Volcano

Managing Gastro-Oesophageal Reflux Disease

Cite this article as:
Sarah Davies. Managing Gastro-Oesophageal Reflux Disease, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.29563

Isobel is a 10 week old, exclusively breast-fed, baby girl. She is brought into the Emergency Department with a history of frequent vomiting and poor weight gain. Her examination is normal, but when you ask Isobel’s exhausted-looking mother to put her to the breast, she becomes fractious and fussy, pulling away, arching her back, and taking very little feed at all.  

What are you going to do? 

At face value, this familiar presentation sounds like gastro-oesophageal reflux disease (GORD), although the differential for a ten-week old with vomiting and weight loss is wide.

Gastro-oesophageal reflux (GOR) is …the effortless retrograde passage of gastric contents into the oesophagus, with or without overt regurgitation. 

It is:

  • Physiological, due to low tone in the immature lower oesophageal sphincter
  • Common, occurring in up to 50% infants under 6m
  • Frequent – can happen up to x6/day

Gastro-oesophageal reflux disease (GORD) can be diagnosed clinically when GOR is accompanied by troublesome symptoms that affect everyday functioning (eg crying, back-arching, food refusal) and may lead to complications (eg failure to thrive).

Alternative diagnoses should be considered when there are additional red flag features (see below) indicative of a different pathology and under these circumstances, investigations should be tailored to rule these in or out.

*Some red flags overlap with symptoms directly related to GORD. The number, duration and severity of these should inform your decision to investigate on a case by case basis

As Isobel has symptoms of GORD with faltering growth you check her head circumference (which is appropriate), dip a urine (which is negative), and send some bloods for a faltering growth screen (although you strongly suspect they will come back as normal). You explain to Isobel’s mother that there is a stepwise approach to the management of GORD starting with non-pharmacological measures.

So, in the absence of red flag symptoms, do I need to prove its GORD?

In short, no. There is no single gold standard test for the diagnosis of GORD, hence the emphasis on clinical diagnosis. 

Invasive testing does have a place, though it is rarely the job of an ED clinician to be considering this. 

Endoscopy is used under the guidance of a Paediatric Gastroenterologist, for infants who fail to respond to optimal medical management. This will diagnose erosions and eosinophilic oesophagitis. 

pH MII (multi-channel intraluminal impedance) monitoring is used in children whose symptoms persist despite optimal medical therapy with normal endoscopy.   For a great explanation of this technique this previous DFTB post on reflux from 2016

Barium is out. Reliable biomarkers don’t yet exist. Scintigraphy, ultrasound and trial of a proton-pump inhibitor (PPI) are not useful in babies. 

OK, so I only need to investigate if I think there may be another cause for the symptom. But what should be my initial approach to treatment?

  • Positional management?
  • Avoiding overfeeding?
  • Thickening feeds?

Positional management – keeping the baby upright after feeds and elevating the head of the cot to sleep – is often advised for reflux. However, a study by Loots and colleagues in 2014 showed that regurgitation was only reduced through the use of side-lying positions which should NEVER be recommended due to the increased risk of SIDS. Head elevation made no difference at all despite some evidence that it can be beneficial in adults. 

And whilst a common-sense approach would support a move to smaller more frequent feedings and keeping a baby upright for 20-30 minutes after a feed, there isn’t any good quality evidence that confirms this. 

Feed thickeners have been shown repeatedly to reduce the frequency of visible regurgitation episodes in babies with reflux and in some studies to decrease cry/fuss behaviour too. They are safe and come highly recommended as a first-line intervention for babies with troublesome reflux. If you are going to advise a thickener for a breastfed infant, it’s important to suggest a carob bean-based product, such as Carobel, because the amylase in breast milk will digest the rice cereal-based thickeners such as Cerelac.  

Acupuncture, probiotics, massage, hypnotherapy have not yet been adequately studied for us to say one way or another if they are of any benefit. And alginates, probably the most familiar to us being Gaviscon? We’ll cover those shortly.

The key thing to remember for any intervention, is to reserve these for your patients with GORD. Happy, thriving, refluxy babies, typically outgrow their symptoms as they transition to solid food and should be left well alone

OK, but what if my patient has tried these already? What should I advise next? 

First, check how long they have persisted with the intervention. 

One of the biggest reasons for the simpler interventions not to help with GORD is that they are not given enough time to make a difference. Having said that, if a tired parent is repeatedly confronted with a grizzly, uncomfortable baby who is refusing to feed, asking them to persevere for two weeks with an intervention they don’t think is helping, may be practically difficult to achieve. 

In the UK, we have a choice of two key guidelines to help us with the next steps in reflux management.  

  1. NICE, last updated 2019

OR

  1. ESPGHAN/NASPGHAN 2018 joint consensus guidelines which are endorsed and recommended by our own BSPGHAN
  • European Society of Paediatric Gastroenterology, Hepatology and Nutrition
  • North American Society of Paediatric Gastroenterology, Hepatology and Nutrition
  • British Society of Paediatric Gastroenterology, Hepatology and Nutrition

Except that these guidelines differ a little on the advice they give for when simple measures don’t help…

NICE recommend a trial of Gaviscon first, and if that doesn’t work 4-8 weeks of a PPI such as omeprazole, and only then suggest a trial of cow’s milk protein exclusion (either through use of a hydrolysed formula or maternal dairy exclusion in breastfed infants) as a last resort, if reflux does not improve after ‘optimal medical management’. 

NASPGHAN/ESPGHAN on the other hand, suggest that ALL infants undergo an initial trial of cow’s milk protein exclusion, and only if this fails do they suggest the use of a PPI or hydrogen receptor antagonist (H2RA) such as Ranitidine. The bottom line is, that no-one has looked at the efficacy of a cow’s milk protein-free diet for symptom relief in babies presenting with reflux as the single symptom of cow’s milk protein intolerance (CMPI).  

The NASPGHAN team argues, that whilst there is no evidence on the topic, there are a number of babies with CMPI manifesting as reflux only who will benefit from this approach. They suggest eliminating cow’s milk protein from an infant’s diet for a minimum of 2 weeks, ideally four. If symptoms resolve and reappear on reintroduction then the diagnosis is clear. 

NASPGHAN then suggest babies who do not respond should be referred to secondary care services and started on a time-limited trial of PPI. 

This is largely so that infants are not left struggling on inadequate therapy for long periods of time, but also because their review found conflicting evidence around the benefit and side effect profile of these medications for young children. 

In six studies looking at PPI versus placebo, four studies showed no difference in regurgitation or other reflux associated symptoms between intervention and control groups. Three studies comparing H2RAs to placebo did show some benefit of the intervention, however, these studies were all in older children with biopsy-proven erosive oesophagitis up to 8 years of age.  Two studies showed endoscopic and histological and clinical features of GORD were reduced with H2RA over placebo, but these were in mixed-age groups including children up to 8 years old.

All studies showed a similar profile of side effects and between drug and placebo arms, however, one study demonstrated an increased rate of infection, in particular lower respiratory tract infection and diarrhoea in the PPI group. 

Given these findings, NASPGHAN cautiously recommends PPI or H2RA therapy in babies who have troublesome reflux despite trying a number of other non-pharmacological management options. 

Their key message is around early referral to secondary care, giving sufficient time for any one intervention to work, and making sure children are appropriately followed up.

So, what should I do? 

Given the somewhat conflicting advice outlined by these two well-respected groups, you could be left feeling unsure how to manage your next case. However, the genuine gap in the evidence market here does mean you are free to exercise your own clinical judgment and tailor your decision making to each individual refluxy baby, whilst empathetically taking on board the thoughts and preferences of the family.  This could, for some babies and parents, be medicine in itself. 

And what about alginates?

Two studies in the large literature review by the NASPGHAN/ESPAGHN group, compare Gavsicon to placebo. They show a reduction in visible regurgitation but no difference in reflux-associated symptoms. Furthermore, infants treated with alginate and then undergoing pH MII for 24 hours, showed no difference in the frequency of regurgitation events between groups. 

Chronic use of alginates causes constipation and poses a theoretical risk of milk-alkali syndrome, which is perhaps why the authors suggest use is limited to short term therapy. NICE do recommend a trial of Gaviscon therapy at an early stage in their pathway, as an alternative to feed thickener, but again on a time-limited basis with a planned review. 

Isobel’s mother had already tried two weeks of feed thickener on recommendation from the GP with no improvement. She was keen to avoid medication if possible so you agreed to a trial of dietary cow’s milk elimination for Mum who would continue to breastfeed and give top-ups with a hydrolysed formula if there was still no weight gain in a week. You gave her a sheet of dietary advice to ensure she maintained her own calcium intake and asked her to see the GP in 2 weeks for a review.  

Take home message

  • The vomiting infant has a wide differential – actively look for red flag features and investigate if you are concerned.
  • Infants with GORD need a management plan; infants with GOR, leave well alone
  • Start simply with an intervention that the family are happy to trial
  • Give time for it to work (up to two weeks)
  • Ensure follow-up for all and onward referral for infants who require acid-suppressive medication 

References

  1. Loots et al. Body positioning and medical therapy for infantile gastroesophageal reflux symptoms. Journal of Pediatric Gastroenterology and Nutrition 2014; 59 (2): 237-243. 
  2. Rosen et al. Pediatric Gastroesophageal Reflux Clinical Practice Guidelines: Joint Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition and the European Society of Pediatric Gastroenterology, Hepatology and Nutrition. JPGN 2018; 66(3): 516-554. 
  3. Winter et al. Efficacy and safety of pantoprazole delayed release granules for oral suspension in a placebo-controlled treatment withdrawal study in infants 1-11 months old with symptomatic GERD. JPGN 2010; 50: 609-618.  
  4. Orenstein et al. Multicenter, double-blind, randomized, placebo-controlled trial assessing the efficacy and safety of proton pump inhibitor lansoprazole in infants with symptoms of gastroesophageal reflux disease. Journal of Pediatrics 2009; 154: 514-520e4. 
  5. Davidson et al. Efficacy and safety of once daily omeprazole for the treatment of gastroesophageal reflux disease in neonatal patients. Journal of Pediatrics 2013; 163: 692-698.e1-2. 
  6. Winter et al. Esomeprazole for the treatment of GERD in infants ages 1-11 months. JPGN 2012; 55: 14-20. 
  7. Hussain et al. Safety and efficacy of delayed release rabeprazole in 1-11 month old infants with symptomatic GERD. JPGN 2014; 58: 226-236. 
  8. Moore et al. Double-blind placebo-controlled trial of omeprazole in irritable infants with gastroesophageal reflux. Journal of Pediatrics 2003; 143: 219-223. 
  9. Cucchiara et al. Cimetidine treatment of reflux oesophagitis in children: an Italian multi-centric study. JPGN 1989; 8: 150-156. 
  10. Orenstein et al. Ranitidine, 75mg, over the counter dose: pharmacokinetic and pharmacodynamic effects in children with symptoms of gastro-oesophageal reflux. Alimentary Pharmacology and Therapeutics 2002; 16: 899-907. 
  11. Simeone et al. Treatment of childhood peptic esophagitis: a double-blind placebo-controlled trial of nizatidine. JPGN 1997; 25: 51-55. 
  12. Miller et al. Comparison of the efficacy and safety of a new aluminium free paediatric alginate preparation and placebo in infants with recurrent gastroesophageal reflux. Current Medicines and Research Opinion 1999; 15: 160-168. 
  13.  Ummarino et al. Effect of magnesium alginate plus simethicone on gastro-oesophageal reflux in infants. JPGN 2015; 60: 230-235.

Ten ‘not to be missed’ paediatric ECGs

Cite this article as:
Megan Thomas, Jordan Evans, Amos Wong and Jeff Morgan. Ten ‘not to be missed’ paediatric ECGs, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.29306

To refresh your memory on how to read paediatric ECGs take a look at Anna McCorquodale’s fantastic article: Approaching the paediatric ECG.

Here we review ten ‘not to be missed’ abnormal ECGs that may be encountered in acute paediatrics. 

#1 Supraventricular Tachycardia (SVT)

What is it?

SVT is a narrow complex tachycardia, the electrical activity originates above the ventricles (‘supraventricular’). SVT is classified based on whether it originates from the atrium or from the AV node. Finding where the position of the P wave is (with respect to the QRS complex) during tachycardia (‘P wave hunting’) is essential for the diagnosis of SVT.

Why does it happen?

