORS and could suit as a more palatable alternative.  Take a look at a sweet summary (pun intended!) of the “apple juice trial”.

Breastfeeding should continue and a child can be supplemented with ORS if this is needed.  Children can go back to a normal diet after the illness has passed.

Enteral (oral / NG) versus IV hydration

Most studies show that enteral rehydration with ORS is just as effective as IV hydration in mild to moderate dehydration with a 2006 Cochrane analysis concluding that enteral rehydration is as effective if not better than IV rehydration with fewer adverse events and a shorter hospital stay.  It is also less invasive (even with NG placement) and anecdotally satisfaction is greater amongst parents.  It is very safe.

Enteral rehydration only fails in approximately 1 in 20-25 children.

Barriers to oral rehydration include unfamiliarity with the benefits, misconception that it takes longer than IV therapy, and that it has a high failure rate.

Contraindications to enteral rehydration include haemodynamic instability, abdominal distension, concern over ileus, absent bowel sounds, or impaired airway reflexes.

IV therapy is more invasive and involves placing and maintaining IV access.  There are also iatrogenic complications including electrolyte disturbance should inappropriate fluids / composition / volume / rate be used. 

But… in severely dehydrated children, put away the ORS and apple juice. They will need IV rehydration as first line.

Antiemetics

How can we support enteral fluids? Well, children who receive Ondansetron are less likely to vomit, have greater oral intake and are less likely to require IV hydration.  A Cochrane review demonstrates that Ondansetron also increases the proportion of children who stop vomiting when compared to placebo [RR1.4] and reduces the proportion of children needing IV therapy (and therefore admission rate) [RR 0.41].  Median length of stay is also shorter in the ED. 

Reported side effects are rare with very few reported side effects other than a few cases of increased frequency of diarrhoea.

Antiemetics alleviate vomiting by acting on the ChemoReceptor Trigger Zone and vomiting centre.  Ondansetron is a 5HT3 receptor antagonist.  This class of antiemetics have fewer adverse effects (than dopamine antagonists, anticholinergics, antihistamines and corticosteroids) and can be safely used in children.  The NICE guideline discusses its off-licence use (at time of publication it’s licence was for post-operative nausea and vomiting and chemotherapy induced vomiting).

Ondansetron prolongs the QT interval.  Recommendations are it should be avoided in those with long QT and should be used in caution where there may be electrolyte imbalance (severe dehydration) or on other QT-prolonging medication.

Ondansetron is relatively cheap  £1.71 for 10 4mg tablets and is available in oro-dispersible form (though these are much more expensive at £36 for 10x4mg tablets) and liquid (£36.82 for 40mg [50ml] bottle).

Probiotics

An ESPGHAN working group position paper on the use of probiotics in acute paediatric gastroenteritis concludes that:

  • Effects seen in clinical trial are probiotic strain specific (this makes ‘trial-life’ difficult to replicate in ‘real-life’).
  • A lack of evidence now doesn’t mean that there won’t be evidence sometime in the future. 
  • Safety profile of certain strains cannot be extrapolated to other strains.
  • Studies that report benefits in certain doses in certain settings have insufficient evidence to support a health benefit at lower doses and different setting.

…the jury’s still out.

Other therapies

Antibiotics and anti-diarrhoeal agents aren’t routinely recommended in the management of paediatric gastroenteritis.

For gastroenteritis in high income countries, the WHO does not recommend adding zinc to a treatment regimen (it is for gastroenteritis in low and middle income countries). 

Investigations

Routine lab testing in mild and moderate gastroenteritis is of little value in these patients and should be avoided unless clinically indicated.

This goes for stool samples too.  Stool cultures are not routinely indicated in immunocompetent children with non-bloody diarrhoea.

Confirmation of viral gastroenteritis after the child has been discharged from the ED, and likely on the road to recovery at home, adds very little to (A) the clinical diagnosis of viral gastroenteritis in the ED, (B) the management plan and (C) the clinical outcome. 

Should the investigation influence management, then stool sampling may be of benefit.  This could be applicable where an outbreak may be suspected in school or creche, where there may be a public health benefit.

Stool samples should be sent in cases of bloody diarrhoea, immunodeficiency and recent foreign travel.

How about tests for dehydration? Sadly there is no one test that correlates clinically with dehydration. Urine specific gravity in infants is unreliable because the kidney reaches adult concentrating abilities after the age of 1.  Also, the child often doesn’t begin urinating until rehydration has begun.

And glucose? Well, almost 10% of GE patients aged 1 month to 5 years in high income countries present with hypoglycaemia.  Risk factors for hypoglycaemia on presentation include a longer duration of vomiting and increased frequency of vomiting.  It would be reasonable to consider point of care glucose testing at triage for young children as identifying hypoglycaemia on clinical ground alone is difficult in this age group. 

Prevention

The key to reducing the burden (and generally for an all-round happier life!) is in the prevention of acute gastroenteritis.  Rotavirus vaccination is now commonplace thought the antibodies, the UK & Ireland and other countries around the world.  It is very effective.

In the home and in the ED…Handwashing, handwashing, handwashing!

Vaccination leads to a profound reduction in presentations and admissions and a fall in overall seasonal workload, often within the first year after the introduction of universal vaccination against rotavirus.  Even though only those under 1 year old are generally vaccinated, it has been shown to contribute to a significant herd effect with fewer cases than expected in older children. In Scotland, where initial vaccine uptake was 93- 94% during the first 2 years, annual rotavirus confirmed gastroenteritis cases fell by 84.7%, bed days reduced by 91% (from 325 to just 29), without any documented cases of intussusception.  Reductions were seen across all age groups despite only infants receiving the vaccine.  Similar results can be seen in other areas of the UK and Ireland.

The not to miss bits

  • Do not assume isolated vomiting in a child is gastroenteritis.  Consider other causes -these very widely from inborn errors of metabolism to diabetes mellitus, surgical obstruction to urinary tract infections. If you’d like to hear more, check out Dani’s talk on vomiting in children in DFTB Essentials.
  • Beware chronic diarrhoea in an infant – do they have malabsorption or is this a presentation of IBD or an immunodeficiency?
  • Beware the non-thriving child with diarrhoea.
  • And beware chronic diarrhoea.

But what happened to Conor?

Conor was given a cup of Dioralyte ORS and his favourite beaker filled with Dioralyte.  His mum was encouraged to give him syringes of 5 mls of Dioralyte frequently or for him to take sips from his beaker and was asked to document on a piece of paper how many he received.  He vomited after 30 minutes of this therapy.

You give him a dose of Ondansetron and place an NG tube and give him 100mls (10ml/kg) over 1 hour after deciding he does not need rapid rehydration but slightly more than normal maintenance.  He then receives maintenance volumes of Dioralyte via his NG, which he tolerates well and then starts to take his own sips from his beaker.

He does not vomit in the ED again, has one episode of loose stools, passes urine, and is tolerating fluids orally.  He’s smiling at you! You feel he can be discharged and council his mum regarding regular fluid intake, choice of fluids, of any red flags, and encouraged to return in the event of any concern.

Conor’s Dad calls to say that Conor’s 3 year old sister at home is now vomiting too!  But it’s OK – He’s not too worried about her and Conor’s Mum has advised his Dad to start giving her regular sips of Dioralyte at home…

References

Colletti JE, Brown KM, Sharieff GQ, Barata IA, Ishimine P. The Management of Children with Gastroenteritis and Dehydration in the Emergency Department. J Emerg Med [Internet]. 2010;38(5):686–98. Available from: https://dx.doi.org/10.1016/j.jemermed.2008.06.015

Elliott EJ. Acute gastroenteritis in children. Br Med J. 2007;334(7583):35–40.

Vecchio A Lo, Dias A, Berkley JA, Boey C, Cohen MB, Cruchet S, et al. Comparison of Recommendations in Clinical Practice Guidelines for Acute Gastroenteritis in Children. Gastroenterology. 2016;63(2):226–35.

Freedman SB, Willan AR, Boutis K, Schuh S. Effect of dilute apple juice and preferred fluids vs electrolyte maintenance solution on treatment failure among children with mild gastroenteritis: A randomized clinical trial. JAMA – J Am Med Assoc. 2016;315(18):1966–74.

BK F, A H, JC C. Enteral vs Intravenous regydration therapy for children with gastroenteritis: A meta-analysis of randomized controlled trials. Arch Paediatr Adolesc. 2004;158(1):483–90.

Hartling L, Bellemare S, Wiebe N, Kf R, Tp K, Wr C, et al. Oral versus intravenous rehydration for treating dehydration due to gastroenteritis in children (Review). 2006;

Fedorowicz Z, Jagannath V, Carter B. Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. [Internet]. Cochrane database of systematic reviews. 2011. Available from: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD005506.pub5/full

NICE. Management of vomiting omiting in children and y young oung people with gastroenteritis : ondansetron. NICE GUIDELINES. 2014. p. 1–20.

Szajewska H, Guarino A, Hojsak I, Indrio F, Kolacek S, Shamir R, et al. Use of Probiotics for Management of Acute Gastroenteritis : A Position Paper by the ESPGHAN Working Group for Probiotics and Prebiotics. 2014;58(4):531–9.

Forrest R, Jones L, Willocks L, Hardie A, Templeton K. Impact of the introduction of rotavirus vaccination on paediatric hospital admissions , Lothian , Scotland : a retrospective observational study. 2017;323–7.

MARLOW RD, MUIR P, VIPOND I, TROTTER CL FA. Assessing the impacts from the first year of rotavirus vaccination in the UK. Arch Dis Child. 2015;100(Supl 3):A30.

Constipation Module

Cite this article as:
Team DFTB. Constipation Module, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.27243
TopicConstipation
AuthorRebecca Paxton
Duration30-60 mins
Equipment requiredNone
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

Billy is an otherwise well 4 year old boy who presents to A&E with a 4 week history of abdominal pain. His pain comes and goes, and seems to be worse after eating. Today he has been doubling over with pain and crying inconsolably.

He has had no fevers or vomiting. He is drinking well but parents think he is a bit off his food. His last poo was 3 days ago, and parents think it was normal but aren’t sure.

What else would you like to know?

What would you look for on examination?
How would you treat Billy?

When should he be seen again?

What is your next step if he doesn’t respond to your treatment?

Red flags – make sure learners have thought to exclude red flags in their history and examination. These include:

  • History of delay more than 48hours in passing meconium
  • Ribbon stools
  • Faltering growth
  • Abdominal distension and vomiting
  • Abnormal anatomical appearance of the anus
  • Severe abdominal distension
  • Abnormal motor development
  • Abnormal gluteal muscles or sacrum
  • Spine or limb deformity (including talipes)
  • Abnormal power, tone or reflexes
  • Safeguarding concerns
  • Ensure external examination of anus for haemorrhoids/fissures that may need treatment 
  • Treatment – assess Billy for signs of impaction and start disimpaction regime if indicated. Discuss non pharmacological treatments.
  • Counselling – prepare parents for duration of treatment, possible side effects and importance of adherence
  • Follow up – prompt and regular follow up, tailored to the families needs
  • Treatment failure – discuss reasons for treatment failure, methods to tackle common problems
  • Red flags
  • Not responding to treatment after 3 months (thyroid, coeliac, allergy) 
  • Failure to thrive
  • Safeguarding concerns

Jakob is a  9 day old baby boy who is brought to the emergency department with vomiting. He is mum’s 3rd baby. Mum is worried that he is vomiting everything he drinks, and is sleepier than she would expect. He seems distressed when awake. He is having 3-4 light wet nappies per day but has only passed a few small stools in his short life.

What else would you like to know? 

What would you look for on physical exam?

Would you order any investigations?

What is your initial management?

  • Red flags on history – delayed passage of meconium and bilious vomiting
  • Examination- look for abdominal distention, careful examination of external genitalia and anus. Document weight and weight loss.
  • Discussion of PR examination – should only be performed by experienced practitioner. May result in forceful expulsion of gas/stool (highly suggestive of Hirschsprung’s). 
  • Investigations – order in consultation with surgical team. Consider abdominal XR to assess for obstruction but keep in mind the surgical team will likely perform contrast study. Rectal biopsy (under surgeons) for definitive diagnosis. 
  • Initial management – resuscitation. NG tube and IV fluids, correction of any electrolyte abnormalities. Look for signs of sepsis (enterocolitis).

Lily is an 8 year old girl with Trisomy 21. She had an AVSD repair as an infant, and is otherwise well and takes no medications. She has been referred to A&E by her GP with worsening constipation. She has been constipated on and off for most of her life, but this has usually been easily managed with movicol. This time around, she has been constipated for 3-4 months and is passing painful, hard stools approximately once per week. Her GP started her on movicol 3 months ago, which parents say she has been happily taking but it doesn’t seem to be working. 

What else would you like to know?

What investigations would you order?

What do you think might be going on?

How would you treat Lily?

T21 and constipation. Constipation is very common in Trisomy 21. Most often it is not due to an underlying disease, but a combination of low muscle tone, decreased mobility and/or a restricted diet. However, T21 is associated with an increased risk of autoimmune disease, including thyroid dysfunction, diabetes and coeliac disease – all of which might cause constipation.

Investigations can be done in an outpatient setting, in this scenario should be followed up by a community paediatrician. Screen for all of the above.

Laxative treatment is unlikely to be entirely effective until the underlying problem is corrected. However, depending on the severity of symptoms treatment escalation is appropriate. Lily doesn’t have any symptoms if impaction, but it may be worth escalating her movicol dose or considering the addition of a stimulant laxative whilst awaiting test results.

Advanced Case 2 (20 minutes)

Georgie is a 12 year old girl with severe autism. She is non verbal. She is otherwise well, but has had trouble with constipation in the past. Her parents attribute this to her being a “picky eater”. Georgie has had abdominal pain for the last 2 weeks, and has been passing small, pellet – like stools every 4-5 days. She has been having more “accidents”, and has been back in nappies for the last 7 days. She has been seen by the GP who has diagnosed constipation and prescribed movicol. She took this as prescribed for the first couple of days, but she is now refusing her medications. Over the past 4 or 5 days, Georgie has begun to refuse all food and will only drink sips of juice with a lot of encouragement. When parents try to give her medications or take her to the toilet, Georgie becomes very upset and aggressive. Her parents are very distressed and not sure what to do.

What are your management options for Georgie? 

Children on the autistic spectrum are more likely to have problems with constipation. Often this is due to a restricted diet, but may also be due to increased levels of anxiety around toileting.

  • Georgie requires disimpaction and this is not being achieved despite the best efforts of the family. There is no right approach to this scenario. Options include
    • Optimise setting and motivators for toileting
    • Change/optimise medications – try mixing movicol into juice, try changing to lactulose, add stimulant laxative
    • Admission for washout – nasogastric tube for washout +/- enema. Strongly consider sedation
    • General anaesthetic for manual disimpaction + washout
  • Support parents and empower them in decision making process
  • Involve multidisciplinary team – community supports will be important on discharge

Macrogol laxatives may cause “lazy bowel” if used for more than 2 months. True or false?

The correct answer is false.

There is some evidence of patients developing dependence on stimulant laxatives if used long term. However, macrogols are safe to use indefinitely without complication.

Which of the following is NOT supportive of a diagnosis of idiopathic constipation?

A: Loss of appetite

B: Ribbon like stools 

C: Urinary incontinence

D: Faecal incontinence

The correct answer is B.

Ribbon like stools suggest an anorectal malformation, and any history of this warrants further investigation. Loss of appetite, urinary and faecal incontinence can all be the result of constipation or faecal impaction. 

In a child with abdominal pain, the diagnosis of UTI makes constipation less likely. True or false?

The correct answer is false.

Constipation can lead to urinary retention and UTI, and as such the two can, and often do, co-exist.  A positive urine dip or culture doesn’t rule out constipation as a cause of abdominal pain. Don’t forget to think about constipation in the child with a history of recurrent UTI. 

National Institute for Health and Care Excellence. Constipation in children and young people. London: NICE, 2014. Available at www.nice.org.uk/guidance/qs62 

The Royal Children’s Hospital. Clinical practice guideline on constipation. Melbourne: RCH, 2017. Available at www.rch.org.au/clinicalguide/guideline_index/Constipation

Zeevenhooven J, Koppen IJ, Benninga MA. The new Rome IV criteria for functional gastrointestinal disorders in infants and toddlers. Pediatr Gastroenterol Hepatol Nutr 2017;20(1):1–13.

Sampaio C, Sousa AS, Fraga LGA, Veiga ML, Netto JMB, Barroso Jr U. Constipation and lower urinary tract dysfunction in children and adolescents: a population-based study. Frontiers in pediatrics 2016;4:101.

Youssef NN, et al. Dose response of PEG 3350 for the treatment of childhood fecal impaction. Journal of Pediatrics. 2002;141(3):410-4



Please download our Facilitator and Learner guides

Top 5 Papers in PEM

Cite this article as:
Tessa Davis. Top 5 Papers in PEM, Don't Forget the Bubbles, 2019. Available at:
https://doi.org/10.31440/DFTB.18476

This post is based on a talk I presented at the RCEM Spring Conference in April 2019 – Top 5 papers in PEM.