It usually occurs due to one of the following mechanisms:

  • An accessory pathway linking the ventricle to the atrium, which impulses can travel along returning into the atria (AVRT, Atrioventricular Re-entrant Tachycardia)
  • A micro re-entrant circuit in the AV node itself (AVNRT, AV node re-entrant tachycardia)
  • An enhanced automatic focus in the atrium which fires impulses out 

These all lead to excessive impulses being conducted to the ventricles.

So what do we see on ECG?

  • A fast narrow complex tachycardia (approx. 150-220 bpm)
  • SVT – The hunt for the missing P wave:  It is a common misconception  in SVT that there are no P waves. Whilst this may appear to be the case, this is because the P wave is in fact hidden elsewhere.  The location of the missing P wave will depend on the type of SVT.
  • Lack of beat to beat variability i.e. you will see on the monitor that the rate stays pretty much constant

Atrioventricular Re-entrant Tachycardia (AVRT)

This is when there is an accessory electrical pathway connecting the ventricles and the atria. This creates a re-entrant circuit, with impulses either being conducted down the AV node and then back up the accessory pathway (orthodromic) or vice versa (antidromic).  You may see a retrograde P wave at the end of the QRS complex. (See #2 for further info on Wolff-Parkinson-White Syndrome, a classic type of AVRT).

Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)

A micro re-entrant circuit forms in, or adjacent to, the AV node itself.  Here, P waves are very hard to find as they are usually buried in the QRS complex. The circuit often stimulates both the atria and ventricles and therefore the P-wave is hidden, buried within the QRS complex. 

AVNRT: N for No P waves!

Permanent junctional reciprocating tachycardia (PJRT)

This is a type of orthodromic AVRT where the concealed accessory pathway is near the coronary sinus. This means it can conduct at a relatively slow rate for a tachycardia. The characteristic of PJRT is Long RP tachycardia where the P wave is inverted in the inferior leads (hence NOT in sinus rhythm!) and the RP interval is longer than PR interval.

PJRT is commonly misdiagnosed as sinus tachycardia.  If PJRT is suspected seek cardiology input as adenosine is often ineffective and therefore needing multiple anti-arrhythmic therapy.

#2 Wolff-Parkinson-White Syndrome (WPW)

What is it?

Wolff-Parkinson-White is a conduction abnormality, where there is an accessory pathway connecting the atria and the ventricles. If this accessory pathway conducts from the atria to the ventricles (anterogradely) then it can be seen on the ECG as ‘pre-excitation’, as the impulse will travel faster down the accessory pathway than the rate-limited AV node.  WPW can lead to SVT (AVRT type).

What do we see on ECG?

A short PR interval (<120ms) is seen.

The most distinguishing feature is a delta wave which appears as a slow upslope between the Q wave and the R wave – with the Q wave being much earlier than usual. This means that the QRS is wide (>100ms).  The delta wave reflects fusion between the accessory pathway and the normal QRS as conducted via the AV node.

#3 Complete Heart Block

What is it?

Complete heart block (also known as ‘Third Degree’ heart block) occurs when an impulse isn’t conducted from the atria to the ventricles, usually due to AV node pathology. This means that whilst the atrial rate is determined by the SA node, the ventricular rate is a ventricular escape rhythm –which is much slower than the rate of the SA node. This means that the ventricles and atria, therefore, contract completely independent of one another. In AVN block a narrow QRS is seen, whereas, in an infranodal block, a wide QRS is seen. The former is more stable as the pacemaker site is more proximal (Bundle of His) so asystole is less likely.

Why does it happen?

Heart block can occur for a variety of reasons in children, but often it is congenital- secondary to either structural disease (i.e congenitally corrected transposition of the great arteries) or maternal antibodies, as seen in neonatal lupus. Congenital heart block associated with underlying structural heart disease has a poorer prognosis.

So what do we see on ECG?

There are regular P waves and regular QRS complexes, but these are completely unrelated to one another.

But what about the other blocks?

#4 Myocarditis

What is it?

As suggested in the name, myocarditis is inflammation of the myocardium. This can occur due to infection (viruses, bacteria, spirochetes, fungi, and other organisms) having a direct toxic effect on the myocardium.  It is important to consider the diagnosis in children who have recently suffered a systemic illness (esp. Coxsackie). Certain drugs may also be responsible (anthracycline chemotherapy and alcohol).  Myocarditis may occur alongside pericarditis. The inflamed myocardium is unable to contract and conduct as well as usual resulting in poor function of the heart.

So what do we see on ECG?

Usually, myocarditis presents with sinus tachycardia and non-specific T-wave and ST-segment changes (e.g. T wave inversion). We may also see:

  • QRS/QT prolongation
  • Low voltage QRS (<5mm in precordial leads)
  • Pathological Q waves
  • Ventricular arrhythmias (can be ectopics or VT)
  • AV block 

#5 Dilated Cardiomyopathy (DCM)

What is it?

Dilated Cardiomyopathy (DCM) is characterized by weak and floppy myocardium.  It may be inherited or develop as a result of myocarditis secondary to infection or drugs.

So what do we see on ECG?

Cardiomyopathies show similar features to myocarditis.  Pathologically it’s a spectrum, the inflammation in myocarditis is the ‘active phase’ leading to muscle damage present in cardiomyopathy. Changes may include:

  • QRS/QT prolongation
  • Low voltage QRS (<5mm in precordial leads)
  • T wave / ST segment changes
  • Pathological Q waves
  • Ventricular arrhythmias (can be ectopics or VT)
  • AV block 

#6 Hypertrophic Cardiomyopathy (HOCM)

What is it?

HOCM is a genetic condition that affects the sarcomeres in the heart causing left ventricular hypertrophy (LVH), which cannot be explained by other causes. It is very important as it’s the most common cause of sudden cardiac death in those <35, and those who have HOCM may require an internal cardiac defibrillator.

So how do we figure out if there is HOCM?

There are many criteria that can be used to describe HOCM, however no one criteria has been determined to be the most reliable (especially in children).

So what do we see on ECG?

Whereas in DCM there are small QRS complexes, in HOCM they are large due to the hypertrophied muscle.  As above with myocarditis and dilated cardiomyopathy: T wave inversion and ST changes indicate unhealthy myocardium. Pathological Q waves may also be seen.

#7 Long QT

What is it?

As the name suggests, this is when the QT interval is prolonged. In order to determine if the QT is prolonged then we need to determine the QTc using Bazetts formula.

Source: litfl.com/bazett-formula/
  • In boys, a prolonged QTc is >450ms
  • In girls a prolonged QTc is >460ms.

The most important tool in trying to determine the cause of a prolonged QT interval is history! Certain features make a congenital cause of a prolonged QT interval much more likely:

  • Syncope (+/- stress)
  • Congenital deafness (suggests LQT5)
  • FHx of sudden cardiac death <30 yr in immediate family
  • FHx of Long QT syndrome
  • Certain medications

What causes it?

There are many causes of a prolonged QT interval, including:

Acquired prolonged QT: This is when a child has a prolonged QT interval secondary to an underlying cause such as:

  • Drugs: antibiotics, antidepressants, antipsychotics, antihistamines, antiarrythmics, antifungals
  • Electrolyte disturbances
  • Hypothermia

Congenital long QT syndrome: This is an inherited channelopathy, where the child has a prolonged QT interval present either at baseline or unmasked by a stimulus.

There are 17 different forms of long QT syndrome (and counting!), which each have a different genetic mutation.

Three main types of Long QT syndrome (LQTS):

NameGeneTriggersFrequencyT waves
LQT1KCNQ1Peak exercise40%Early onset broad based.
LQT2KCNH2Sudden loud noises, swimming, emotion, stress30%Low voltage double bumped ‘bifid’ T wave with notching
LQT3SCN5ARest, sleep10%Late onset T wave  

ECG changes may be seen at rest or the child may need to go through exercise tolerance testing or an adrenaline challenge in order to unmask the prolonged QT interval.

So what do we see on ECG?

Nice one, Sherlock, you guessed it!  The main feature is a prolonged QTc interval.      

Why do we care so much about a prolonged QT interval?

Those who have a prolonged QT interval are at a higher risk of developing VT or Torsades de Pointes and therefore sudden cardiac death. This means it is important to identify these children so that they can receive medical therapy or an ICD if deemed necessary.

In paediatric cardiology, Schwartz criteria is used to determine the likelihood of Long QT syndrome. Whilst we do not reach an ultimate diagnosis in the ED, it is useful to note the risky features.

#8 Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)


What is it?

As the name suggests, it is a polymorphic (i.e. of multiple morphologies) ventricular tachycardia that is stimulated by catecholamines such as adrenaline. It is an inherited condition, which affects ion channels causing altered calcium flux leading to delayed after-depolarisations causing VT. Whilst baseline ECG may be normal, states in which there is a high adrenaline surge can unmask the CPVT (i.e. heavy exercise). If detected, these children need to be sent for further investigation for medical management or potentially an ICD.

So what do we see on ECG?

A polymorphic ventricular tachycardia. There are two types:

  • Normal baseline ECG!
  • Typical polymorphic / bidirectional VT – where both QRS complexes and T wave change in axis.

Differential for bidirectional VT = CPVT, LQTS Type 7 and Digoxin toxicity.

Do not shock CPVT! This may induce ‘electrical storm’ perpetuate the catecholamine release.  Seek advice from your local Paediatric Cardiologist.

#9 Brugada Syndrome

What is it?

This is an inherited channelopathy which affects impulse conduction, causing ventricular tachyarrhythmias and potentially sudden cardiac death. It is more common in males and commonly seen in carbohydrates consuming nations e.g. rice in South East Asia and pasta in the Western population. Interestingly, the same gene that causes LQT3 (see above) causes Brugada (SCN5A), however in the former there is a gain in function, whereas in Brugada there is a loss of function.

#10 Anomalous Left Coronary Artery arising from the Pulmonary Artery (ALCAPA)

What is it?

This is when the left coronary artery is connected to the pulmonary artery instead of the aorta. This means that instead of receiving oxygenated blood, the left side of the myocardium will receive deoxygenated blood. This can lead to myocardial ischaemia, which is initially transient occurring only in periods of increased myocardial demand (feeding, crying). However, as oxygen demand increases, infarction of the anterolateral left ventricular wall can occur.

So what ECG changes do we see?

  • Pathological Q waves (esp. in leads I, aVL and V6) – 50% of kids with Q waves in aVL have ALCAPA!
  • Ischaemic / T wave changes in inferolateral leads (II, III, aVF, V5-6).  Note on ECG below T waves in V5 and V6 are flattened

Maxilla and zygoma injuries

Cite this article as:
Jessie Lynch. Maxilla and zygoma injuries, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.21700

A 2-year-old child called Lucy is brought to your ED by ambulance. She was the right-sided rear seat passenger in a high-speed head-on road traffic collision. The driver of the other car died on impact. She was restrained in a car seat, however, the seatbelt holding the car seat in place had broken and the car seat was thrown forward. She had a 4-minute episode of loss of consciousness. She had a GCS of 14/15 on arrival, she was maintaining her airway and she was haemodynamically stable. She had significant swelling, bruising, and superficial abrasions to the right side of her face, and her right eye was swollen shut.

Facial injuries in children are relatively common. The most common facial injuries encountered in a paediatric population are dental trauma, oral trauma and facial lacerations. Facial fractures, however, are exceedingly rare in this population, with an incidence of <15% in those under the age of 16 years, and only 0.87% – 1% in those under the age of 5 years.

There are a number of factors which make children less prone to facial fractures. These include:

  • Retruded position of the midface relative to the skull
  • Structural stability increased by the presence of tooth buds within maxilla and mandible and lack of sinus pneumatisation
  • A thick layer of adipose tissue coverage
  • More elastic bones and flexible suture lines
  • High level of adult supervision

These factors also make children more prone to greenstick and minimally displaced fractures as opposed to comminuted or complex fractures. These factors become less significant as the child grows older.

History

Common causes of facial fractures include falls, road traffic collisions, sports-related injuries and, less commonly, interpersonal violence. 2.3% of victims of non-accidental injury have facial fractures and the possibility of this should always be taken into account.

Examination

The presence of a midfacial fracture in a child implies that a significant velocity impact has occurred. 40% of children with a midfacial fracture have an associated skull fracture, and associated cervical spine injury is also common. The primary survey should be undertaken following APLS protocols, with particular attention paid to cervical spine immobilisation and airway management. A detailed craniomaxillofacial examination should be performed as part of the secondary survey, after initial stabilisation.

Fractures of different parts of the face will lead to different clinical signs.

Zygomatic arch and zygomaticomaxillary complex (ZMC) 

The zygomaticomaxillary complex (ZMC) is made up of four parts:

  • lateral orbital wall
  • zygomatic-maxillary junction
  • zygomatic arch
  • orbital floor

An approach to the assessment of ZMC fractures includes:

  • Inspect the orbit. There may be periorbital swelling or ecchymosis, enophthalmos, subconjunctival haemorrhage and diplopia (due to extraocular muscle dysfunction). The orbital examination should also include visual acuity, visual fields and extraocular muscle function.
  • Palpate the facial bones. There may be a palpable depression or step in the infraorbital rim or zygomatic arch as well as tenderness or widening of the frontozygomatic suture.
  • Oral assessment. There may be trismus (lock jaw) and bruising and tenderness of the upper buccal sulcus.
  • Infraorbital nerve assessment, documenting any paraesthesia.

Maxilla

Maxillary fractures are classified according to the Le Fort classification system*

  1. Le Fort I: A horizontal fracture through the floor of maxillary sinuses with the teeth contained within the detached fragment. Only palate moves.
  2. Le Fort II: A fracture which can be one-sided or bilateral fracture through the maxilla extending into the floor of the orbit, the nasal cavity and hard palate. This results in a pyramidal shaped fracture.
  3. Le Fort III: A fracture through the orbits in which the entire maxilla and one or more facial bones, the entire midface, becomes separated from the base of the skull. This is called craniofacial disjunction.

*Rene Le Fort was a French physician at the turn of the 20th century. He discovered that the midface tended to fracture in three different ways when traumatising cadavers in quite gruesome, but scientifically important, ways.

Clinical signs of Le Fort fractures are much the same signs as for ZMC and zygomatic arch fractures but signs are, for the most part, bilateral. Facial asymmetry, flattening or elongation may be evident in older children.

Management

Manage pain with non-pharmacologic and pharmacological measures. Oral and intravenous analgesia may be required but avoid intranasal analgesia in case of fracture.

Investigations

Facial bone x-rays may give you some valuable information, but the caveat is that they can be difficult to interpret in children. If you have a high clinical suspicion of a facial bone fracture, a CT scan is the imaging modality of choice and can be argued to be the cornerstone of investigation for facial bone fractures in children.

A chest x-ray may be indicated to exclude aspiration of foreign bodies or dental fragments.

Specific treatment

All fractures should be discussed with the local maxillofacial service and/or ophthalmology if orbital involvement is present. A formal ophthalmological review should be carried out as early as is feasible in children with any suspected midfacial fracture.

Most greenstick or minimally displaced fractures can be managed conservatively with soft diet, advice not to blow nose or hold nose closed while sneezing, antibiotic prophylaxis and a nasal decongestant.

There is no clear consensus on the best choice of antibiotic for facial fractures, and there is much variety among papers. The most commonly used would appear to be co-amoxiclav, cefuroxime, and clindamycin in penicillin-allergic patients.

Surgical intervention range from an intraoral approach for minimally displaced zygoma fractures to open reduction and internal fixation for comminuted fractures.

Potential complications, including mal/non-union, are less common in paediatric patients than in adults.

The do not miss bits

  • Reduced or lost vision, severe eye pain or proptosis of the globe are all features of retro-orbital haemorrhage, an ophthalmological emergency which requires immediate surgical intervention to avoid permanent blindness.
  • Although facial fractures are rare in children they have the potential to cause significant disruption to future growth, function & cosmesis and thus it is vital that they are recognised.
  • It takes significant velocity to cause a facial fracture in a child, and examination & investigations must be thorough to identify any other potential injuries. Consideration should be given to the possibility of non-accidental injury when assessing a child with a facial fracture.

Lucy’s CT brain & c-spine showed no significant abnormalities. CT facial bones showed a minimally displaced fracture of the frontal process of the right zygoma. She was reviewed by ophthalmology & maxillofacial specialists & was treated conservatively with oral antibiotics with a soft diet until her fracture had healed.

Selected references

Alcalá-Galiano A,  Arribas-García IJ,  Martín-Pérez MA, et al. Paediatric Facial Fractures: Children Are Not Just Small Adults. RadioGraphics. 2008; 28:441-461

Kumaraswamy SV, Madan N, Keerthi R, Singh DS. Paediatric injuries in maxillofacial trauma: a 5 year study. J Maxillofac Oral Surg. 2009; 8(2):150-153

Braun TL, Xue AS, Maricevich RS. Differences in the Management of Paediatric Facial Trauma. Semin Plast Surg. 2017;31:118-122

Cole P, Kaufman Y, Hollier LH. Managing the Pediatric Facial Fracture. Craniomaxillofac Trauma Reconstruction. 2009;2:77-84

Kidd AJ, Beattie TF, Campbell-Hewson G. Facial injury patterns in a UK paediatric population aged under 13 years. Emergency Medicine Journal. 2010;27:603-606

Mundinger GS, Borsuk DE, Okhah Z, et al. Antibiotics and facial fractures: evidence-based recommendations compared with experience-based practice. Craniomaxillofac Trauma Reconstr. 2015;8(1):64–78

The Royal Children’s Hospital Melbourne.The Paediatric Trauma Manual. Maxillofacial Injury. https://www.rch.org.au/trauma-service/manual/maxillofacial-injury/

Post ROSC care

Cite this article as:
Costas Kanaris. Post ROSC care, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.29109

Or some pointers on clinical management following the successful return of spontaneous circulation in children. 

It’s 5:40 am at Bubblesville ED. The red phone rings. The paramedic crew informs you that they are five minutes away with a 7 kg, 6-month-old, previously thriving, baby boy called Tarquin. He has had a witnessed out of hospital cardiac arrest at home and there was no prodromal illness according to the family. He choked during a breastfeed, turned blue, and stopped breathing. He had 5 minutes of CPR by the parents by the time the ambulance arrived and had ROSC by the paramedic team after a further 8 minutes. The rhythm strip was consistent with a PEA arrest. They are hand-ventilating him through an LMA.

This is his capillary gas on arrival in the ED
  1. What are your clinical priorities?
  2. What clinical problems do you anticipate in the immediate post-arrest phase?
  3. Who do you call for help?
  4. What do you do with the family whilst you’re managing the patient?
  5. What investigations do you need?

A systematic, collaborative, well-led approach to advanced paediatric life support can maximize the chances of the clinical team achieving a return of spontaneous circulation in a child that has arrested. We’ve seen the drill be before. We can go through our algorithms expertly and the 5-H’s and 5-T’s roll off the tongue, even under duress. The return of a pulse is heralded as the “hallelujah moment”, almost as if the patient is now healthy and safe and all we have to do is wait for the paediatric critical care retrieval team to arrive.

Whilst traditional APLS teachings are vital for the dissemination of knowledge and it’s application in everyday clinical life, their main focus is on the initial phase of achieving a pulse with very little attention placed on the all-important post-resuscitation phase.  This part of care is crucial, not only if we are to minimize secondary brain injury to the child but also to improve the chances of permanent returns of spontaneous circulation. Good short and long term outcomes rely heavily on how well we manage the post-resuscitation stage. 

There are four phases of cardiac arrest:-

Phase one: Prevention. This is the pre-arrest phase. Child safety and injury prevention strategies are in place to recognize deterioration. Adequate monitoring by using early warning systems and a pro-active approach to management is likely to contribute to avoiding an arrest.

Phase two: No flow arrest. This is a period of cardiac arrest prior to us commencing CPR. Our aim here is to minimize the time it takes to start life support. It is key that we involve the cardiac arrest team quickly, we start chest compressions early, and that we do not delay defibrillation if this is needed. 

Phase three: Low flow resuscitation. This phase describes when CPR is in progress. The aim is to achieve high-quality CPR in order to allow adequate coronary and cerebellar perfusion. Maintaining good ventilation and oxygenation whilst avoiding aggressive over-ventilation is paramount. It is during this phase that we systematically approach and threaten the reversible causes of cardiac arrest. 

Phase four: This is the post-resuscitation phase after ROSC has been achieved. Our aim here is to optimize coronary and cerebral perfusion. Neuroprotection and treatment of arrhythmias as well as treatment of post-cardiac arrest syndrome come under this phase. 

Adult v paediatric arrest: What’s the difference?

Out of hospital cardiac arrests in children >16 years of age are relatively rare – reported at 8-20/100000/ year. The incidence is only comparable to that of the adult population, estimated at 70/100000/year. The incidence of in-hospital paediatric arrests is much higher, with a nearly one-hundred-fold increase, compared to the out-of-hospital incidence for the <16’s. 

Survival, and especially a “good” survival from a neurological perspective still remain poor. Out of hospital survival rates are estimated to be 5 – 12%. Only 0.3 to 4% of those that survive have no long-term neurological insult.

Children have cardiac arrests due to severe respiratory insult or circulatory collapse, in the main. Either can lead to a respiratory arrest coupled with hypoxia, which then results in a cardiac arrest. The overwhelming majority of cardiac arrests present with a non-shockable rhythm.  It is also worth noting that almost half of the paediatric population that have a cardiac arrest have other chronic comorbidities such as respiratory conditions e.g. asthma, congenital cardiac disorders, or neurodisability. 

In the adult population, cardiac arrest is more likely due to long-term comorbidities such as ischaemic heart disease. This contributes to the development of an acute myocardial insult and (usually) a shockable rhythm. Understanding the difference in pathology leading to a cardiac arrest between adults and children is vital. Reversing the cause of the respiratory compromise can make the impalpable pulse palpable, allowing us to perfuse our patient once again. 

The recommended CPR ratio of 15:2 for children aims to provide adequate ventilation for oxygenation as well as satisfactory cardiac compressions to maintain sufficient perfusion of the coronary and cerebral circulation. Adult studies looking at compression-only CPR in patients with VF arrest have shown that success in achieving ROSC is due to pre-existing pre-arrest aortic blood oxygen and pulmonary oxygen stores.  As a mere 14% of cardiac arrests are due to a shockable rhythm, combining ventilation and compressions is vital. 

What is the Post Cardiac Arrest Syndrome (PCAS)? 

PCAS describes the period in which our patients are at the highest risk of developing ventricular arrhythmias and reperfusion injuries after ROSC. This is secondary to prolonged ischaemia then reperfusion of vital organs, primarily the myocardium and central nervous system. Its systemic effects are not dissimilar to those encountered in severe sepsis. There are four stages to PCAS:

  • Immediate post-arrest – First 20 minutes. 
  • Early post-arrest – 20 minutes to 6-12 hours. 
  • Intermediate phase – 6-12 hours up to 72 hours.
  • Recovery phase – From 72h onwards. 

Neuroprotection

Even high-quality closed-chest CPR can only achieve 50% of normal cerebral blood flow at best. It is not a secret that the brain does not tolerate hypoxia or ischaemia, the effects on both of these processes are exponential during a cardiac arrest, the longer the downtime, the worse the neurological hit

The pathophysiological cascade for neurodegeneration following cardiac arrest is complex and multi-factorial. Following a hypoxic or ischaemic period the brain develops cerebral oedema and cerebral hyperaemia. There is impaired cerebral vascular reactivity and like any other organ trying to reperfuse, the post-ischaemic biochemical cascade is activated. All these factors contribute to a secondary brain injury. Of course, the duration of hypoxia will in large part dictate how severe the primary brain injury is and whether the patient is likely to survive or not. Brain injury can manifest as myoclonus, stroke, seizures, coma, or brain death. 

We can minimize the extent of secondary brain injury with simple proactive, neuroprotective measures:

  • Strict normothermia
  • Aggressive seizure prophylaxis
  • Avoiding hypoxia and hyperoxia
  • Tight circulatory monitoring and support
  • Patient position
  • Eucapnia and normoventilation
  • Vigilant glucose monitoring
  • Frequent neurological assessment, especially before the administration of anaesthetic agents and paralysis

Strict normothermia

Therapeutic hypothermia following a cardiac arrest during the intermediate phase (after VF in adults), as well as newborns with birth asphyxia, has shown some correlation with better neurological outcomes and reduced neurodisability.  Similarly, there is strong evidence linking core temperature above 38° with worse neurological outcomes in patients following cardiac arrest. There is a wide variation in practice in relation to therapeutic hypothermia.  Mild hypothermia after paediatric cardiac arrest is in the policy of some PICU’s. Patients are cooled to 33-34°C for 1 – 2 days and are then gradually rewarmed. Paralysis can be used as an adjunct to stop shivering. Temperatures below 32°C should be avoided as they are associated with worse survival, immunosuppression, arrhythmias, coagulopathies, and infections.  The decision to “cool” must be made early and in conjunction with your critical care transport team. You have many tools at your disposal to achieve this such as cold IV fluids, cooling blankets, and catheters. 