Kylie and Jason are enjoying their time at home with their first baby. The highs of being new parents is at its peak and true sleep deprivation is yet to set in. Jayden is two weeks old and is simply perfect. They spend hours staring at him each day marvelling at the perfect human they have created. 

As we follow Jayden through his journey to adulthood, we’ll encounter some common paediatric problems. The 5.5 papers I have chosen were selected because: they cover common presentations; they use large patients groups; and they were conducted by well-respected and highly regarded research groups. But back to our story…

 One night Jayden seems a bit more unsettled than normal. When they check his temperature it’s 38.4. They get in the car and bring Jayden to ED

 Febrile neonates are a huge source of concern – we know that they can deteriorate quickly and we usually err on the side of caution by doing a full septic screen, IV antibiotics, and admission. Actually many of these babies don’t have a serious bacterial infection. Is there a way to tell which ones do?

When you see Jayden in your ED, you ask yourself is…should I do a full septic screen?

Paper 1 - Kupperman et al, 2019, A clinical prediction rule to identify febrile infants 60 days and younger at low risk for serious bacterial infections, JAMA Pediatrics


This paper aimed to derive and validate a highly accurate prediction rule to identify infant at low risk of SBI. The patients were febrile infants 60 days and younger (who had a rectal temp of >38 in the ED or a fever at home within the preceding 24 hours)

They excluded those who were critically ill, who had antibiotics in the preceding 48 hours, those born premature, and those with other medical conditions.

There were 1821 febrile infants included.

The authors considered clinical suspicion of SBI. They then look at various markers: blood culture; urine culture and urinalysis; CSF; FBC; and procalcitonin levels. The outcomes  considered were serious bacterial infection – that is bacterial meningitis, bacteraemia, or urinary tract infection.

Overall, the rates of SBI in this group was 9%. The authors formulated a rule with a very high sensitivity (97.7%) for identifying those at low risk of serious bacterial infection. They were low risk if they fulfilled three criteria:

  • negative urinalysis
  • neutrophil count of less than 4/mm3 
  • procalcitonin of less than 0.5ng/ml

61.3% of their patient group were low risk.

Interestingly their low risk rule does not include use of  lumbar puncture67.4% of the low risk group had a lumbar puncture that would not have been necessary.

Key take away: There may be some febrile neonates that are low risk, and therefore we could avoid a lumbar puncture and full work up. In practical terms, this is unlikely to change our practice at the moment. Many of us cannot send a procalcitonin in the ED, and we might have to wait several hours to get a neutrophil count back. However this does bode well for the future in identifying which of these well febrile neonates are low risk.

Jayden does get a full septic screen. He has IV antibiotics for 48 hours and remains well. His blood cultures are negative so his antibiotics are stopped and he is discharged.

FLASH FORWARD…

 

 

Jayden is growing well. At 7 months of age, he is looking great and developmentally normal. Dad, Jason, smokes, but reassures you that he never does so in the house. Jayden develops a cough and two days later starts breathing very quickly and noisily. They head to the emergency department.

Jayden has bronchiolitis. This is very common and your departments and wards have no doubt been filled with these children over the winter. We know that little works with these children. So you force yourself to hold back the ‘trial of salbutamol’ because it won’t make any difference.. But high flow does seem to be the one thing (along with oxygen) that might make a difference.

You ask yourself the question...should I start high flow?

Paper 2 - Franklin et al, A Randomized Trial of High-Flow Oxygen Therapy in Infants with Bronchiolitis. NEJM. 2018. 378(12):1121-1131

This study looks at infants under 12 months old with a clinical diagnosis of bronchiolitis and a need for supplemental oxygen. 1472 were included (after exclusions). Patients were excluded if: they had an alternative diagnosis; they had cyanotic heart disease; or they were on home oxygen.

Patients were randomised to either high flow or low flow. The high flow group were given heated humidified high flow oxygen – 2L/kg/min via Optiflow. The oxygen was then weaned to achieve target saturations, and they were taken off high flow once they had been on air for four hours. The low flow group were given wall oxygen via nasal cannulae at 2L/min max.

The outcome  was escalation of care. This meant who in the low flow group was escalated to high flow, and who in the high flow group was escalated to BiPAP or was intubated. Treatment failure was based on: an increase in heart rate; if the respiratory rate increased or didn’t drop; if they were needing oxygen in >2L/min of flow or >0.4 FiO2 to maintain their saturations; or if they achieve a high early warning score. Clinicians could also escalate care themselves (34% were escalated in this way).

Escalation of care occurred much more commonly in the low flow group – with 12% being escalated in the high flow group and 23% in the low flow group.

 

Interestingly there was no difference in the length of stay between the two groups.

Key take away: High flow does reduce the need for escalation. Escalation itself is significant – it requires increased nursing attention for low flow patients while they are transferred onto Optiflow.  There may be less medical staffing on the wards if the child deteriorates on high flow overnight. Although they aren’t comparing like with like, escalation itself is an important clinical event. They also demonstrated that high flow does not increase the number of adverse events (for example there was no difference in the number of pneumothoraces between the groups). High flow is safe to use and we should consider starting it early in ED.

You start Jayden on high flow in ED and he stabilises. 12 hours later he is weaned off on the ward and is discharged the following day.

FLASH FORWARD…

Jayden is now a healthy 3 year old boy. He loves Paw Patrol.  He hates vegetables and won’t eat any food that is the colour green or yellow. Kylie and Jason are expecting their next child, and Jason has finally quit smoking. Unfortunately Jayden is prone to wheezy episodes and now has his very own inhaler which he hates using. The change in weather in London, from quite cold to…colder, seems to have triggered something and he’s now pretty wheezy and short of breath. They head into their favourite emergency department.

 Jayden is now firmly in the realm of viral-induced wheeze. Yes, it’s all on a spectrum, but he’s now 3 years old with an inhaler. You asses him and think he should have a salbutamol burst.

As you are writing the salbutamol up, your SHO asks  you – should I give him steroids?

Paper 3 - Foster SJ, Cooper MN, Oosterhof S, Borland ML. Oral prednisolone in preschool children with virus-associated wheeze: a prospective, randomised, double-blind, placebo-controlled trial. The Lancet Respiratory Medicine. 2018 Jan 17.

 This paper aimed to assess the efficacy of oral prednisolone in children presenting to an ED with viral wheeze.

The patients included were 2-6 years old. They were excluded if: saturations were less than 92% in air; they had a silent chest; they had sepsis; there was a previous PICU admission for wheeze; they had prematurity; or they had recently had steroids.

605 patients were included and they were randomised to receive either prednisolone or placebo. The prednisolone group received 1mg/kg prednisolone once a day for three days. The placebo group received a placebo medication (matched for volume and taste to prednisolone) once a day for three days.

Patients were assessed for their wheeze severity using a validated pulmonary score.

The outcome measures were length of stay (until clinically fit for discharge). They also considered re-attendance, readmission, salbutamol usage, and residual symptoms.

The results are tricky to interpret. Those who were discharged from ED within four hours did not benefit from prednisolone. However there may be some benefit in the mild to moderate wheeze group, and some in those who used salbutamol at home prior to presenting to ED. Interestingly this paper did not support our previously held belief that those children with atopy respond better to prednisolone.

 Key take homes: Some pre-schoolers are steroid responsive, but identifying which ones is a challenge. As Damian Roland discusses here, it is likely that we are seeing lots of children presenting with the same symptoms (wheeze) but with different pathology behind it. Once we can identify the pathology we can start to target specific groups of patients with management that works.

You decided not to give Jayden prednisolone and after his salbutamol burst he stretches to 4 hours and is discharged home.

FLASH FORWARD…

Jayden is 5 years old and in his excitement of building the new Hogwarts Lego castle he accidentally swallows a Lego head. Kylie and Jason aren’t sure whether to worry or not? So they take him into ED.

Children ingesting random objects is a common presentation to ED.

When you see Jayden in the department, his parents ask you…should I search through his poo?

Paper 3.5 - Tagg, A. , Roland, D. , Leo, G. S.Y., Knight, K. , Goldstein, H. , Davis, T. , DFTB, (2018), Everything is awesome: Don’t forget the Lego. J Paediatr Child Health. doi:10.1111/jpc.14309

Myself and 5 of my fearless, and brave, paediatric colleagues swallowed a Lego head each to see how quickly it passed. The paper was generously published in the Journal of Paediatrics and Child Health.

To ensure serious scientific rigour, we put together some scoring systems.

The Stool Hardness and Transit time (the SHAT score) took into account how hard our stools were, and whether that impacted (no pun intended) on the time to retrieve the Lego head.

And out main outcome was the Found And Retrieved Time (the FART score). This was the time to get our Lego heads back, and the average FART score was 1.71 days.

Unfortunately one of the six of us didn’t find his Lego head. After valiantly searching through his own faeces for two weeks, he gave up. And it may still be up there.

Key take home: Don’t search through poo, it’s gross.

Jayden heads home happily to finish building his Lego Castle.

FLASH FORWARD.

Jayden is 6 years old. He thinks Paw Patrol is for losers. Fortunately he still loves Lego and Harry Potter. He also enjoys climbing. Unfortunately, two days ago he fell off the ladder coming down from his bunk bed. He seemed okay at the time, and Kylie and Jason had other plans that evening, so they decided to keep him at home. Now, two days later, he has a massive egg on his head and has been complaining of a headache. He also vomited yesterday. They bring him to ED.

 

We have fabulous head injury guidance for kids thanks to PECARN, CHALICE, and CATCH. But actually PECARN and CATCH specifically exclude injuries more than 24 hours old, and CHALICE doesn’t publish data on this group. So, for Jayden you need to put the NICE guideline away because it doesn’t apply. This is a common grey area.

The question you ask is….should I scan his head?

Paper 4 - Borland M, Dalziel SR, Phillips N, Lyttle M, Bressan S, Oakley E, Hearps SJC, Kochar A, Furyk J, Cheek J, Neutze J, Gilhotra Y, Dalton S, Babl F. Delayed Presentations to Emergency Departments of Children With Head Injury: A PREDICT Study, Annals of Emergency Medicine, DOI: https://doi.org/10.1016/j.annemergmed.2018.11.035

This paper aimed to establish the prevalence of traumatic brain injuries in children presenting more than 24 hours after the head injury.

Traumatic brain injury (TBI) was defined as: intracranial haemorrhage; contusion; cerebral oedema; diffuse axonal injury; traumatic infarction; shearing injury; or a sigmoid sinus thrombosis.

The also looked a clinically significant traumatic brain injury (cTBI) – this included death, intubation for more than 24 hours, neurosurgery, or admission for 2 or more nights to hospital.

The patients were from the Australian Paediatric Head Injury Study Cohort which was 20,137 patients. 5% of these presented over 24 hours after the injury. 981 children were included in this study.

The authors considered the injury characteristics and demographics, trying to find an association between mechanism and delay in presentation. Those presenting were more likely to have: a non-frontal scalp haematoma; headache; vomiting; and assault with NAI concern. Those with loss of consciousness and amnesia were more likely to have presented within the first 24 hours.

The CT rates were much higher in the late presentation group – 20.6% being scanned in the delayed group and only 7.9% in the early group. This probably reflects the lack of evidence in this area, and therefore we feel safer doing more scans.

But the rates of TBI also varied. 3.8% in the delayed presentation group had a TBI, whereas only 1.2% in the early presentation group did.

The rates cTBI were the same between the groups at 0.8%

Key take homes: There is an increased risk of TBI when presenting more than 24 hours after a head injury injury. The authors found that risk is increased if the patient has a non-frontal scalp haematoma or a suspicion of a depressed skull fracture.

You decide to scan Jayden’s head, but it turns out to be normal and he is discharged home.

FLASH FORWARD… 

Jayden is 8. He’s been drinking a LOT of water over the last few weeks and seems to be weeing constantly. His clothes seem a bit big for him too. He looks so bad one day (and has vomiting and abdominal pain) that Jason finally reneges and takes him into ED.

Jayden has DKA. The debate about over-zealous fluid administrations and its relationship to the dreaded cerebral oedema is long-standing. Previous research suggested a link but only by association, not causality.

You ask yourself…how fast should I give IV fluids?

Paper 5 - Kupperman et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis NEJM 2018 vol 378 (24) pp 2275-2287

The study examines the causal effect between fluid resuscitation and cerebral oedema.

They included 1389 episodes of DKA. Exclusions were mainly due to too much management prior to contact with the study team, as well as children with a GCS<12. The median age was 11. It should be noted that the very young and the very sick are probably lost in this cohort.

Patients were randomised to received either fast or slow rehydration, and then were split again into received either 0.9% NaCl or 0.45% NaCl.

The fast rehydration group received 20ml/kg bolus and then replacement of 10% deficit, half over 12 hours and rest over next 24 hours. The slow rehydration group received a 10ml/kg bolus and then replacement of 5% deficit over 48 hours. Maintenance fluids and insulin were given in addition.

The outcomes looked at were deterioration of neurological status within first 24 hours of treatment. They also assessed short term memory during treatment, and IQ 2-6 months after the episode of DKA.

In short, they found no difference between the groups. There was a 0.9% rate of brain injury overall and it didn’t matter which type of fluids or how fast. Patients were more likely to get hyperchloraemic acidosis in the 0.9% NaCl group but this is of debatable clinical significance.

Key take homes: The evidence does not support our traditionally cautious approach to DKA. The speed of IV fluids does not seem to be the cause of brain injury in DKA.

You resuscitate Jayden and send him off to the ward. He is discharged a few days later with good support from the Endocrine team for management of his diabetes.

FLASH FORWARD…

Jayden is now 16 years old and next time he comes to ED, he’ll be in the harsh world of Adult ED. We have navigated him through his common childhood presentations to ED and answered the key questions we ask ourselves every day in the Paeds ED.

 

Should I do a full septic screen on this hot baby?

Should I start high flow on this infant with bronchiolitis?

Should I give prednisolone to this 2 year old with wheeze?

Should I scan this child with a head injury?

How fast should I give fluids to my DKA?

And most importantly, do I ever need to sift through my child’s poo, or my own ever again?

Don’t Forget The Lego

Cite this article as:
Team DFTB. Don’t Forget The Lego, Don't Forget the Bubbles, 2018. Available at:
https://doi.org/10.31440/DFTB.17375

It might have escaped your notice but the team at DFTB recently had a paper published by the Journal of Paediatrics and Child Health that has garnered a lot of interest.

Tagg, A. , Roland, D. , Leo, G. S.Y., Knight, K. , Goldstein, H. , Davis, T. , DFTB, (2018), Everything is awesome: Don’t forget the Lego. J Paediatr Child Health. doi:10.1111/jpc.14309

We are sure you have questions. Lots of questions. So we thought we should answer them for you in the best way we know how.

What pressing scientific question did you ask?

We know that coins are the most commonly swallowed foreign object in the paediatric population and there is a lot of data surrounding transit time. The second most commonly swallowed objects are small toys but there is very little data out there. We wanted to know how long it would take for a small piece of plastic toy, in this case a Lego head, to pass through.

How on earth did you come up with the idea?

In one of our regular editorial meetings we were discussing some of our upcoming publications and musing how we could do something a little lighter, akin to the great Peppa Pig paper in last years Christmas BMJ. And then Andy Tagg said, “I’ve got this idea but you might think it a bit strange.” Within a short space of time we had an international team of researchers literally chomping at the bit to undertake the study.

Did you really swallow those poor heads?

Of course we did! Do you want proof?

Then what happened?

We waited to see what would happen. We all know corn kernels can whip through the colon in seemingly no time at all, but what about a little yellow piece of plastic? There was really only one way to find out.

And you searched through your own poo to find them? How?

As with any piece of research it is important to have a robust search strategy in place prior to commencement. A variety of techniques were tried – using a bag and squashing, tongue depressors and gloves, chopsticks – no turd was left unturned. And although we only used a very small sample size the fact that one of our heads went missing suggest that you really shouldn’t worry if you can’t find it.

What happened to the missing head?

Who knows? Perhaps one day many years from now, a gastroenterologist performing a colonoscopy will find it staring back at him.

But what about Ben Lawton? Where was he when all this was going on?

Don’t Forget the Bubbles was founded by four curious doctors – Tessa Davis, Andy Tagg, Henry Goldstein and Ben Lawton. Unfortunately Ben was travelling at the time we undertook the study and we didn’t think searching through his colonic contents in an aeroplane toilet was exactly fair.

And then you kept it quiet, right?

It can take an average of 17 years for science to go from benchside to bedside. Leveraging social media we managed to go from online publication on a Thursday evening to global saturation by Saturday evening.

By Saturday morning Damian Roland was speaking on Canadian radio and the DFTB group made Forbes, ars technica, and the BBC World Service by the afternoon.

But surely this isn’t hard science?