What is, and should be, more aggressively targeted is strict normothermia (temperatures between 36-37°C), and depending on local practice hypothermia can be targeted to 33-36°C. Avoidance of pyrexia is crucial. Fever can result in an increased metabolic demand of the brain. This contributes to more ischemic injury and more infarcts as the threshold for ischemia in the injured brain is lower than that of the normal brain. The brain can no longer auto-regulate the mismatch between cerebral blood flow and metabolic demand.

Aggressive seizure prophylaxis

Seizures after paediatric cardiac arrest can occur in up to 47% of cases. 35% of these can lead to refractory status epilepticus.  Whilst CFAM/EEG monitoring is unlikely to be available in your local PED, it is important to have a low threshold to administer a long-acting anti-epileptic or a continuous infusion of a short-acting medicine to prevent/avoid this from happening. Ideally, a continuous infusion of midazolam +/- levetiracetam (less arrhythmogenic than phenytoin but both will work) and standard national guidelines should be followed. 

Clues as to whether a patient is still fitting include:

  • Unexpected changes in the pupillary size (beware of the child that had atropine on induction with the “fixed dilated pupils”).
  • Sudden changes in BP or heart rate.  

If you have given a paralytic for intubation, do not fall into the trap of thinking that the patient is not seizing, only an EEG or CFAM can tell you that. It is better to err on the side of caution.

Avoiding hypoxia and hyperoxia

Avoiding hypoxia and hyperoxia are also key components in minimizing secondary brain injury.  Whilst hypoxia will further exacerbate secondary brain injury, hyperoxia  (PaO2 > 40 kPa) is also be associated with worse survival due to oxygen free-radical formation that can inactivate intracellular enzymes, damage DNA, and destroy lipid membranes. It is reasonable to have high concentration oxygen therapy during the low-flow resuscitation and early post-resuscitation phases (as the commonest causes are respiratory). In the subsequent phases, we should target oxygen saturations between 94 and 96% and be proactive in how we reduce the FiO2 whilst avoiding hypoxia. There is a caveat in cases of severe anaemia or carbon monoxide poisoning. Then it is clinically appropriate for the highest concentration of oxygen to be administered.

Tight circulatory monitoring and support

Inotropic support may also be needed early. A degree of myocardial dysfunction/stunning is expected following CPR. To ensure adequate cerebral perfusion we need to target an age-specific, physiologically normal blood pressure. Both hypo and hypertension can exacerbate secondary brain injury. Because of this, monitoring the blood pressure through an arterial line is preferred. If the local set-up or skillset does not allow for arterial line placement, especially in smaller children, having non invasive blood pressure on 1-2 minute cycles can be a useful proxy.  

The paediatric myocardium is much more resilient than its adult counterpart.  If the arrest is not secondary to congenital heart disease the paediatric heart can regain normal function within 12-24 hours.  During the first 20 minutes following ROSC poor cardiac function is due to profound systemic vasoconstriction and cellular acidosis. We can support the myocardium by supplying adequate fluid resuscitation, targeting normal (age-appropriate) blood pressure and inotropic support. Point of care ultrasound, CVP monitoring, or assessing for hepatomegaly/rales if there is no access to the former, can help us prevent fluid overload

Inotrope choice is usually made with the help of the critical care team and depends on the balance between the need for inotropy and vasoconstriction.  Adrenaline is preferred for inotropy, noradrenaline for vasoconstriction.  Be aware that severe acidosis can cause catecholamine resistance, so giving some bicarbonate if the pH <7 may help your inotropes work better. Routine administration of bicarbonate has not been shown to improve clinical outcomes. There are some special circumstances in which we should consider its use such as cases of hyperkalaemia or hypermagnesaemia and arrests due to tricyclic antidepressant overdose. 

Patient position

The patient position that can achieve optimum cerebral perfusion is with the patient semi-sat up at a 30-45 degree angle.

Eucapnia and normoventilation

Avoidance of hypercapnia or hypocapnia is important in preventing secondary brain injury. It is, therefore, recommended that eucapnia is achieved by targeting a PaCO2 between 4.5 and 5.5 kPa. Hyperventilation can cause hypoxia and increase intracranial pressure due to hyperaemia, it can also cause further cerebral ischemia. As the intrathoracic pressures increase, cardiac venous return is impaired. Since the myocardium is already injured this can have catastrophic effects causing the BP to plummet and subsequently impair cerebral perfusion.

Vigilant glucose monitoring 

Following ROSC, children are also at risk of developing hypoglycemia (glucose <3 mmol/L). There is good evidence to suggest that hypoglycaemia negatively impacts neurological outcome and cause hypoglycaemic seizures, especially in the younger ages. Vigilant glucose monitoring and correction as per APLS guidelines is important. If regular dextrose boluses are needed, consider a continuous glucose infusion. If the patient mounts an adequate stress response, they may become hyperglycaemic.  There is no evidence to suggest that aggressive glucose control with insulin in the non-diabetic patient is beneficial; wait with watchful deliberation and the glucose will usually return to normal levels with no intervention.

Frequent neurological assessment

It is important to frequently assess neurological status frequently after ROSC as this can help us prognosticate. Take the time to do a very quick assessment ideally before the administration of anaesthetic agents and paralysis. Document clearly pupillary size/reactivity, GCS (and its break down) and any respiratory effort or gasping. 

Adjunctive investigations

Following ROSC a number of investigations will be needed to guide diagnosis and therapy. Routine bloods such as renal function, electrolytes, liver function tests, full blood count, and clotting are a basic standard. In cases of lactaemia and/or severe metabolic acidosis ammonia and toxicology is useful. Arterial blood sampling is invaluable to allow quick correction of any electrolyte abnormalities and help titrate ventilation settings and (in part) guide inotropic support. Arterial samples will also help uncover any exposure to carbon monoxide, especially in burns cases. 

From an imaging perspective, a chest X-ray is vital in ascertaining tube positioning and lung pathology as well as cardiac contours in case a congenital or acquired heart disease is suspected. Head CT is obviously useful in cases in keeping with traumatic arrest and NAI but timing of the CT and whether it should take place pre-departure to PICU or after depends largely on local trauma network protocols so should ideally be discussed with the regional trauma team lead and paediatric critical care transport team. 

Children that die or arrest unexpectedly in the UK are subject to a sudden unexpected death in infancy investigation (SUDI) so the appropriate referrals need to be made to the child protection team, police and social care. It is important to clarify that even near-miss cases merit triggering the same SUDI process to ensure that any NAI cases don’t slip through the net. 

Transport pearls

After ROSC the patients will need stabilisation and transfer to PICU for on-going management. Depending on the geographical location of your hospital and the availability of a critical care retrieval service you may have to transfer the patient yourselves or look after them until he/she is retrieved by transport team. A good transport and adequate neuroprotection can be achieved by applying these simple pearls: 

  1. Aggressive temperature monitoring and control between 33°C and 37°C.
  2. Monitor for seizures and pre-empt with long-acting antiepileptic accordingly.
  3. Correct electrolytes and hypoglycaemia and monitor frequently.
  4. Nurse the patient a 45° degree angle.
  5. Aim for a higher end of normal BP and use inotropes to achieve this. If you can’t insert an arterial line, have the NIVBP cycle every couple of minutes. 
  6. In cases of trauma, blood products should be used for volume. In an atraumatic arrest, balanced solution boluses are less harmful than 0.9% saline; don’t forget that you are still likely to need blood products. 
  7. Aim for a pCO2 of 4.5-5.5 kPa; use your continuous EtCO2 monitor to titrate ventilation. 
  8. Vigilant and through history/examination to rule out NAI. Free up a member of the team to do a thorough history from the family, always suspect NAI until proven otherwise especially in children under 6 months. 
  9. Know your anaesthetic drug side-effects (atropine dilates pupils for example so impairs our ability to monitor for seizures). Primum non nocere. 
  10. Intraosseous access can be used instead of a central line, have a low threshold to insert one and do it early.
  11. Have a member of the team check-in with the family every 10-15 minutes to explain what is happening, this is a bad day at work for you but probably the worst day of their lives. 

Conclusion

Achieving ROSC is an important step to give our patients a shot at survival. In some cases, achieving ROSC can only give us enough time to prognosticate and understand that survival is not possible. In some other cases ROSC can be the stepping-stone for a good, meaningful survival with a good quality of life. To achieve that, we must be able to apply good quality post–ROSC care and aggressive, pre-emptive neuroprotection. Learn the PCAS disease process to beat the PCAS disease process.  The APLS algorithm has become the bread and butter of anyone that is involved in paediatric care. Understanding and applying the principles of post-cardiac arrest syndrome is equally vital in improving survival outcomes for our patients. Learn the pearls, use them, teach them and I guarantee that it will make a difference.

Safety Netting

Cite this article as:
Carl van Heyningen. Safety Netting, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.28803

Safety netting is a cornerstone of paediatric practice. 

Children are a vulnerable group. Their condition can deteriorate and improve rapidly. Uncertainty is inherent in paediatric emergency medicine. From the child with a fever to the infant with vomiting, it is up to us to safeguard children from harm.  

Of course, we can’t admit every child to the hospital. Nor should we. The vast majority of patients in A&E return home with reassurance. Easy right? Reassure. Give advice. Send home. Simple?

You’re at the end of a busy shift and you have a train to catch. You’ve put in blood, sweat, and tears and feel happy your last patient has a simple throat infection. You advise fluids, paracetamol for symptoms of headache and neck pain and to come back if worried. The mother is anxious, you give them a leaflet on fever and rush out the door. 

Typically, our focus is on the front door of care not the exit. Discharge care is often overlooked. Even in the best of circumstances, we are under pressure to maintain patient flow especially as our emergency departments begin to become busy again. 

The next morning, coffee in hand, you walk in the department and hear the words that strike fear into the hearts of all that hear them… 

“Do you remember that child you saw yesterday? They’re being admitted to intensive care, it looks like meningitis.”

What could you have done differently? More tests? Not necessarily needed, no? More time? They had been observed and appeared well for several hours. Senior review? You’d seen them with the Consultant and agreed on the diagnosis. Then what? 

Safety netting

Why is it important? 

Acute illness remains one of the most important causes of childhood mortality in the UK. Early illness is notoriously non-specific. Take meningitis. In only half of cases, diagnosis is made at the first presentation. So what do we do? We must educate parents about uncertainty. Discuss the potential for deterioration. Explain the importance of seeking further help if necessary. We must safety net. 

What is it?

The term was first formally described in 1987. Today, it has come to mean “advice about what to do and what to look out for to empower parents and carers to seek help if the child’s condition deteriorates further or if they need more support.”  

What else should it cover? 

In addition to the above, it is critical to cover how they should seek help, what they should expect ahead (the disease course) and when to become worried.

How should it be done? 

Whilst verbal and written formats exemplify current practice, ranging from information leaflets to printed discharge letters, audiovisual and online resources are growing in abundance. Families report wanting this varied range of approaches.

Let’s consider the options. 

Face to Face – individualized, personal but highly variable and time-dependent

TOP TIP – be adaptable (don’t just simply recite the same information each time)

Social, educational, and cultural differences may all necessitate adapting your usual spiel in order to truly achieve understanding. Remember, the parents are in an unfamiliar, often noisy, and stressful environment in addition to feeling worried about their child. Expect them to be distracted a little. 

Leaflets – standardised, quality assured but not necessarily up to date and potentially bland and uninteresting. 

TOP TIP – use leaflets to re-enforce verbal information

When taken home written materials can often act as an aide memoire.  

Audio-visual – engaging and memorable with the potential to overcome literacy and language barriers if well designed, though resource intensive and expensive upfront   

Internet, social media, websites, apps – there are many innovative methods of connecting families with health information. Our responsibility is thus to navigate the clutter, signpost reliable resources, dispel myths and thus champion true evidence based materials. 

TOP TIP – keep the message simple, it can be easy to overwhelm parents with information. 

Remember, many parents may not wish to go on the internet. A few may even not have access to it. 

Why tailor the information? 

As ever, before talking we must first listen. For example, one interview based study found a mother worrying about “their child with cough dying at night through choking on phlegm.” If we do not listen to such fears how can we expect our own advice to be heard. 

Parental priorities

Parents priorities include… 

Emotional distress (addressing this)

Physical symptoms (addressing these)

Information (providing this, particularly reassurance, diagnosis and explanation)

Care (basic care, including food drink and friendliness)

Closure (finding out what’s wrong and, where possible, going home)

An awareness of these priorities can inform our conversations, helping us to better look after our patients from their perspective.

Ok, but what is the reality?

“You don’t actually know how much of that leaflet they’re gonna actually understand, take in, comprehend… going through things step by step, listening, understanding and explaining, I think is more beneficial” (Paediatric ED doctor). 

“It’s very difficult to know ‘cause often they’ll nod their heads and say “yes I understand everything you say” and walk off and they might have no idea what we’ve just said”  (ED staff nurse). 

“If you’ve got a sick child at home and they’re moaning at you, you haven’t got the time to go on the internet… you’ve got a child hanging off your leg going, “Mummy I feel poorly, mummy I want this, mummy I want that”” (Mother).

“My doctor did give like an information leaflet… and I did read through it, because when you’ve got a sheet at least you can find time to do that” (Mother).

So how can we do it best?

After reviewing the literature and FOAMed (see further resources) here are my top tips for giving the very best safety netting advice, enjoy! 

  • Sit down – it has been shown to increase the perception of empathy 
  • Verbalize back concerns – be explicit important conditions have been excluded 
  • Explain things – share reasoning, show your process 
  • Highlight red flags – signs that necessitate reattendance
  • Be specific – ‘If x happens, do y’
  • Reinforce – provide written leaflets
  • Avoid criticism, foster understanding – put yourself in their shoes 
  • Document advice – yes, write down what you said 

And as with all good communication, ensure a quiet, private area and avoid using jargon. 

Finally, directly ask if parents understand and are happy. Don’t assume they are. 

Here is one good example to get you started… 

“…your little guy is likely to continue to have vomiting and diarrhoea. If he remains well in himself, is drinking the amount of fluid we have discussed and is having wet nappies then he is unlikely to become dehydrated. If, however, he becomes drowsy, develops a fever or fails to stay hydrated please call this number and come back to us.” 

We must stop thinking of reattendance as a failure – patients do get worse and some need to return. 

Good quality safety netting means both you and your patients can get a better nights sleep. 

References

Gill P, Goldacre M, Mannt D, Heneghan C, Thomson A, Seagroatt V and Harnden A (2013) ‘Increase in emergency admissions to hospital for children aged under 15 in England, 1999–2010: national database analysis’, Archives of Disease in Childhood 98, 328–34.

Wolfe I, Cass H, Thompson MJ, Craft A, Peile E, Wiegersma PA, Janson S, Chambers T, McKee M: Improving child health services in the UK: insights from Europe and their implications for the NHS reforms. Bmj 2011, 342:d1277.2. 

Thompson MJ, Ninis N, Perera R, Mayon-White R, Phillips C, Bailey L, Harnden A, Mant D, Levin M: Clinical recognition of meningococcal disease in children and adolescents. Lancet 2006, 367(9508):397–403.3. 

Neighbour R. The inner consultation. Lancaster: MTP Press, 1987.

NICE guideline [NG143], Fever in under 5s: assessment and initial management, November 2019

Available at https://www.nice.org.uk/Guidance/Ng143/evidence

Almond S, Mant D, Thompson M: Diagnostic safety-netting. The British journal of general practice: the journal of the Royal College of General Practitioners 2009, 59(568):872–874

Jones CH, Neill S, Lakhanpaul M, et al. Information needs of parents for acute childhood illness: determining what, how, where and when of safety netting using a qualitative exploration with parents and clinicians. BMJ Open 2014;4:e003874.

Neill SJ, Jones CH, Lakhanpaul M, et al. Parent’s information seeking in acute childhood illness: what helps and what hinders decision making? Health Expect 2015;18:3044–56. 

Austin PE, Matlack R, Dunn KA, et al. Discharge instructions: do illustrations help our patients understand them? Ann Emerg Med 1995;25:317–20.

Scullard P, Peacock C, Davies P. Googling children’s health: reliability of medical advice on the internet. Arch Dis Child 2010;95:580–2.

Mackert M, Kahlor L, Tyler D, et al. Designing e-health interventions for low-health-literate culturally diverse parents: addressing the obesity epidemic. Telemed J E Health 2009;15:672–7.

Knight K, van Leeuwen DM, Roland D, et al. YouTube: are parent-uploaded videos of their unwell children a useful source of medical information for other parents? Arch Dis Child 2017;102:910–4.

CS Cornford, M Morgan, L Risdale, Why do Mothers Consult when their Children Cough?, Family Practice, Volume 10, Issue 2, July 1993, Pages 193–196

Body R, Kaide E, Kendal S, et al. Not all suffering is pain: sources of patients’ suffering in the emergency department call for improvements in communication from practitioners, Emergency Medicine Journal 2015;32:15-20.

(15) Jones, C.H., Neill, S., Lakhanpaul, M. et al. The safety netting behaviour of first contact clinicians: a qualitative study. BMC Fam Pract 14, 140 (2013)

Jones, C.H.D., Neill, S., Lakhanpaul, M., Roland, D., Singlehurst-Mooney, H. and Thompson, M., (2014) Information needs of parents for acute childhood illness: determining ‘what, how, where and when’ of safety netting using a qualitative exploration with parents and clinicians. BMJ Open 4 (1). 

Further resources

RCPCH (2015) Facing the Future: Standards for acute general paediatric services. RCPCH.

RCPCH Safe System Framework, resources accessed 19th November 2019,  https://www.rcpch.ac.uk/resources/safe-system-framework-children-risk-deterioration

Dr. Natalie May, MBChB, MPHe, MSc, PGCert Medical Education, FRCEM, FACEM, #CommunicatED 1: Discharge & Safety Netting in ED, available at https://www.stemlynsblog.org/communicated-discharge-safety-netting/

Bruera, Eduardo & Palmer, J Lynn & Pace, Ellen & Zhang, Karen & Willey, Jie & Strasser, Florian & Bennett, Michael. (2007). A randomized, controlled trial of physician posture when breaking bad news to cancer patients. Palliative medicine. 21. 501-5.

Sarah Jarvis, Medico-legal adviser

BSc MBBS MRCGP, Playing it safe – safety netting advice, available at https://mdujournal.themdu.com/issue-archive/issue-4/playing-it-safe—safety-netting-advice

Damian Roland, BMedSci (Hons) MBBS MRCPCH, PhD, TIGHTEN UP YOUR SAFETY NET #WILTW, available at 

https://rolobotrambles.com/tightenyoursafetynet/

Safety netting – a guide for professionals and parents of sick kids from GP Paedtips

Shame. How it affects patients and their relationships with health care professionals. https://abetternhs.wordpress.com/2012/11/16/shame/ 

The febrile infant conundrum

Cite this article as:
Dani Hall. The febrile infant conundrum, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.28850

It’s fair to say that febrile infants can be challenging. Often presenting with insidious symptoms but looking reasonably okay, they may still have life-changing or life-limiting illnesses like sepsis or meningitis. You could argue that we should take the view of eliminating risk, performing septic screens on all febrile babies, and admitting for IV antibiotics until their cultures are returned. The vast majority will have a benign viral illness but at least you can rest assured you didn’t miss a seriously sick infant.

And that’s what we did when I started my paediatric training back when the dinosaurs roamed the earth – every baby under 6 months (yes, you heard it right, 6 months) with a fever got a full septic screen, including lumbar puncture, and was admitted to the ward for at least 48 hours pending cultures. But, from a health economics point of view, this is, let’s just say, perhaps not the best way to allocate healthcare resources.

Over the years, researchers have tried to rationalise our approach to febrile infants. 2013 saw the first NICE fever in under 5s guideline; a year later a group from Spain published the Step by Step approach to identifying young febrile infants at low risk for invasive bacterial infection; and last year, the PECARN group published a clinical prediction rule for febrile infants under 60 days, which had excellent sensitivity and negative predictive values to rule out serious bacterial infections.

Last month, the Spanish group published an article looking at the external validity of the PECARN rule in their dataset.

Velasco R, Gomez B, Benito J, et al. Accuracy of PECARN rule for predicting serious bacterial infection in infants with fever without a source. Archives of Disease in Childhood Published Online First: 19 August 2020

PICO image

Before we plunge into the paper, let’s stop and think about a couple of important definitions here:

Serious bacterial infection (SBI) is used to describe bacteraemia, meningitis and urinary tract infections, also including infections such as pneumonia, skin, bone and joint infections, bacterial gastroenteritis and sometimes ENT infections.

Invasive bacterial infection (IBI) are infections where bacteria are isolated from a normally sterile body fluid, such as blood, CSF, joint, bone etc. An IBI is a type of SBI in a sterile site.

Who did they study?

Velasco’s group looked back at their registry of infants with a fever without source from a busy paediatric ED (> 50,000 presentations a year) in a tertiary hospital. To match the cohort in the PECARN paper, they used the following inclusion and exclusion criteria:

Inclusion: infants younger than 60 days who presented with a recorded fever, or history of recorded fever, of >38 C over an 11 year period between 2007 (when they started measuring procalcitonin) and 2018.

Exclusion: any infants whose history and/or examination pointed towards a focus, whose results didn’t include those used in the PECARN rule (absolute neutrophil count, PCT, urine dip), who didn’t have culture results, who were critically ill on presentation or who had a past history of prematurity, unexplained jaundice, previous antibiotics or other significant past medical history.

What were they looking for?

The group were interested to see how the PECARN rule fared in their dataset by looking at how many infants were predicted to be low-risk and yet had an SBI or IBI to assess the external validity of the rule.

What did they find?

1247 infants were included in this study. Of these, 256 (20.5%) were diagnosed with an SBI, including 38 (3.1%) with an IBI.

Of the 256 infants with an SBI, 26 (10%) were considered low risk by the rule. Of the 38 with an IBI, 5 were considered low risk (13.2%) by the rule. The PECARN rule would have missed 10% of infants with an SBI.

The PECARN rule’s sensitivity dropped from 97.7% in the original study to 89.8% and specificity dropped to from 60% in the original study to 55.5%.

So, how did Velasco’s group calculate the sensitivities and specificities of the PECARN rule for different groups in their dataset? They’ve nicely shown their data in 2 x 2 contingency tables in their figures. This is the data for SBI.

Table of data from Velasco study

So, we can see that sensitivity (those patients testing positive for the SBI as a proportion of all patients who definitely have SBI) = 230 / 256 = 89.8%. This means that 10.2% are falsely negative.

Specificity (those patients who test negative for SBI as a proportion of all of those who don’t have SBI) = 550 / 991 = 55.5%. This means that 44.5% are falsely positive.

What about infants with a really short duration of fever?

When the group looked at infants with a history of less than 6 hours of fever (n=684, a little over half of the cohort), the sensitivity dropped further to 88.6%.

Why did the PECARN rule perform less well in this study?

The authors offer up a number of suggestions, some of which are outlined below.

The populations may be slightly different. Although the authors attempted to exclude ‘critically ill’ infants from this study (as the PECARN study excluded ‘critically ill infants’), a precise definition wasn’t coded in the original Spanish registry. Instead, they excluded infants from this study if they were ‘not well looking’ or admitted to ICU. Because of the way the data was coded, some critically ill infants may have been included in this study’s dataset, skewing the results.

The Spanish database was of febrile infants without a source, excluding babies with respiratory symptoms, which may explain why the rates of SBI and IBI were much higher in this study than the PECARN database of febrile infants. So, although the PECARN rule was highly sensitive in their group of febrile infants, as in this study it may not perform so well in febrile infants without a source.

This study showed that the PECARN rule performed less well in infants with a short duration of fever. Overall, infants in the PECARN study had a longer history of fever at presentation – over a third of the PECARN infants had fever >12 hours compared to 11% in this study. Over half of the infants in this study presented within the first 6 hours. Blood tests are less sensitive in the first few hours of a febrile illness and this may well partially explain why the rule performed less well outside the PECARN dataset.

It’s important not to ignore this study’s limitations. The PECARN dataset recruited infants from multiple centres, while the registry for this study came from only one ED. As this study was a secondary analysis of a dataset, a power calculation wasn’t performed. Generally, a minimum of 100 cases is recommended for validating a model, but only 38 infants in this study had an IBI.

Study bottom line

This study showed that in the Spanish dataset of infants under 60 days with a fever without source, the PECARN rule performed less well than in the original study. This was especially true for infants with a short history of less than 6 hours of fever.