Of course it’s not, it’s a bit of fun in the run up to Xmas.

With such a small sample size it is important that you don’t extrapolate the data to the entire population of Lego swallowers. Anecdata from Twitter suggests that a large number of people accidentally ingested bits of Lego throughout their life with no adverse effects*.

It is also worth noting that most people who swallow Lego are children, not fully grown adults. Data that is applicable to the adult population may well not be applicable to children.

For a more scientific approach to ingested foreign bodies in children then take a look at these two papers.

Yeh HY, Chao HC, Chen SY, Chen CC, Lai MW. Analysis of Radiopaque Gastrointestinal Foreign Bodies Expelled by Spontaneous Passage in Children: A 15-Year Single-Center Study. Frontiers in pediatrics. 2018;6:172.

Macgregor D, Ferguson J. Foreign body ingestion in children: an audit of transit time. Emergency Medicine Journal. 1998 Nov 1;15(6):371-3.

You may also enjoy exploring the following posts about foreign bodies on DFTB:

Andy’s blog post on Foreign Body Ingestion

Chantal McGrath’s DFTB17 talk Batteries Not Included on button battery ingestion

A case study by Loren on ‘the magic coin’ 

What’s next for the group?

Whilst this may be the pinnacle of our publishing careers we hope we have not peaked too early. Next up is finalizing all the details for our upcoming conference in London – www.dftb19.com, and then? Who knows?

*Please do not try this at home.

DFTB in the papers

Ars Technica

Forbes

BBC World Service

CBC Radio Canada – As it happens

10 Daily

Herald Sun

FPIES

Cite this article as:
Clementine David. FPIES, Don't Forget the Bubbles, 2018. Available at:
https://doi.org/10.31440/DFTB.16444

A 6-month-old male is brought to ED by his mother with multiple episodes of profuse vomiting after eating lunch. No diarrhoea, fevers or unwell contacts. He is usually a well child and had a normal neonatal period.

He is immunised and otherwise thriving from a growth and developmental perspective. The mother, a nurse, reports that the infant was mottled, pale and lethargic at home but began to pick up whilst being triaged in ED.

Gastroesophageal Reflux Disease

Cite this article as:
Li-Zsa Tan. Gastroesophageal Reflux Disease, Don't Forget the Bubbles, 2016. Available at:
https://doi.org/10.31440/DFTB.2754

A 5-month-old infant is brought into the Emergency Department by her parents because they feel she has been persistently irritable and back arching after feeds for the last month. They have looked up ‘infant reflux’ on the internet, but upright positioning and changing formulas several times has not made any difference. They are now intensely sleep-deprived and are keen for something to be done for her.

Examination reveals a cheerful baby girl with no signs of being unwell or irritable. She is gaining weight according to her centiles and is developmentally appropriate for age.

Bottom Line

  • Gastroesophageal reflux is a physiological phenomenon
  • Gastroesophageal reflux disease is when the child is symptomatic and results in complications such as poor weight gain
  • 67% of healthy infants have some form of reflux at 4 months of age
  • It is important to consider factors which may worsen reflux or contribute to reflux disease, such as hiatus hernia or eosinophilic esophagitis
  • Most infants will improve on transitioning to solids

What is gastroesophageal reflux disease?

Gastroesophageal reflux (GER) is a physiological phenomenon.  It is defined as the retrograde passage of gastric contents into the esophagus and is a normal physiological phenomenon that occurs in healthy children several times a day after meals and lasts <3 minutes. Reflux disease (GERD) occurs when it results in symptoms and complications.

Regurgitation is the passage of refluxed contents into the mouth. Vomiting is the expulsion of said contents from the mouth.

Primary GER results from a primary disorder of the upper GI tract.

Factors which influence incidence of GOR include: mastication, saliva secretion; swallowing; esophageal clearance; esophageal innervation and receptors; mucosal resistance; LES pressure and relaxation; abdominal esophagus; sphincter position; angle of His; gastric volume and accommodation; gastric emptying; gastric acid output; gastric acid feed buffering; feeding regimen: type frequency and volume; pepsin/trypsin/ bile salts; H. Pylori; intra abdominal pressure; genetic factors; environmental factors; posture; physical activity; sleep state; respiratory disease; medications.

Sometimes GER is protective: e.g. when the stomach is overdistended after a meal GER decompresses it.

Which mechanisms are in place to prevent or limit GERD?

The first line of defense against GERD is the lower esophageal sphincter (LES), and the diaphragmatic pinchcock and angle of His which physically limits the frequency and volume of gastric contents refluxing into the esophagus.

The second defense is esophageal clearance, when gravity and peristalsis remove the contents from the esophagus and secretions serve to neutralise the acid.

The third defence is the esophageal mucosal defence against luminal acid.

How does the LES work?

The LES is an extension of the circular muscle of the esophagus. The anti-reflux barrier consists of the LES and the crural portion of the diaphragm. The esophagogastric angle (or the angle of His) is the angle between the esophagus and the greater curvature of the stomach and is normally acute. It is a functional barrier, and its intraluminal pressure is greater than that of the stomach and esophagus. In adults, it is 3-6 cm long and has a pressure of 20 mmHg. (range 10-40 mmHg). An absolute pressure of <6 mmHg is required for GER.  In infants, the length is only a few millimeters. The LES relaxes 2.5 secs after the initiation of a swallow, and remains open during 10-12 secs until the food bolus passes through. LES pressure is decreased postprandially, and is also decreased by among others: the presence of fat in the duodenum, progesterone, cholecystokinin, glucagon, estrogen, nitric oxide, dopamine, nicotine, alcohol, mint and chocolate.

Most physiologic reflux episodes occur in relation to Transient LES Relaxations  (TLESRs) or when the LES tone adapts inadequately to changes in intra-abdominal pressure. TLESRs are induced by gastric distension and incomplete swallowing (normal mechanism for burping and belching). The larger the meal the more TLESRs, the more reflux episodes! Higher intragastric osmolarity and greater gastric secretory volume also contribute towards more TLESRs which may contribute to the efficacy of Proton Pump Inhibitors and H2 receptor antagonists in decreasing secretory gastric volume and reducing TLESRs.

The angle of His is usually acute. When the angle is obtuse, such as in hiatal hernias, this favors GER episodes

How does esophageal clearance help in reflux episodes?

This is influenced by peristaltic waves, gravity and saliva. Swallowed saliva contributes towards neutralising the pH of the refluxed acid. Swallowing itself stimulates antegrade peristalsis which clears the esophageal contents.

Esophageal mucosal resistance against injury to acid consists of:

  • Pre-epithelial: mucous layer, surface bicarbonate ion concentration, unstirred water layer
  • Epithelial defense: The esophagus is lined by moist, partially keratinized stratified squamous epithelium. Tight junctions act as a barrier to molecules passing from lumen to blood.

What are the symptoms of GERD?

GERD can range from minor symptoms such as regurgitation, heartburn and epigastric pain to more complicated disease such as erosive esophagitis or esophageal stricture. Hiatal hernia is the only endoscopic observation that predicts erosive esophagitis.

Reflux disease may also cause respiratory symptoms through micro aspiration. This may manifest as apneas, chronic coughs or chest infections, particularly in neurologically compromised infants.

How common is reflux or regurgitation in normal children?

In healthy infants, the prevalence of regurgitation has been reported at 50% at age 0-3 months, 67% at 4 months then declining to <5% by 10-12 months.  In a study of 509 healthy infants aged 0-11 months, as many as 73 physiologic reflux episodes per day was normal.

How do we investigate GERD?

pH monitoring

Intraluminal pH monitoring measures the frequency and duration of acid esophageal reflux episodes. A drop in intraesophageal pH <4.0 is considered an acid reflux episodes.

pH monitoring has limitations because of its inability to detect nonacidic bolus movement into the esophagus in particular in infants who are fed milk. This is problematic when evaluating reflux as a contributing factor towards respiratory disease in infants. Studies showed that in infants with apparent life-threatening events or apnea, 48% were nonacid. In a study of preterm infants with apnea, Magista et al found that 76% of reflux events were only weakly acidic (4

Impedence technique

Multichannel intraluminal impedance (MII) detects GER episodes based on changes in electrical resistance to the flow of an electrical current between 2 electrodes placed on the MII probe when a liquid, semisolid, or gas bolus moves between them. The combined pH and impedance monitoring are therefore able to detect reflux regardless of pH and provide symptom correlation with parental reports.

Endoscopy

Upper GI endoscopy can also be performed to look for esophagitis (macroscopic and histological changes) and gastritis. As this involves a general anaesthetic in children and has its own risks and complications, endoscopy is not usually a first line investigation for simple suspected reflux disease.