Clinical bottom line by Damian Roland

In Kuppermann et al’s original 2019 study febrile infants 60 days and younger were demonstrated to be at low risk of SBIs using 3 laboratory test results: Urinalysis, Absolute Neutrophil Count (ANC), and serum procalcitonin (PCT) levels. The study was well designed and therefore compelling in providing a framework in which to manage these challenging presentations. However, with respect to knowledge translation, external validity is critical. The availability of PCT is a significant limiting factor to being able to show the PECARN approach could be reproduced internationally. While PCT is used in Europe and Australia, it’s certainly not widespread in the UK where I practice, and then it is only used routinely in a very small number of hospitals. This makes Velasco and colleagues’ work really important as they were able to replicate the requirements of the original study and helps answer an important question: should centres start introducing PCT into their diagnostic pathology panels? The results of this study will be interpreted differently by different observers as ultimately the question is of risk tolerance. Personally, a 10% false-negative rate (if this is indeed the case) for an outcome that could result in long term disability feels uncomfortable. Counselling a parent that they could return home without treatment knowing this would probably be quite challenging. I am not sure many departments would be rushing to buy point of care PCT.

However, there are two very important caveats.  Firstly, is the validation cohort different from my own local cohort? The prevalence of disease has a huge bearing on the accuracy of any test. Knowing the local incidence of SBI and IBI in your own institution is important (but actually getting the numbers is harder than you may think!). It is likely that the PECARN approach may perform more effectively in other centres. Importantly the original paper highlights that implementation may be more effective in the second month of life due to the impact of HSV and other peri-natal infections present at 0-30 days. Secondly, what is the threshold for undertaking the blood tests in the first place? Fever in an infant less than 3 months is an interesting area as it’s one of the very few presentations in which a solitary symptom or sign is independently predictive of risk. Regardless of how the child appears to a health care professional, there is a risk of SBI and IBI (of anywhere between 2-10%) just by having a fever. This does mean that sometimes there is variation in approaches when there is a history of fever rather than a documented fever (for fear of not wanting to do a battery on tests on a neonate who in front of you appears completely well and has normal observations). But more importantly, this has led to an approach where although blood tests are taken, the results are often disregarded as an LP will be done and antibiotics will be given regardless. There are many cultural practices that have evolved around the management of the febrile neonate both within individuals and institutions. While in a study situation these are controlled for, their influence in the real world can not be underestimated and this is why it’s so important we have some pragmatic studies in this area.

This study makes me more determined to define our incidence of SBI locally and work out what impact new approaches to management may have. I think all centres should probably be doing this. However knowing the potential uncertainty in the sensitivity of the PECARN approach means it’s unlikely to be adopted in the immediate future without further validation.  

**post blog addendum 1st September 2020**

While this blog was in post production phase Kuppermann and colleagues have released further data on implementing their original predictive rule. This work has been summarised by Dr. Kuppermann below (click on to go to the original thread) and provides useful context to the discussion about external validity and implementation – DR.

Prehospital analgesia: part 2

Cite this article as:
Joe Mooney + Dani Hall. Prehospital analgesia: part 2, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.27501

You’re in the rapid response vehicle, having just handed over a 2 year old with a femoral fracture. As you clear the hospital, a call comes in: 8 year old, fall from slide, deformed left arm, conscious and breathing. When you arrive in the house you find him lying on the sofa, with bruising and deformity of his left elbow. The paracetamol and ibuprofen given by his mother has not controlled his pain*, so you take out a methoxyflurane inhaler and explain to him to suck in and blow out through ‘the whistle’. After a few breaths he begins to relax.

Methoxyflurane is a fluorinated hydrocarbon, used as an inhaled anaesthetic in the ’60s and early ’70s, until it fell out of favour after case reports describing renal failure at anaesthetic doses. But, when given in small doses, methoxyflurane has excellent analgesic properties, with no nephrotoxic side effects. It has been used extensively in Australia and New Zealand by prehospital clinicians as a self-administered analgesic for short-term pain relief in adults and children. After being licenced in 2015 in the UK and Ireland for the emergency relief of moderate to severe pain in conscious adults with trauma, methoxyflurane was included in the Irish prehospital CPG for EMTs, paramedics and advanced paramedics with permission under the seventh amendment to allow its use in children.

Added as a liquid to a Penthrox® inhaler, methoxyflurane vaporises, to be inhaled on demand. It has revolutionised prehospital pain control due to its quick onset and easy, pain free administration and, because of its light weight, crews can carry it over rough ground easily. Known as ‘the green whistle‘, each 3ml dose is quoted to last between 20 and 30 minutes, but in practice can sometimes last up to 45 minutes or an hour, depending on a child’s respiratory rate and depth and the way in which they self-administer. The Irish prehospital CPGs allow two inhalers to be administered in 24 hours to a patient, so when there’s an extended journey time, methoxyflurane inhalers used back-to-back can provide up to two hours of analgesia, which can be supplemented by the simple analgesics, paracetamol and ibuprofen, or morphine, fentanyl and ketamine, as needed.

But what’s the evidence for methoxyflurane in children?

Pop methoxyflurane in the PubMed search bar, and a lot comes up. It’s safe, it works, but there are surprisingly few randomised controlled trials (RCTs) that include children. A couple of observational studies are noteworthy. An Australian study in the prehospital setting, published in 2006 by Franz Babl and colleagues, describes an observational case series of 105 children, ranging in age from 15 months to 17 years, who received methoxyflurane while by being conveyed to hospital by ambulance. The children’s pain scores dropped from 7.9 to 4.5, with few side effects, although there was a tendency towards deep sedation in the under 5s. The following year Babl’s team published an ED-based observational case series of 14 children aged 6 to 13 years with extremity injuries who received methoxyflurane for painful procedures in the hospital setting. Although methoxyflurane was a useful analgesic agent, Babl’s team found it did not work as well as a procedural analgesic for fracture reduction.

The first double-blind RCT of methoxyflurane in children was published almost two decades ago by Chin et al in 2002. Forty-one children over the age of 5 with upper limb fractures were randomised to receive either methoxyflurane or placebo. Unsurprisingly, methoxyflurane resulted in a lower pain score at 10 minutes than placebo. Adverse events weren’t reported, but the apparent safety and efficacy of methoxyflurane demonstrated in this study paved the way the some bigger and better RCTs.

A better known, and more recent, RCT involving children was the STOP! trial, published in the EMJ in 2014. This randomised, double-blind placebo-controlled trial was conducted at six EDs in the UK. Three hundred patients, 90 between the ages of 12 and 17, with minor trauma (such as burns, fractures, dislocations and lacerations), were randomised to receive either methoxyflurane or saline via an inhaler. In a nifty way to keep the patients, doctors and nurses blinded to which drug was being administered, a drop of methoxyflurane was added to the outside of every inhaler so both drug devices smelled the same. Pain scores dropped significantly lower in the methoxyflurane group, with a median onset of action of 4 minutes. But what about those adolescents? Although 45 12 to 17 year olds were included in each group, their data wasn’t analysed separately, and children under the age of 12 were excluded from the study, so although we can probably assume methoxyflurane works well and is safe in adolescents, more trials would be helpful.

Segue to the Magpie trial, which is currently recruiting in the UK and Ireland via the PERUKI network. This international multi-centre randomised, double-blind placebo-controlled trial is specifically investigating the efficacy and safety of methoxyflurane in children and young people so that its UK license can be extended to include children. Like STOP!, participants are being randomised to either methoxyflurane or placebo (again saline) via an inhaler. To ensure younger children are well represented in the study data, the study team are aiming to recruit higher numbers of 6 to 11 year olds than adolescents, with a recruitment target of 220 children and adolescents in total. We’re awaiting the results eagerly…


*A top tip on top up dosing

This child had been given 500mg of paracetamol and 280mg of ibuprofen by his mother before the crew arrived. He was 8 years old, with an estimated weight of 31kg. Based on Irish CPGs allowing a paracetamol dose of 20mg/kg (620mg) and ibuprofen dose of 10mg/kg (310mg) he was underdosed. It’s important to top-up simple analgesics as part of your approach to pain relief in children.


But what happened to the 8 year old?

You check CSMs (circulation, sensation and movement) before and after applying a splint and transfer him to the ambulance on a stretcher. His pain is very well controlled, and he asks his mother to take a photo for his friends. This sentence is hard for him to say and he gets the giggles. You transfer him uneventfully to hospital where he’s diagnosed with a supracondylar fracture.

Read more about assessing pain, prehospital analgesia in children and the evidence behind intranasal fentanyl in part 1 of the DFTB prehospital analgesia series.

References

Hartshorn, S., & Middleton, P. M. (2019). Efficacy and safety of inhaled low-dose methoxyflurane for acute paediatric pain: A systematic review. Trauma21(2), 94–102. https://doi.org/10.1177/1460408618798391

Babl FE, Jamison SR, Spicer M, Bernard S. Inhaled methoxyflurane as a prehospital analgesic in children. Emerg Med Australas. 2006;18(4):404-410. doi:10.1111/j.1742-6723.2006.00874.x

Babl FE, Barnett P, Palmer G, Oakley E and Davidson A. A pilot study of inhaled methoxyflurane for procedural analgesia in children. Pediatric Anesthesia. 2007;17:148-153. doi:10.1111/j.1460-9592.2006.02037.x

Chin, R, McCaskill, M, Browne, G A randomized controlled trial of inhaled methoxyflurance pain relief in children with upper limb fracture. J Paediatr Child Health 2002; 38: A13–A13.

Coffey F, Wright J, Hartshorn S, et al. STOP!: a randomised, double-blind, placebo-controlled study of the efficacy and safety of methoxyflurane for the treatment of acute pain. EMJ 2014;31:613-618

Hartshorn, S., Barrett, M.J., Lyttle, M.D. et al. Inhaled methoxyflurane (Penthrox®) versus placebo for injury-associated analgesia in children—the MAGPIE trial (MEOF-002): study protocol for a randomised controlled trial. Trials 20, 393 (2019). https://doi.org/10.1186/s13063-019-3511-4

POCUS: Russ Horowitz and Cian McDemott at DFTB19

Cite this article as:
Team DFTB. POCUS: Russ Horowitz and Cian McDemott at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.22174

Where would the world of paediatrics be without POCUS? We’d still be trying (and failing) to cannulate chubby toddlers by feel alone, we’d still be using radioactive waves to determine if the child in front of us has pneumonia and we wouldn’t have this eye-opening talk from Russ and Cian.

©Ian Summers

 
Russ and Cian co-ordinated the wonderful pre-conference ultrasound workshop in London.  Here is one of our favourite pearls is you want to help identify the bladder before performing a SPA. The bladder, looking just like a slice of toast, makes the perfect target.
 
 
 
If this talk has whetted your appetite then why not sign up for one of the www.dftb20.com ultrasound workshops.

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal.

If you want our podcasts delivered straight to your listening device then subscribe to our iTunes feed or check out the RSS feed. If you are more a fan of the visual medium then subscribe to our YouTube channel. Please embrace the spirit of FOAMed and spread the word.

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Selected References

Sii F, Barry RJ, Abbott J, Blanch RJ, MacEwen CJ, Shah P. The UK Paediatric Ocular Trauma Study 2 (POTS2): demographics and mechanisms of injuries. Clinical ophthalmology (Auckland, NZ). 2018;12:105.

Haemolytic Uraemic Syndrome

Cite this article as:
Jennifer Watt. Haemolytic Uraemic Syndrome, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.26233

What is HUS?

Haemolytic Uraemic Syndrome is a combination of findings which involves the triad of:

  • Microangiopathic haemolytic anaemia with red blood cell fragmentation on blood film
  • Acute renal failure
  • Thrombocytopenia

 What causes HUS?

About 90% of cases follow an infection, most commonly with entero-haemorrhagic E. Coli (EHEC). Other infective causes to be considered include Shigella and Streptococcus pneumoniae.

These infections are commonly contracted by the ingestion of contaminated food or water sources. In the US and UK, E. Coli 0.157 forms part of the natural intestinal microflora of cattle and sheep, therefore infection can be caused by direct contact with animal faeces. This can take place at farms or petting zoos, or via undercooked contaminated meat or dairy products.

The other 10-15% of cases represent atypical HUS and are due to a variety of causes, which will not be discussed here.

How do children present?

In children infected with EHEC about 10-15% of them will go on to develop HUS.

The common presentation includes bloody diarrhoea +/- cramping abdominal pain, fever and/or vomiting. The average onset of HUS after development of diarrhoea is about 7-10 days, with children under the age of 5 at highest risk.

Dependent on the extent of HUS progression, children may present with pallor, oedema, lethargy, or reduced urine output.

How to approach the examination

As with any unwell child, an A to E assessment is critical to rule out any immediate, life threatening complications.

Specific attention should be paid to assessing their fluid status, especially for evidence of dehydration.

*Although they may be oedematous, it is important to assess if they are intra-vascularly dry.

Things to examine for:

  • Prolonged capillary refill time
  • Observations: Tachycardia; hypotension or hypertension
  • Are they are cool peripherally?
  • Assess fontanelle tension (if applicable)
  • Dry mucus membranes/reduced skin turgor
  • Oedema (common locations in children include lower limbs, sacral and peri-orbital)

Is there evidence of neurological sequelae?

  • Irritable/restlessness
  • Confusion
  • Reduced GCS

Key investigations to perform

A. Initial blood samples:

  • Full blood count with blood film to assess for RBC fragmentation
  • Coagulation
  • Group and Save +/- cross match if haemoglobin low
  • Biochemistry: U&Es, calcium, phosphate, magnesium, bicarbonate
  • Glucose
  • CRP
  • Liver function including albumin
  • Amylase/Lipase (hospital dependent)
  • LDH
  • Blood gas
  • Blood cultures

B. Stool MC&S + E. Coli PCR

C. Urinalysis + MC&S

How to approach the management of HUS

Management should always be discussed with your local paediatric nephrologist in order to individualise/optimise management.

This is a generalised framework for the approach to management. Treatment involves supportive therapy to allow time for the infection to clear and the HUS process to cease.

1. Fluid Management:

  • IV access
  • Assess fluid status
  • Monitor for electrolyte disturbances and correct as per local guidelines
  • Daily weight, In/Out fluid balance, close monitoring of patient observations

*Fluid rehydration should be administered cautiously and in the setting of oliguria/anuria and oedema, fluids given should not exceed insensible loss + urine output.

*Evidence has shown that children presenting to hospital with dehydration in the prodromal phase of EHEC-induced HUS have a higher risk of developing an oliguric AKI and the requirement for dialysis. The administration of isotonic fluid in this phase has shown to be nephroprotective. 

2. Hypertension:

  • Can be secondary to fluid overload or as a result of the HUS process
  • Trial of diuretics or if receiving dialysis, fluid can be offloaded
  • If unresponsive to diuretics, consider a vasodilator (For example, amlodipine/ nifedipine *hospital dependent)

3. Anaemia:

  • Target Haemoglobin: 70-100g/L
  • Avoid excessive transfusion due to the associated risk of development of hyperkalaemia or fluid overload

4. Thrombocytopenia:

  • Consideration for platelet transfusion if platelets <10 x109
  • If undergoing surgery may require platelets > 50 x 109

5. Abdominal pain/vomiting:

  • Secondary to colitis
  • Regular paracetamol for pain relief
  • Avoid opiates if possible due to constipating side effects

*NSAIDS like Ibuprofen should not be prescribed*

6. Nutrition:

  • All patients should be reviewed by a dietician
  • NG tube and feeding regime

7. Dialysis (Peritoneal Dialysis or Haemodialysis) Indications:

  • Intractable acidosis
  • Diuretic resistant fluid overload
  • Electrolyte abnormalities Hyperkalaemia
  • Symptoms of uraemia

In children with HUS, peritoneal dialysis is the preferred treatment option as it is a gentler form of dialysis.

Haemodialysis is indicated for children with severe colitis, severe electrolyte abnormalities and those with neurological complications.

 HUS Complications

  • AKI:  Oliguria/anuria; hyperkalaemia; hypertension
  • Neurological: Irritable, confusion, seizures
  • Bleeding Risk
  • Cardiac: Hypertensive cardiomyopathy/myocarditis
  • Gastrointestinal: Severe colitis with bleeding/perforation
  • Pancreatitis
  • Pulmonary oedema

Selected references

Mayer CL, Leibowitz CS, Kurosawa S and Stearns-Kurosawa DJ. Shiga Toxins and the Pathophysiology of Hemolytic Uremic Syndrome in Humans and Animals. Toxins (Basel). Nov 2012. [Cited June 2020]; 4 (11): 1261-1287. doi: 10.3390/toxins4111261

Kausman. J 517 Haemolytic uraemia syndrome. Royal Hospital for Children- Nephrology. Dec 2013. [Cited June 2020]; Available from:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509707/

Hughes D. Management and investigation of bloody diarrhoea and haemolytic uraemic syndrome [draft].  GG&C Paediatric Guidelines- Kidney Diseases. Oct 30 2019. [Cited June 2020]; Available from: https://www.clinicalguidelines.scot.nhs.uk/ggc-paediatric-guidelines/ggc-guidelines/kidney-diseases/management-and-investigation-of-bloody-diarrhoea-and-haemolytic-uraemic-syndrome-draft/

Balestracci A et al. Dehydration at admission increased the need for dialysis in hemolytic uremic syndrome children. Pediatr Nephrol. 2012. [ Cited June 2020];27: 1407-1410. Doi: 10.1007/s00467-012-2158-0

Scheiring J. Andreoli SP. Zimmerhackl LB. Treatment and outcome of Shiga-toxin-associated hemolytic uremic syndrome (HUS). Ped Neprhrol. 2008. [Cited June 2020]; 23: 1749-1760. Doi: 10.1007/s00467-008-0935-6

Grisaru Silviu. Management of hemolytic-uremic syndrome in children. Int J Nephrol Renovasc Dis. 2014 [Cited June 2020]; 7: 231-239. Doi: 10.2147/IJNRD.S41837.

Metabolic presentations part 1: neonates

Cite this article as:
Taciane Alegra. Metabolic presentations part 1: neonates, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.28423

You are working in the Paediatric Emergency Department and are called in to see a neonate with a history of irritability and seizures. You enter the room and are told the following: “Emma is a 3 day old, term baby who has been refusing feeds and crying excessively. Her mother says she has been irritable since birth. There has been no history of fever or cough. At home she had seizure-like activity with tonic posturing”. When you examine her, you find an awake, extremely irritable baby with flexed upper limbs flexed, extended lower limbs and global hyperreflexia. She is not dysmorphic and has no cardiac murmurs, respiratory distress or abdominal organomegaly.

Babies cry (a lot!) and we all know that, however Emma is presenting some red flags: she’s irritable and has an acute onset of seizures, without any obvious trigger.

The basics

In this post we will discuss some acute metabolic presentations in the neonatal period, how to identify potential problems and emergency treatment in the ED. You don’t need to make a diagnosis (bonus points if you do) but do need to remember that spotting the zebra will lead to more favourable outcomes. Metabolic diseases / disorders are also called inborn errors of metabolism (IEM).

How common are metabolic conditions?

Individually, metabolic conditions are rare, most having an incidence of less than 1 per 100,000 births. However, when considered collectively, the incidence may reach 1 in 800 to 1 in 2500 births (Applegarth et. al, 2000; Sanderson et.al, 2006). 

Remember: some symptoms can be unspecific and can mimic sepsis; or a child with an undiagnosed metabolic condition can decompensate with an intercurrent infection. 

An easy-to-understand classification by Saudubray divides the IEM in three groups of disorders, depending on how they present. 

Intoxication disorders

An acute or progressive intoxication from the accumulation of toxic compounds, usually small molecules. 

These usually present with a symptom-free interval and clinical signs of ‘intoxication’, which may be acute, although can be intermittent.

  • disorders of amino acid catabolism: e.g. phenylketonuria, maple syrup urine disease, homocystinuria, tyrosinemia 
  • most organic acidurias: e.g. methylmalonic, propionic, isovaleric acidaemia
  • urea cycle defects: e.g. Ornithine transcarbamylase deficiency (OTC deficiency), Citrullinemia type I (ASS1 deficiency).
  • sugar intolerances: galactosemia
  • metals: Wilson’s, Menkes, hemochromatosis
  • porphyrias

Disorders involving energy metabolism

A deficiency in energy production or utilization, within the liver, myocardium, muscle, brain or other tissues. 

Common symptoms include hypoglycemia, hyperlactatemia, hepatomegaly, failure to thrive and cardiac failure. 

  • Mitochondrial defects: congenital lactic acidemias (defects of pyruvate transporter, pyruvate carboxylase, pyruvate dehydrogenase, and the Krebs cycle), mitochondrial respiratory chain disorders and the fatty acid oxidation defects (MCAD deficiency).
  • Cytoplasmic energy defects: disorders of glycogen metabolism (collectively known as glycogen storage diseases), hyperinsulinism.  

Complex molecules disorders

Problems in the synthesis or catabolism of complex molecules, leading to storage of big molecules. 

Symptoms are chronic, progressive and independent of intercurrent events or food intake. 

  • Mucopolysaccharidosis (I-IV, VI and VII). The eponymous names are used less frequently now, particularly in the literature, but you might come across them in clinical practice (MPS I, Hurler’s Syndrome; MPS II, Hunter’s Syndrome; MPS VI, Maroteaux- Lamy) 
  • Gaucher disease
  • Peroxisomal disorders: e.g. X-linked adrenoleukodystrophy (X-ALD) and Zellweger’s Syndrome.

Treatment strategies

Remember your biochemistry: a substrate is transformed by an enzyme into a product .

If there is a problem with the enzyme, the substrate will accumulate. If this substrate accumulation is a problem, we eliminate it, like avoiding protein in the diet or removing toxins with treatments such as ammonia scavengers.  If a lack of the product is the problem, we can supplement it (for example the administration of carbohydrate in glycogen storage disease). And for some diseases the  enzyme can be “corrected” with organ transplantation or enzyme replacement therapy.

A bonus on smells

Due to accumulation of “unusual” products in their body fluids, people with certain metabolic conditions have distinctive odours (better observed in urine, for practical reasons):

  • Maple syrup, burnt sugar, curry: Maple syrup urine disease
  • Sweaty feet: glutaric aciduria type II, isovaleric acidaemia
  • Cabbage: tyrosinemia
  • Mousy, musty: phenylketonuria
  • Rotting fish: trimethylaminuria
  • Swimming pool: Hawkinsinuria 

Back to Emma. You explain to Emma’s mother that there are lots of things that could be making her unwell so you’re going to send some tests to help work out what the problem is. You put in a cannula, take a gas, send some bloods to the lab and set her and her mother up to collect a urine.

Seeing that Emma has a metabolic acidosis on her gas you send a metabolic screen: plasma amino acids, urine organic acids, acylcarnitine profile. Her urine dip has some ketones but is otherwise unremarkable, except for a strange smell of sweaty feet…

Remembering a fabulous infographic about the importance of calculating the anion gap in children with a metabolic acidosis (and how to interpret them!), you get out your pen and paper and do the following calculations: 

Just as you’re pondering the causes of a raised anion gap, the lab phones with Emma’s blood results… Her ammonia is 184!

Emma has an acute neurological presentation, with metabolic acidosis, increased anion gap and mildly elevated ammonia, suggestive of an organic acidaemiaIn the context of a sick neonate with a raised anion gap, a normal lactate and normal ketones, think organic acids.

Are you familiar with ammonia?

A normal ammonia level is <50 mol/l but mildly raised values are common, up to 80 mol/l.

In neonates, any illness may be responsible for values up to 180 mol/l.

Artifactually high values can be caused by muscle activity, haemolysis or delay in separating the sample. Capillary samples are often haemolysed or contaminated and therefore should not be used.

There’s debate as to whether a level of >100 or 200 should be discussed with a metabolic specialist, but if in doubt, follow the RCPCH DeCon guideline and seek advice for any patient presenting with a level >100 mmol/l.

Urine organic acids and blood acylcarnitines will also be sent as part of this baby’s metabolic work-up. Although the results won’t be available in ED, the urine organic acid profile will confirm a diagnosis of an organic acidaemia, while the blood acylcarnitine profile will support the diagnosis as the organic acids conjugate with carnitines creating compounds such as isovalerylcarnitine.

The emergency treatment of suspected organic acidaemias

It’s important to think about your differentials. Sepsis is the most common – these conditions can mimic sepsis, or decompensation can be triggered by an infection, always cover with broad spectrum antibiotics. But don’t forget non-accidental injury and other differentials – the baby is likely to need a CT head if presenting encephalopathic or with seizures. If she continues to seize, load with an anticonvulsant.

 Specific emergency treatment of her metabolic presentation requires:

  • stopping sources of protein (milk)
  • avoiding catabolism (by giving glucose IV – 2mL/kg 10% glucose) 
  • rehydration (IV fluids resuscitation and maintenance)

What about that urine?

The “sweaty feet” smell of the urine points towards the diagnosis of Isovaleric Acidaemia. Remember that this condition can be part of the Newborn Screening in some countries (Ireland, UK, Australia, New Zealand).