What are the pharmacological options to treat reflux disease?

Proton Pump Inhibitors are the most potent inhibitors of gastric acid secretion, and are superior to H2 Rreceptor antagonistis in healing esophagitis and maintaining remission.

What about other approaches?

There is no clear evidence that upright positioning post feeds helps limit reflux episodes in infants. In fact GER seems to occur most in seated upright position! Changing formulas or from breastfeeding to bottle feeding also does not appear to have an effect on reflux disease.

Thickening feeds under the supervision by a dietician may be useful.

It is important to rule out contributing factors such as concurrent infection in infants, congenital abnormalities such as a hiatus hernia and eosinophilic esophagitis and H pylori infection in older children.

Transitioning to solids usually marks clinical improvement in symptoms.

References

Vandenplas Y, Hasall E. Mechanisms of Gastroesophageal Reflux and Gastroesophageal Reflux Disease. Journal of Pediatric Gastroenterology and Nutrition 2006; 35: 119-136.

Colletti R, Di Lorenzo C. Overview of Pediatric Gastroesophageal Reflux Disease and Proton Pump Inhibitor Therapy. Journal of Pediatric Gastroenterology and Nutrition 2003; 37: S7 – S11.

Mousa HM, Rosen R, Woodley FW, Orsi M, Armas D, Faure C, Fortunato J, O’Connor J, Skags B, Nurko S. Esophageal Impedance Monitoring for Gastroesophageal Reflux. Journal of Pediatric Gastroenterology and Nutrition 2011;52:129 – 139

Upper GI Bleed

Cite this article as:
Li-Zsa Tan. Upper GI Bleed, Don't Forget the Bubbles, 2016. Available at:
https://doi.org/10.31440/DFTB.3205

A 7 year old boy is referred from a peripheral hospital for a 2 day history of passing black tarry stool. On the 3rd day he passes loose stools mixed with dark maroon blood clots. For the last week he had been having upper respiratory tract symptoms and had daily doses of ibuprofen for his low grade fever.

Biliary atresia

Cite this article as:
Li-Zsa Tan. Biliary atresia, Don't Forget the Bubbles, 2016. Available at:
https://doi.org/10.31440/DFTB.3555

A 5 week old infant is seen for the first time at the paediatrics outpatient’s clinic with jaundice. The baby boy was being followed up by his GP for jaundice since the age of 6 days. As he was otherwise a well child, his mother was assured that the jaundice was likely related to breastfeeding. His GP grew concerned when his jaundice persisted and performed a formal serum bilirubin when he was 4 weeks old, which showed that he had a predominantly conjugated hyperbilirubinaemia. After his thyroid function tests returned as normal and a urinary tract infection was excluded, he was referred to a tertiary hospital for further evaluation. Radioisotope excretion studies showed good hepatic uptake but absent excretion into the intestine within 24 hours.

Bottom Line

Any infant with jaundice lasting more than 14 days must have a formal serum bilirubin checked with conjugated/unconjugated differentials

Pale stools may not easily be identifiable and so may provide false reassurance

The most important prognostic factor for a Kasai portoenterostomy is age. The older the patient at the time of surgery, the less successful the outcome

What is biliary atresia?

Extrahepatic biliary atresia is a destructive inflammatory obliterative cholangiopathy which affects both intra and extra hepatic ducts with progressive destruction leading to cholestasis, fibrosis and cirrhosis.

The disease is classified according to the most proximal biliary obstruction:

Type 1 (~ 5%):         Patency to the level of the common bile duct and proximal cystic duct

Type 2 (~ 2%):         Patency to the level of the common hepatic duct

Type 3 (> 90%):      The entire extra hepatic biliary tree is non patent [/toggle]

How common is it?

In UK and France, the prevalence is 1 in 17000 -19000 livebirths.

In east Asian countries it is much more common, with the frequency in Taiwan being quoted at 1 in 5000.

What else is associated with biliary atresia?

Biliary atresia is associated with other congenital malformations in up to 20% of cases. The most common of these is the biliary atresia splenic malformation syndrome, (10% in Europe and the US).

CharacteristicsEstimated frequency
Pancreatic anomalies11%
Cardiac anomalies (VSD, ASD, HLH)45%
Absent inferior vena cava70%
Preduodenal portal vein40%
Intestinal malrotation60%
Situs inversus37%
Splenic malformation (polysplenia, asplenia)100%

Biliary atresia has also been described with other genetic disorders, for example in trisomies 18 and 21.

In 80-90% of neonates, it is an isolated finding. Thus two clinical phenotypes are described: the syndromic or embryonic forms associated with other congenital/genetic abnormalities, and the far more common perinatal or acquired form in which BA is an isolated finding.

The theory is that in the perinatal or acquired form, the obliterative process begins later in the perinatal period than it does in the syndromic form (which may begin in the embryonic phase

Any theories of pathogenesis?

The cause of biliary atresia is unknown but is likely to be multifactorial:

Genetic: Genes associated with different parts of the inflammatory pathway (e.g. CFC1, ICAM1,CD14 endotoxin receptor gene) have variable polymorphism frequency in children with biliary atresia.

Viral: Studies inoculating mice with rotavirus strains, reovirus and cytomegalovirus have resulted in jaundice and intrahepatic histology similar to biliary atresia. Liver biopsies from human patients showed 90% of infants expressed a protein linked to inflammation secondary to a viral immune response.

Immunological: It is unlikely that a direct viral cause is responsible for the pathogenesis of biliary atresia as viral particles have not been isolated in biopsies. Rather, viral infection may be the trigger to activation of the innate immune response which causes apoptosis and cell death. It is more likely that infection is a second injury to a liver which is already susceptible to damage through genetic or immunological dysregulation. Lymphocyte mediated biliary inflammation seems the most likely mechanism by which bile duct obliteration occurs but the trigger for this response is unknown.

How do patients present?

Typically biliary atresia presents in early infancy with persistent jaundice, dark urine and pale stools. A 2012 study however concluded that even experienced professionals often fail to recognize stool colour associated with biliary obstruction

How is it diagnosed?

All term infants who remain jaundiced after 14 days should have serum bilirubin levels measured with conjugated/unconjugated differentials.

Physiological and breast milk jaundice manifests as unconjugated hyperbilirubinaemia, whereas most forms of liver disease present with raised conjugated bilirubin.

Liver function tests typically show raised transaminases, especially serum gamma-glutamyltransferase.

An abdominal ultrasound is an essential basic investigation which may demonstrate an enlarged liver, and an absent or contracted gallbladder after a 4 hour fast. Biliary dilatation is not seen.

Radio isotope excretion studies scan after pretreatment with phenobarbitone 5mg/kg per day for 3-5 days will typically will show good hepatic uptake but absent or reduced excretion into the intestine within 24 hours. This result is not specific for biliary atresia however and is also found in children with Alagille’s syndrome.

Percutaneous liver biopsy is the usual diagnostic method and shows evidence of extrahepatic biliary obstruction such as portal tract fibrosis, oedema, ductular proliferation and cholestasis. Biopsies done before 6 weeks of age might not have typical features.

The gold standard for diagnosis, particularly if there is any doubt prior to a Kasai portoenterostomy, is an operative cholangiography. Other investigations include an endoscopic retrograde cholangiopancreatography or a magnetic resonance retrograde cholangiopancreatography although these are technically difficult and not widely available.

How is it managed?

i. Kasai portoenterostomy:

The entire extrahepatic biliary tree is excised so that the porta hepatis is transected at the level of the liver capsule and anastomosed to the jejunum via a Roux loop. Success is measured by clearance of jaundice and is defined as achievement of normal bilirubin concentration within 6 months of the procedure.

A Kasai is not curative, and the disease will continue to progress in 70% of children who have had a successful surgery.

The most important prognostic factor for the Kasai portoenterostomy is the patient’s age at the time of the procedure. The older the infant, the less successful the outcome.

Age at Kasai4 year survival with native liver10 year survival with native liver
>90 days23%15%
31-90 days36%25%
<30 days49%49%

Because timing is such a factor in outcome, some countries (Taiwan, Japan) are considering implementing a screening program based on stool colour cards to increase awareness of biliary atresia among parents and physicians. A 2011 study showed that stool colour card screening may be associated with a decline in late referrals.

Complications of Kasai:

Ascending cholangitis presents in the first few months post surgery and manifests as a recurrence of jaundice, acholic stool and abdominal pain. Recurrent or late cholangitis suggests an obstruction of the Roux loop.