Isovaleric acidaemia is a type of organic acidemia, inherited in an autosomal recessive way. It is caused by a problem with the enzyme that usually breaks down the amino acid leucine. This amino acid accumulates and is toxic at high levels, causing an ‘intoxication’ encephalopathy. The sweaty feet smell is stronger without treatment or  during acute exacerbations.

Maple Syrup Urine Disease (MSUD) is another organic acidaemia, associated with sweet smelling urine during decompensation. These children cannot break down leucine, valine and isoleucine. They may not have hypoglycaemia, hyperammonemia or acidosis and, if not picked up on newborn screening, can be diagnosed late, resulting in neurological sequelae.

Organic acidaemias: the take homes

  • Always measure the anion gap and send an ammonia sample in any sick neonate.
  • Sick neonates with metabolic acidosis, increased anion gap and mildly elevated ammonia may have an organic acidemia.
  • Treatment is to stop feeds, prevent catabolism with 10% dextrose (and standard electrolytes for IV maintenance) and cover for sepsis with IV antibiotics, whilst considering other differentials.

The next case feels like déjà vu…

The next baby you see is remarkably like Emma but with a subtle difference. Lucy is a 3 day old baby, presenting with poor feeding, irritability and seizures at home. There has been no fever, cough, coryza, or sick contacts. On examination she’s awake, extremely irritable, with upper limbs, extended lower limbs extended and global hyperreflexia. She has no dysmorphic features, cardiac murmur or abdominal organomegaly. You notice that she seems tachypnoeic at 70, although her lungs are clear. The rest of her observations are normal. 

The key differences between Emma and Lucy’s presentations is that Lucy is tachypnoeic and has a respiratory alkalosis; this should make you suspicious of hyperventilation. Always check an ammonia level in sick babies, but particularly in this case as hyperammonemia stimulates the brain stem respiratory centre, causing hyperventilation and, as consequence, respiratory alkalosis. 

The lab phones you with Lucy’s ammonia result…

Acute neurological presentations, with respiratory alkalosis and extremely elevated ammonia point towards a urea cycle disorder. Respiratory alkalosis is a common early finding caused by hyperventilation secondary to the effect of hyperammonemia on the brain stem, although later the respiratory rate slows as cerebral oedema develops and an acidosis is seen. Lucy also has a low urea and mildly deranged liver enzymes and INR, all of which support the diagnosis of a urea cycle disorder.

The emergency treatment of suspected urea cycle disorders

Overall the acute treatment is similar to the first case: cover for sepsis, manage seizures and consider differentials.

And as in the first suspected metabolic case:

  • stop sources of protein – stop feeds 
  • avoid catabolism – giving glucose IV – 2mL/kg 10% glucose 
  • rehydrate – IV fluids resuscitation and maintenance

In urea cycle disorders, the toxic metabolite is ammonia, so ammonia scavengers are used, all given intravenously:

  • sodium benzoate
  • phenylbutyrate 
  • arginine

A nice guideline on the management of hyperammonemia secondary to an undiagnosed cause can be found on the British Inherited and Metabolic Disease Group website.

Urea cycle disorders are autosomal recessive inborn errors of metabolism. A defect in one of the enzymes of the urea cycle, which is responsible for the metabolism of nitrogen waste from the breakdown of proteins, leads to an accumulation of ammonia as it cannot be metabolised to urea. The urea cycle is also the only endogenous source of the amino acids arginine, ornithine and citrulline.   The most common urea cycle disorder is Ornithine Transcarbamylase (OTC) deficiency. Unlike the other urea cycle disorders (which are autosomal recessive), OTC deficiency is x-linked recessive, meaning most cases occur in male infants. Female carriers tend to be asymptomatic.

CPSI: Carbomoyl Phosphate Synthetase; OTC: Ornithine Transcarbamylase; ASS: Arginosuccinate Acid Synthase; ASL: Arginosuccinate; ARG: Arginase

Classically, urea cycle disorders present in the neonatal period with vomiting, anorexia and lethargy that rapidly progresses to encephalopathy, coma and death if untreated. In these circumstances, ammonia accumulates leading to a very high plasma ammonia. 

Children presenting in infancy generally have less acute and more variable symptoms than in the neonatal period and include anorexia, lethargy, vomiting and failure to thrive, with poor developmental progress. Irritability and behavioural problems are also common. The liver is often enlarged but, as the symptoms are rarely specific, the illness is initially attributed to many different causes that include gastrointestinal disorders. The correct diagnosis is often only established when the patient develops a more obvious encephalopathy with changes in consciousness level and neurological signs. 

Adolescents and adults can present with encephalopathy and or chronic neurological signs. 

What are ammonia scavengers?

In urea cycle defects, ammonia cannot be converted to urea so instead is converted to glutamine and glycine. 

Ammonia scavengers phenylbutyrate and sodium benzoate offer alternative pathways for ammonia excretion through urinary pathways.

Phenylglutamine and hippurate are produced and are excreted in urine.

Urea cycle disorders: the take homes

  • Always measure the anion gap and send an ammonia sample in any sick neonate.
  • Sick neonates with respiratory alkalosis, normal anion gap and very elevated ammonia may have a urea cycle defect. 
  • Emergency treatment of urea cycle disorders is the same as for an organic acidaemia (stopping feeds, starting dextrose and rehydrating) PLUS intravenous ammonia scavengers.

Thank you to Dr Roshni Vara, Consultant in Paediatric Inherited Metabolic Disease at the Evelina London Children’s Hospital for her help with this post.

References

Adam , HH. Ardinger, RA. Pagon, S. E. Wallis, L. J. H. Bean, K. Stephens, & A. Amemiya (Eds.), GeneReviews® [online book].

Applegarth DA, Toone JR, Lowry RB. Incidence of inborn errors of metabolism in British Columbia, 1969-1996. Pediatrics. 2000 Jan;105(1):e10.

Sanderson S, Green A, Preece MA, Burton H. The incidence of inherited metabolic disorders in the West Midlands, UK.Arch Dis Child. 2006 Nov;91(11):896-9. 

Saudubray J-M, Baumgartner MR, Walter JH. (editors) Inborn Metabolic Diseases. Diagnosis and treatment. 6th Edition. Springer 2016. 

Elbow dislocations

Cite this article as:
Becky Platt. Elbow dislocations, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.28344

You are called to assess 14-year old Oliver who has presented to your ED by ambulance with an elbow injury.  He dived to make a save while playing football and landed on his outstretched hand.  He reports feeling a click in his elbow, followed by excruciating pain.  He was given methyoxyflurane in the ambulance which has helped. 

Assessment of any child and examination of their elbow should be approached in an age-appropriate and systematic way.  In addition to examining for bony tenderness, vascular and neurological status should be tested.

Oliver’s elbow looks significantly swollen, deformed and bruised.  You feel for a radial pulse – it’s there – and  undertake a neurovascular assessment, which is intact.  You prescribe him some intranasal fentanyl and order AP and lateral x-Rays of his elbow.

The elbow is an incredibly stable joint due to the way the humerus and ulna articulate (giving anterior-posterior and varus-valgus stability), strengthened by the medial and lateral collateral ligaments and the joint capsule.  Muscles and tendons further strengthen this ring.  A significant amount of force is needed to dislocate the elbow. 

Traumatic dislocation of the elbow is rare in the paediatric population comprising only 3-6% of all childhood elbow injuries, but the most common large joint dislocation (Lieber et al., 2012).  It is usually the result of a fall onto an outstretched hand, often with a large amount of force involved.  

Clinically, it is obvious that there is significant injury around the elbow; this is not something you will miss or be tempted not to x-ray.  Displaced supracondylar fractures can sometimes be confused with elbow dislocation as both present with a grossly swollen elbow and significant pain.  A quick and easy way to distinguish the two clinically is to palpate for the equilateral triangle formed by the olecranon and the two epicondyles: this is lost in elbow dislocation as the humerus creates a fullness in the antecubital fossa. There is no need to check movements in a deformed elbow but be sure to undertake a neurovascular assessment as a priority.  

The easiest way to classify simple elbow dislocations is by describing the direction of ulna dislocation in relation to the distal humerus.

Classification of elbow dislocations

90% of paediatric elbow dislocations are postero-lateral with the radiographic appearance as below:

But beware: elbow dislocations rarely present in isolation.  They often coexist with other elbow injuries. Associated fractures are likely to occur prior to closure of the epiphyses; when they are closed, collateral ligaments are likely to be ruptured (Lieber et al., 2012). The most common associated fracture is a medial epicondyle avulsion which can become incarcerated in the joint – scrutinize the elbow x-rays for associated fractures. This illustrates the importance of knowing CRITOE.

Elbow dislocation with medial epicondyl avulsion from Orthobullets.com. The white arrow points to the avulsed medial epicondyl while the red arrow shows where it has been avulsed from.

Oliver returns from x-ray and you review his films. You note the posterior dislocation but cannot see any associated fractures on Oliver’s films. You contact your orthopaedic team for further assistance.

Management

Many elbow dislocations reductions can be carried out in the emergency department with adequate muscular relaxation and appropriate analgesia.  A reasonable amount of force is often required to achieve reduction using traction on the forearm with counter-traction around the elbow.  This should be carried out or supervised by a clinician experienced in the procedure. 

Common pitfalls in elbow reduction

Be very careful to conduct a thorough neurovascular assessment before attempting reduction. The brachial artery and median nerve may become stretched over the displaced proximal ulna and ulnar nerve can become damaged when medial epicondyle avulsions complicate elbow dislocations. If a deficit is found after reduction you need to know whether it was present before you attempted relocation…

And if you can’t reduce the dislocation go back and have another look at the x-ray – it could be due to an avulsed medial epicondyle in the joint. Any elbow dislocation with an incarcerated piece of avulsed bone in the joint must be reduced in theatre and not in the ED.

Complications

Possible complications following elbow dislocation include residual limitation of the range of movement, recurrent instability, neurovascular injury, avascular necrosis of the epiphyses and degenerative arthritis. Early diagnosis and stable reduction, with fixation of concomitant fractures if necessary, are generally associated with better outcomes.  For the Emergency department clinician, it is therefore critical that children with this injury are assessed and managed with the minimum possible delay, ensuring that associated fractures are recognised and managed appropriately.

After sedation with ketamine, Oliver’s elbow is reduced in the department with a satisfying clunk signifying reduction.  His elbow is put through a full range of movement to test joint stability and an above elbow backslab applied.  You order repeat x-Rays to evaluate the position and to check for the joint spacing and any fracture fragments within the joint as this would require surgical intervention.  The post-reduction films are good and Oliver’s neurovascular assessment remains normal and he leaves your ED with a follow-up appointment in fracture clinic in a week’s time.

References

Cadogan, M. (2019) Elbow Dislocation https://lifeinthefastlane.com/elbow-dislocation/

Edgington, J. (2018) Elbow Dislocation – Pediatric.  

https://www.orthobullets.com/pediatrics/4013/elbow-dislocation–pediatric

Lieber, J., Zundel, S., Luithle, T., Fuchs, J., & Kirschner, H-J. (2012) Acute traumatic posterior elbow dislocation in children.  Journal of Pediatric Orthopaedics B. 21(5) 474-481

Rasool, M. N. (2004). Dislocations of the elbow in children. The Journal of Bone and Joint Surgery, 86, 1050–1058. 

Sibenlist, S. & Biberthaler, P. (2019) Simple Elbow Dislocations in Biberthaler, P., Sibenlist, S. & Waddell, J.P. Acute Elbow Trauma.  Fractures and dislocation injuries (eBook).  Springer

Sofu, H., Gursu, S., Camurcu, Y., Yildirim, T., & Sahin, V. (2016). Pure elbow dislocation in the paediatric age group. International Orthopaedics, 40(3), 541–545

Does Every Child With Fever Have Sepsis? Damian Roland at DFTB19

Cite this article as:
Team DFTB. Does Every Child With Fever Have Sepsis? Damian Roland at DFTB19, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.20382

Damian Roland is a Paediatric Emergency Medicine and Honorary Associate Professor, who is also the chair PERUKI (Paediatric Emergency Research United Kingdom and Ireland). Damian delivered this thought-provoking talk on guidelines, gestalt and real-world practice on behalf of Rachel Rowlands, who was unable to attend. You can follow him in Twitter at @Damian_Roland 

#doodlemed on this talk by @char_durand below

This talk was recorded live at DFTB19 in London, England. With the theme of  “The Journey” we wanted to consider the journeys our patients and their families go on, both metaphorical and literal. DFTB21 will be held in Brisbane, Australia.

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