A degree of hepatic fibrosis or cirrhosis is apparent even in children with a successful Kasai. Portal hypertension is present in most cases and has its own complications such as ascites or variceal bleeds.

Regular ultrasound scans and annual alpha feto protein levels should be part of a long term review to screen for development of malignancy secondary to cirrhosis.

ii. Liver transplantation:

Indications and timing for a liver transplant depends on the success of the Kasai portoenterostomy and the rate of complications. Infants who had failed Kasai surgeries will require transplantation within 6 months to 2 years. Children with BASM syndrome have an increased risk of early mortality and morbidity and thus the need for transplantation is greater. Living related liver transplantation is successful in Taiwan and Japan and allow for planned and timely transplantation with good reported outcomes. [/toggle]

References

Biliary Atresia. Hartley J, Davenport M, Kelly D. Lancet 2009; 374:1704-13


Current management of biliary atresia. Kelly D, Davenport M. Arch Dis Child 2007; 92:1132-35

Prolonged Neonatal Jaundice and the Diagnosis of Biliary Atresia: A single center analysis of trends in age at diagnosis and outcomes. Wadhwani S, Turmelle Y, Nagy R, Lowell J, Dillon P, Shepherd R. Pediatrics 2008; 121 (5): 1438-40

Biliary Atresia: The timing needs a changin’. Chitsaz E, Schreiber RA, Collet JP, Kaczorowski J. Canadian Journal of Public Health 2009;100(6):475-77

Stool color card screening for Biliary Atresia. Tseng J, Lai M, Lin M, Fu Y. Pediatrics 2011; 128(5) 1209

Probiotics in review

Cite this article as:
Henry Goldstein. Probiotics in review, Don't Forget the Bubbles, 2016. Available at:
https://doi.org/10.31440/DFTB.9304

Like almost every other human entering a pharmacy in the ten last years, I was offered some probiotics when I collected a prescription recently. On my walk back to the car I mused about the evidence behind the shop assistants attempted up-sale. I reminded myself of the use of probiotics to prevent necrotising enterocolitis, and was starting to think of some other indications. Some days later, this review by Hania Szajewska in the Archives of Disease in Childhood popped up; here’s a precis of an excellent paper:

Szajewska, H.What are the indications for using probiotics in children? Arch Dis Child. Published Online First: 7 September 2015

Probiotics are “live microorganisms that, when administered in adequate amounts, confer a health benefit on that host.” The most common strains used therapeutically are the lactobacillus strains L. reamnosus GG (LGG) and L. reuteri DSM 17938 as well as bifidobacterium and saccharomyces. There are also some novel probiotics in development.

Probiotic preparations differ to standard medications as the dose, viability and even agent (organism) are harder to control. There is significant industry influence and, in my opinion, therapeutic development has likely suffered at the expense of populist marketing. Research into probiotics is strain specific; with that comes the challenges of extrapolating the findings to any over-the-counter product. Specifically, probiotics are not regulated as drugs, hence significant concerns exist with respect to labelling and quality.

In this paper, Szajewska reviews the evidence for a number of paediatric indications for probiotics. I’ve simplified and summarised the findings here;

What do we think works?

Necrotising enterocolitis – Multiple RCTs and a Cochrane review, mostly using L. reuteri DSM 17938 show a reduction in NEC in preterm infants. Additionally, there was a reduced time to full feeds, reduced admission length and reduced rates of late-onset sepsis.

Antibiotic associated diarrhoea – Szajewska references her own meta analysis – albeit primarily an adult population – which identified a NNT of 13 for antibiotic associated diarrhoea; the database is predominantly adults. Most effective probiotic agents for this indication are saccharomyces boulardii and LGG.

Infantile colicL. reuteri DSM 17938 was assessed in 4 RCTs; their combined results showed that the use of reduced crying times in breastfed infants with infantile colic. In one analysis (3 trials), L. reuteri DSM 17938 vs placebo reduced crying times at 21 days of life by an average of 43 minutes/day. Probiotics appear more helpful in breastfed by comparison to formula fed infants.

Functional abdominal pain – A meta analysis of LGG for a range of abdominal pain-related functional gastrointestinal disorders (FGDs) showed that LGG was significantly better than placebo in this population, with a NNT = 7. Szajewska doesn’t appear to have much faith in these results with respect to FGDs as a whole, but notes that patients with Irritable bowel syndrome showed the most benefit (NNT = 4).

Acute gastroenteritis – ESPGHAN (the European Society for Paediatric Gastroenterology, Hepatology & Nutrition) recommend consideration of probiotics (LGG > S. boulardii > L. reuteri DSM 17938) for children with acute gastroenteritis, in addition to hydration therapy.

What might work?

Nosocomial infection – The review considers a number of nosocomial infections, and briefly mentions the importance of rotavirus immunisation, where available. A handful of trials showed that probiotics (LGG) vs placebo had no significant differences for risk of post-admission diarrhoea in children under 2 years old; the results contradict some earlier trials in this area, which showed promise.

Prevention of allergy – This is controversial – two studies published by opposing peak bodies disagree. This includes maternal probiotics to reduce long-term outcomes.

H.Pylori – May improve eradication rate, but limited evidence in children.

IBD – Some evidence for inducing remission of Ulcerative colitis; insufficient evidence in Crohn’s disease. 

What doesn’t work?


Functional constipation – no evidence of benefit; not recommended via ESPGHAN 

Within the review, two positive studies jumped out at me, so I went back to the primary literature for a deeper dive.

Firstly, I was fascinated by the idea of preventing infections in daycare centres – Szajewska’s overall verdict was that there was not currently sufficient evidence, but that LGG and L. reuteri DSM 17938 may have some effect on community-acquired infections. Particularly, the review describes this study;

Gutierrez-Castrellon, P., Lopez-Velazquez, G., Diaz-Garcia, L. et al. Diarrhea in Preschool Children and Lactobacillus reuteri: A Randomized Controlled Trial. Pediatrics Mar 2014, peds.2013-0652; DOI: 10.1542/peds.2013-0652

P: 336 children born at term aged 6-36 months attending a daycare in Mexico
I: 5 drops L. reuteri DSM 17938 for 12 weeks
C: placebo drops
O: The primary outcome was the number of days with diarrhoea per child, which was defined as days when 3 or more loose or watery stools were passed within a 24-hour period with or without vomiting, both during the intervention and for 12 weeks afterwards.

  • About ¼ of families offered enrolment decline; which means we should question the (?social) acceptability of the intervention in this population.
  • Semi blinded – one of the authors was overseeing the block-randomisation.
  • Interesting exclusion criteria including birth weight < 2500 g, chronic disease, failure to thrive, allergy or atopic disease, recent (previous 4 weeks) exposure to probiotics, prebiotics, or antibiotics, or were participating in other clinical trials.
  • A reasonably well defined list of secondary outcomes.
  • Parents were educated about stool descriptors using the Bristol stool scale, and upon a loose motion had to contact the study centre, and then report for assessment. I wonder if this call-presentation process lent itself to underreporting (in both groups.)
  • All four primary outcomes: Number of diarrhea episodes, Episodes of diarrhea per child, Mean duration of diarrhea episodes and Days with diarrhea per child were significantly better in the treatment arm, both during the intervention and afterwards. With p values ranging from 0.03 to 0.01.


Secondly, the idea that probiotics could reduce infantile colic seemed immensely appealing; it’s an area that has had a myriad of debunked therapies over the last several millenia. T

Indrio F.,Di Mauro A., Riezzo G., et al..Prophylactic use of a probiotic in the prevention of colic, regurgitation, and functional constipation: a randomized clinical trial. JAMA Pediatr. 2014 Mar;168(3):228-33.

P: 589 term infants aged less than one week, in 9 centres across Italy.
I: 5 drops of L reuteri DSM 17938 (1×10^8 cfu) for 90 days
C: placebo
O: Primary outcomes were daily crying time, regurgitation, and constipation during the first 3 months of life. Cost-benefit analysis of the probiotic supplementation.

  • Infants receiving antibiotics in the first week of life were excluded; (in Australian maternity units, this would account for a significant number.)
  • Trial was independently randomized and double blinded.
  • Around ⅙ patients were lost to follow-up; a significant number were withdrawn from the treatment arm for protocol violations by the investigator.
  • Parents recorded data in a structured diary and sought advice as required via usual channels.
  • At both one and 3 months of life, the infants in the treatment arm cried for significantly shorter periods of time and stooled more frequently. At three months, there were fewer episodes of regurgitation in the treatment arm.
  • Although this is a single study, there are a number along similar lines; Szajewska’ paper mentions 4 in total. The results are most striking in this paper, hence my curiosity.

The organism of the hour, L. reuteri DSM 17938 was first cultured from breast milk of a Peruvian mother; it is patented by BioGaia whom provided the study drug and placebo for both trials above.

Conclusions


There’s a growing body of evidence for the potential benefits of probiotics in a number of paediatric conditions.

There is a bias in this review (and pretty much all of academic medicine) towards positive trials. That being said, I haven’t given the details of every study mentioned; Szajewska’s review does so nicely and I also recommend a read of the primary literature.

Most importantly, communicating with parents about the uncertainties about over-the-counter probiotics with respect to labelling, quality, dose and organism remain central to this discussion.

Key points:

  • Probiotics are “live microorgnaisms that, when administered in adequate amounts, confer a health benefit on that host.”
  • There are many vested interests & popular marketing with issues around labelling and quality in this area.
  • Research is strain specific.
  • Main strains researched are; Lactobacillus reuteri DSM 17938, Lactobacillus reamnosus GG (LGG), Bifidobacterium and Saccharomyces
  • Presently, benefit has been demonstrated in NEC, Antibiotic associated diarrhoea, infantile colic, functional abdominal pain and acute gastroenteritis.

References:

Szajewska, H.What are the indications for using probiotics in children? Arch Dis Child archdischild-2015-308656 Published Online First: 7 September 2015

Gutierrez-Castrellon, P., Lopez-Velazquez, G., Diaz-Garcia, L. et al. Diarrhea in Preschool Children and Lactobacillus reuteri: A Randomized Controlled Trial. 

Pyloric stenosis

Cite this article as:
Erin Sharwood. Pyloric stenosis, Don't Forget the Bubbles, 2016. Available at:
https://doi.org/10.31440/DFTB.2768

Key points:

  • Think of pyloric stenosis in a vomiting infant.
  • Only about 1 in 7 cases will have the classic triad of projectile vomiting, visible peristalsis and the palpable “olive”.
  • Hypokalemia suggests several weeks of symptoms.
  • Ultrasound is the most common diagnostic modality, in addition to Hx & Examination.
  • Rehydrate and correct electrolyte disturbances before operative management.

Jackson is a 5-week-old baby brought into the emergency department by his mum Gina. Over the past four days he has had increasing vomiting, and today he seems lethargic. Gina tells you he hasn’t kept anything at all down in the past 24 hours, and has had only one slightly wet nappy since last night.

On examination, Jackson looks pale and mottled. His heart rate is 180 beats per minute, and his respiratory rate is 45. He is afebrile, and his central capillary return is around 3 seconds. You decide to organise an IV cannula for a fluid bolus while continuing to take more history from Gina.

What blood tests would you like to take as you cannulate? What further questions do you have for Mum?

Gina tells you Jackson is her first baby, he was born at term has been fully breast fed. She knows that lots of babies have small vomits after feeding, so wasn’t too concerned initially. The vomit is milky, with no blood or bile. Gina notes that as soon as Jackson vomits he seems hungry and extremely eager to feed again right away. Jackson usually has one or two soft yellow bowel motions a day, and hasn’t had any diarrhoea. Gina doesn’t know of any family history on her side, but isn’t sure about Jackson’s father’s side as they live overseas.

Happily, your cannula goes in beautifully, but yields only enough blood for a venous blood gas. Now what?

While you run through a fluid bolus of 10mL/kg of 0.9% sodium chloride, you take the opportunity to examine Jackson a little further. You find he has a slightly sunken anterior fontanelle. He is sleepy, but sucks vigorously at the pacifier Gina has provided. His abdomen is soft, and you can’t feel any masses in the supine position. There is no respiratory distress, and his lung fields are clear, with dual heart sounds and no murmurs.

What do you expect the gas to show?

As you finish your examination, your blood gas result becomes available. It shows a pH of 7.50, a pCO2 of 50, with a bicarbonate of 38, and a base excess of +5. The electrolytes provided on the gas readout show a sodium of 129, potassium of 3.6, and a chloride of 92.

Jackson has picked up following his fluid bolus, and is now looking for a feed. While keeping maintenance fluids running, you suggest to Gina that offering a breast feed might actually help you confirm the diagnosis. In the meantime, you decide to ask the sonographer if they can help out with an abdominal ultrasound.

As you head back to the room, you run into the surgical registrar and ask them to come and take a look at Jackson. You both note that after the feed, you can see waves of peristalsis across Jackson’s epigastrium going from left to right. You step away just in time to narrowly miss Jackson vomiting forcefully, with milky vomit making it across the cubicle to hit the wall 2 metres away!

The surgical registrar agrees this is very likely pyloric stenosis, and shows you how to palpate his right upper quadrant with Jackson resting prone on her hand. She is suitably impressed by Jackson’s presentation, and happily accepts his care, though she asks you to cancel the ultrasound as she is so confident of the diagnosis. She explains to Gina that Jackson will need surgery to release the muscle between his stomach and duodenum, but first he will need to be rehydrated over night.

Jackson went on to have a laparoscopic pyelomyotomy the following day, with no complications. As they are leaving, they come by to say goodbye, and to let you know it turns out Jackson’s dad also had pyloric stenosis at around about the same age.

What about POCUS?

Sivitz et al established a prospective study assessing the accuracy of POCUS for diagnosis of Pyloric Stenosis; it’s an interesting comparator, but essentially the vast majority of the scans were done by a only one of the participants. It’s also worth noting that the sonographic features become more marked as the stenosis progresses – in the study this meant that all POCUS-negative, sonographer-positive scans were given a free pass. The data suggest that POCUS is suitable as a rule-in test, but is not appropriate for excluding Pyloric Stenosis.

Practice Points

Idiopathic Hypertrophic Pyloric Stenosis typically occurs between 2 and 12 weeks of age, and is around 4-6 times more common in boys, particularly if they are first-born. A family history is often present.

Historically, the diagnosis was made clinically, with a ‘classic triad’ of projectile vomiting, visible peristalsis and a palpable ‘olive’ (the thickened pylorus) in the right upper quadrant at the border of the rectus abdominus muscle. More recently (possibly due to a trend toward earlier presentation to hospital), the ‘olive’ is often not easy to palpate, and ultrasound examination is often employed to confirm the suspected diagnosis. Gotley et al found At least one classic symptom or sign was present in 87% of infants but only 1 in 7 cases had the ‘classic triad’.

Blood gas analysis classically reveals a hypochloraemic metabolic alkalosis. Studies suggest hypokalaemia often doesn’t occur until 3 weeks worth of vomiting. A retrospective study of blood gas results showed that a pH of >7.45, a base excess of >+3, and a chloride of <98 were particularly useful in predicting the diagnosis in babies presenting with vomiting.

Metabolic disturbance needs to be corrected prior to surgery, as this dramatically reduces the risk of intra- and post-operative complications.

 

References

Gotley, LM, Blanch, A, Kimble, R, Frawley, K, and Acworth, JP, “Pyloric stenosis: A retrospective study of an Australian population” Emergency Medicine Australia 21 (2009) 407-413. https://www.ncbi.nlm.nih.gov/pubmed/19840091

Taylor ND, Cass DT, Holland AJ. Infantile hypertrophic pyloric stenosis: has anything changed? J Paediatr Child Health. 2013 Jan;49(1):33-7. doi: 10.1111/jpc.12027. Epub 2012 Dec 2. https://www.ncbi.nlm.nih.gov/pubmed/23198903

Sivitz et al. Evaluation of Hypertrophic Pyloric Stenosis by Paediatric  Emergency Physician Sonography Acad Emerg Med. 2013 Jul;20(7):646-51. doi: 10.1111/acem.12163. Epub 2013 Jun 19. https://www.ncbi.nlm.nih.gov/pubmed/23781883

Oakley EA and Barnett PLJ, “Is acid base determination an accurate predictor of pyloric stenosis?” Journal of Paediatrics and Child Health 36 (2000), 587-589. https://www.ncbi.nlm.nih.gov/pubmed/11115037

Gastrostomy Week – Complications

Cite this article as:
Camille Wu. Gastrostomy Week – Complications, Don't Forget the Bubbles, 2015. Available at:
https://doi.org/10.31440/DFTB.6390

You review a patient on the ward for abdo pain and pyrexia, and they have some sort of tube with feeds going into their stomach. You need to call the surgeons for a consult for their abdo pain. But what you call it? Do you know the difference between your PEGs and gastrostomies? Do you understand about tube calibres and lengths? In this four-part series, Camille Wu covers everything the general paediatrician needs to know about enteral feeding via gastrostomies….